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

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  • #61
    Dr. Silver, I don't know if you have Facebook and watch the chondroitinase dog trial or not. I see today a video was posted showing a little dog named Toby. His owners say he finished the trial 6 months ago and can now stand strong for a few seconds and holds his tail up. The video showed him moving about. Of course we have no idea who is a control and who isn't. I just want to say it's fun being able to see people post their pet dog video's and make comments about a drug we're hoping makes it to humans for clinical use. We've never had this kind of opportunity before. It's been quite amazing watching it unfold at Facebook.
    http://spinalcordresearchandadvocacy.wordpress.com/

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    • #62
      Love that on Facebook too.
      Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

      T-11 Flaccid Paraplegic due to TM July 1985 @ age 12

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      • #63
        How do i find that on fb?

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        • #64
          Dr. Silver--In your rat model, have you tried using your peptide alone without using ch'ase? If yes, any positive results? Understood what you said about using both together to get the best results.

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          • #65
            Originally posted by #LHB# View Post
            How do i find that on fb?
            https://www.facebook.com/ChondroDogs...f=ts&ref=br_tf

            The title page is "Clinical Trial for Paralyzed Dogs"

            I just see a note on one of the posts that says they are enrolling new patients until May. I think they were around 50 dogs completed the last time I looked. May would probably wrap it up pretty much if they're planning on the last 10 over the next few months or so. They were wanting a total of 60. I think they will meet that number.
            Last edited by GRAMMY; 02-22-2016, 11:06 AM.
            http://spinalcordresearchandadvocacy.wordpress.com/

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            • #66
              Originally posted by 6 Shooter View Post
              Dr. Silver--In your rat model, have you tried using your peptide alone without using ch'ase? If yes, any positive results? Understood what you said about using both together to get the best results.
              Thought he covered that in one of this vids. His peptide addresses scar ... I'm really dumbing it down though. I can barely follow him in his videos at times. lol
              Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

              T-11 Flaccid Paraplegic due to TM July 1985 @ age 12

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              • #67
                Originally posted by 6 Shooter View Post
                Dr. Silver--In your rat model, have you tried using your peptide alone without using ch'ase? If yes, any positive results? Understood what you said about using both together to get the best results.

                At acute stages following contusive SCI the peptide by itself is remarkable (Nature Lang et al, 2015). However, so far and at low doses the peptide has not been successful as a stand alone treatment for chronic contusive cord injury. Our goal is to dramatically increase the dose to see if it might work on its own but my thinking is that for chronic injury the combination approach will work best especially when we add rehab training.

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                • #68
                  Originally posted by jsilver View Post
                  OK let me have a go at these but it is difficult to pinpoint an exact timeframe.

                  The major reason that chondroitinase has not gone to clinical trials is because there has not been compelling research showing that the enzyme by itself could restore robust function
                  at chronic stages following cord injury. With our new results I hope that this will stimulate the ISRT to move forward even more rapidly. However, they are a small foundation with limited resources.
                  You might wish to contact the ISRT and