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Thread: ChinaSCINet Update

  1. #951
    Senior Member Imight's Avatar
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    Dr. Young,

    Since Dr. Zhu is already doing intensive locomotor training with individuals that haven't received stem cells, why not combine data between the 2 of you, instead of doing a separate controlled group? Your data with stem cells and ILT, and Dr. Zhu without stem cells.

  2. #952
    Quote Originally Posted by Imight View Post
    Dr. Young,

    Since Dr. Zhu is already doing intensive locomotor training with individuals that haven't received stem cells, why not combine data between the 2 of you, instead of doing a separate controlled group? Your data with stem cells and ILT, and Dr. Zhu without stem cells.
    It takes a lot of time and effort to collect data according to protocol. While Dr. Zhu of course collects data on her patients, they are not doing so on a rigorous schedule. For example, in order to have followup data on our patients, she must send a doctor-nurse team to the patients' homes for the followup exams.

    When one does clinical trials, the patients must be randomized to the therapy and control groups. You can't just use a group of patients just as controls because they paid for the therapy or did not want to join the trial. You have to get informed consent from all of them and randomize them.

    Wise.

  3. #953
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    Quote Originally Posted by Wise Young View Post
    James,

    The spinal cord ends below L1. The examination and diagnosis of injury to the lower spinal cord is quite complex and most doctors are not sufficiently experienced to do that examination properly. I have a few questions.

    How is your bladder function and anal sphincter? If you have anal sphincter tone and your bladder is spastic, this suggests that your conus (the tip of the spinal cord) is intact. In that case, you may have injured the spinal cord just above the conus (which is at L1) or the cauda equina below the conus.

    Do you have sensation in your T12 dermatome? I attach a picture of the dermatome. How is your sensation in the L1, L2, L3, L4, and L5 dermatomes? This will give you a clue as to where your injury is and whether it involves the spinal cord or cauda equina.

    Wise.
    Hi Dr Young

    Thank you for your reply. My bladder is spastic, I take vesicare which allows me to urinate less frequently, but I still go more often than normal with occasional accidents. I have sensation in my anal sphincter and can contract, but neither sensation or muscle contraction is normal. I can hold it when I need to use the restroom, unless I have diarrhea, in which case I sometimes cant feel the urge to go.

    In my left leg, I have pretty good sensation down to L4/L5 and a little bit in my foot and toes. On the right side I have pretty good sensation to about L2 and very little sensation below that.

    When I was originally diagnosed, the dr said I damage to the cauda equina, and that there was peripheral nerve damage as well as to the spinal cord. But they also said that my spinal cord was severed.

    Please let me know if you have any other questions

    James

  4. #954
    Quote Originally Posted by Oocofficial View Post
    Hi Dr Young

    Thank you for your reply. My bladder is spastic, I take vesicare which allows me to urinate less frequently, but I still go more often than normal with occasional accidents. I have sensation in my anal sphincter and can contract, but neither sensation or muscle contraction is normal. I can hold it when I need to use the restroom, unless I have diarrhea, in which case I sometimes cant feel the urge to go.

    In my left leg, I have pretty good sensation down to L4/L5 and a little bit in my foot and toes. On the right side I have pretty good sensation to about L2 and very little sensation below that.

    When I was originally diagnosed, the dr said I damage to the cauda equina, and that there was peripheral nerve damage as well as to the spinal cord. But they also said that my spinal cord was severed.

    Please let me know if you have any other questions

    James
    What is the basis for the comments that you have a severed spinal cord? Did they see this at surgery or was this something from an MRI?

    Wise.

  5. #955
    Dr. Wise,

    The researchers in Japan think they have found that they can manipulate MUSE cells into becoming neurons. You have indicated that umbilical cord blood contains close to 1% MUSE cells. Is it possible that after injecting a subject with umbilical cord blood cells, <1% of the injected cells could turn into neurons? If so, do you think that seemingly very small increase in neurons could make any difference in return of function?
    Last edited by crabbyshark; 07-02-2012 at 06:12 PM.

  6. #956
    Quote Originally Posted by crabbyshark View Post
    Dr. Wise,

    The researchers in Japan think they have found that they can manipulate MUSE cells into becoming neurons. You have indicated that umbilical cord blood contains close to 1% MUSE cells. Is it possible that after injecting a subject with umbilical cord blood cells, <1% of the injected cells could turn into neurons? If so, do you think that seemingly very small increase in neurons could make any difference in return of function?
    crabby,

    Excellent questions. Let me first define the cells that we are transplanting. We are using HLA-matched umbilical cord blood mononuclear cells (UCMBC). Umbilical cord blood contains four major categories of cells: red blood cells (RBC), platelets, neutrophils (polynuclear cells), and mononuclear cells. UCMBC are usually isolated by density centrifugation into what is called the "buffy-coat" layer, which excludes RBC, platelets, and neutrophils. Mononuclear cells include monocytes (40%), lymphocytes (30%), and other cells (macrophages, basophils, mast cells, etc.).

    Mononuclear cells contain several populations of known stem cells and progenitor cells in cord blood.
    • CD34+ cells. These are usually endothelial progenitor cells but some hematological and pluripotent stem cells may express CD34+. These are the cells that are most commonly counted in umbilical cord blood as a marker of the number of stem cells. They are usually about 0.5% of the UCBMC.
    • CD133+ cells. These are pluripotent stem cells, many of which co-express CD34+. They are generally fewer in number than CD34+ cells.
    • VSEL cells. These "very small embryonic-like" cells are believed to be pluripotent. They are usually less than CD133+ and, because of their size, often lost during the density centrifugation procedure.

    We recently found CD105/SSEA3 positive cells in umbilical cord blood. We are now trying to identify these cells. Although we believe that they are MUSE cells, we need to prove that they are pluripotent and can be expanded. If they are MUSE cells and as much as 1% of UCBMC, then this would be the richest source of MUSE cells. In bone marrow, less than 1 out of 300,000 mesenchymal cells are MUSE cells. In any case, this is work in progress but I am hopeful that these cells will be rich source of HLA-matchable pluripotent stem cells.

    Irv Weissman, a former professor of mine at Stanford, once pointed out that one does not need a huge number of stem cells to do the job. Perhaps as few as a couple hundred stem cells can repopulate the bone marrow or gut. All of this presupposes that the stem cells find a "niche" in the tissue that tells them to make tissue-appropriate cells. If they go in like embryonic stem cells or induced pluripotent stem cells and reproduce without regard to the tissue, they would create a teratoma (a stem cell tumor). If they find a niche and make only tissue-specific cells that the niche tells them to make, then they should not produce tumors.

    Umbilical cord blood is the richest source of stem cells of any adult tissue. The mononuclear cells that we are transplanting into the spinal cord of patients a high concentration of CD34+ and CD133+ cells (adding up to about 5%) and about 1% appear to be MUSE cells. We know that these cells produce neurotrophins and some of the cells respond to lithium to make more neurotrophins. That is why we chose to use these cells and lithium for our first clinical trial. We do not really expect these cells to produce neurons but we hope that the cells will "bridge" the injury site and produce neurotrophins that will stimulate growth of axons.

    On the other hand, we and others have shown that lithium stimulates the person's own neural stem cells to produce neurons. Our hope is that it will do so in those patients that received the combined therapy. That is of course why we are doing the trial. Of course, we won't be able to prove that it produces new neurons in humans since we won't be able to take spinal cord samples to confirm. On the other hand, we believe that we can see white matter growth in the spinal cord and that is why we are going to a lot of trouble to do magnetic resonance diffusion tensor imaging to visualize the white matter in the spinal cord.

    Wise.

  7. #957
    Senior Member Imight's Avatar
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    Dr. Young.

    Sorry to bother you again. I have started my own intensive locomotor training altho it's more of a 5:4:6 due to work schedule - I am a walking T4 ASIA C (forearm crutches). I noticed you said Dr. Zhu doesn't like to use the treadmill because it's a form of gait training/harness assistance? What about those that can walk without the harness and independently? Isn't it like walking on a track for us? I'm just trying to figure out how I can walk for long periods of time and where, because I don't think it's safe to walk around the block, esp since the pavements here aren't even, whereas the treadmill, I can stay on it for a good 2-3 hours nonstop and straight forward.

    I'm busy this month with moving, but I'm probably going to take a couple of days next month to head over to Kunming and have a sit down with Dr. Zhu. I'm at level V, so I should be able to do a lot of the exercises independently.

    So far I'm doing treadmill, pool walking, regular walking, and leg presses. My main problem, is my right foot is bouncy, but once that goes away I should be able to recover a lot faster. How exactly are these patients fighting such problems? spasms, spasticity, bouncy feet? are they just going away on their own or do they still have them, but since they're so recovered they can fight through them? I always thought this was all because of the nervous system, and I'm pretty sure they're learning how to walk with existing nerves (unless you mean the cns is bridging on it's own from all the training), so the nerves should still be absent and triggering these spastic issues, but if they're walking unassisted how are they fighting this? what's to keep someone who is walking from randomly getting a spasm and falling over in public, or being throw around by his own legs? I'm confused, how they're getting past something I've had MAJOR issues with and prevents me from walking despite being able to trigger most of my muscles.
    Last edited by Imight; 07-04-2012 at 01:08 AM.

  8. #958
    Quote Originally Posted by Imight View Post
    Dr. Young.

    Sorry to bother you again. I have started my own intensive locomotor training altho it's more of a 5:4:6 due to work schedule - I am a walking T4 ASIA C (forearm crutches). I noticed you said Dr. Zhu doesn't like to use the treadmill because it's a form of gait training/harness assistance? What about those that can walk without the harness and independently? Isn't it like walking on a track for us? I'm just trying to figure out how I can walk for long periods of time and where, because I don't think it's safe to walk around the block, esp since the pavements here aren't even, whereas the treadmill, I can stay on it for a good 2-3 hours nonstop and straight forward.

    I'm busy this month with moving, but I'm probably going to take a couple of days next month to head over to Kunming and have a sit down with Dr. Zhu. I'm at level V, so I should be able to do a lot of the exercises independently.

    So far I'm doing treadmill, pool walking, regular walking, and leg presses. My main problem, is my right foot is bouncy, but once that goes away I should be able to recover a lot faster. How exactly are these patients fighting such problems? spasms, spasticity, bouncy feet? are they just going away on their own or do they still have them, but since they're so recovered they can fight through them? I always thought this was all because of the nervous system, and I'm pretty sure they're learning how to walk with existing nerves (unless you mean the cns is bridging on it's own from all the training), so the nerves should still be absent and triggering these spastic issues, but if they're walking unassisted how are they fighting this? what's to keep someone who is walking from randomly getting a spasm and falling over in public, or being throw around by his own legs? I'm confused, how they're getting past something I've had MAJOR issues with and prevents me from walking despite being able to trigger most of my muscles.
    Imight,

    I am not sure that Dr. Zhu and her colleagues have solved the problem that you describe. To my knowledge, most of their work has focused on intensive locomotor training of patients during the first year after injury, to enhance the spontaneous recovery of those who are incomplete and to maximize the recovery of those with ASIA A. Regarding the latter, only half recover to the point of being able to walk without human assistance but still require the rolling cart. I don't know the Kunming results of training people with ASIA A chronic SCI but my impression is that probably very few recover substantially from the training alone, without any therapy. This is something that we need to test in future clinical trials. Our current trial does not have a locomotor training alone arm.

    The question whether intensive locomotor training would be beneficial to somebody who is incomplete and already walking but want to improve their gait, endurance, and speed was addressed by Anton Wernig in Germany over a decade ago. He reported treadmill training of people with incomplete SCI. Apparently, over 75% of the people with incomplete SCI, many of whom had never walked after injury, showed substantial improvement over several months of training and retained their training effects for more than a year afterward. But, they too have limited walking recovery, endurance, and speed. I don't think that locomotor training alone is sufficient to restore walking to normal even in so-called incomplete chronic SCI.

    Wise.

  9. #959
    Senior Member Imight's Avatar
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    Quote Originally Posted by Wise Young View Post
    Imight,

    I am not sure that Dr. Zhu and her colleagues have solved the problem that you describe. To my knowledge, most of their work has focused on intensive locomotor training of patients during the first year after injury, to enhance the spontaneous recovery of those who are incomplete and to maximize the recovery of those with ASIA A. Regarding the latter, only half recover to the point of being able to walk without human assistance but still require the rolling cart. I don't know the Kunming results of training people with ASIA A chronic SCI but my impression is that probably very few recover substantially from the training alone, without any therapy. This is something that we need to test in future clinical trials. Our current trial does not have a locomotor training alone arm.

    The question whether intensive locomotor training would be beneficial to somebody who is incomplete and already walking but want to improve their gait, endurance, and speed was addressed by Anton Wernig in Germany over a decade ago. He reported treadmill training of people with incomplete SCI. Apparently, over 75% of the people with incomplete SCI, many of whom had never walked after injury, showed substantial improvement over several months of training and retained their training effects for more than a year afterward. But, they too have limited walking recovery, endurance, and speed. I don't think that locomotor training alone is sufficient to restore walking to normal even in so-called incomplete chronic SCI.

    Wise.
    So the person you had in the bw photo, is acute? I thought most of your patients were chronic. I also thought they were walking unassisted. It sounds like you've already taken note that they DO need stem cell therapy AND her training to walk again. She's clearly not accomplishing the results without the injection.

    I guess I'm just doing this for endurance at this point. That hurts.

  10. #960
    Quote Originally Posted by Imight View Post
    So the person you had in the bw photo, is acute? I thought most of your patients were chronic. I also thought they were walking unassisted. It sounds like you've already taken note that they DO need stem cell therapy AND her training to walk again. She's clearly not accomplishing the results without the injection.

    I guess I'm just doing this for endurance at this point. That hurts.
    Let me clarify. The BW photo is just a methods photo illustrating the stages of training and the Kunming Locomotor Score (KLS), using several different patients. They have treated hundreds of patients in Kunming with the intradural decompression followed by intensive locomotor training. Close to 50% of those patients reach KLS V.

    We started the clinical trial of chronic SCI with them last fall and they transplanted 20 ASIA A chronic SCI subjects with escalating doses of umbilical cord blood mononuclear cell transplants, then the cell transplants with methylprednisolone, and then the cell transplants plus methylprednisolone plus a 6 week course of lithium. We don't have 6 month followup data from the last two groups yet. That is why I am urging people to be patient.

    I don't think that there is enough data to conclude that intensive locomotor training alone does or does not do anything for people who are chronic ASIA A SCI. I pointed out that Anton Wernig has already shown that nearly 75% of those are incomplete after injury will benefit from treadmill training. Presumably you belong to that category of people with incomplete injury.

    Wise.

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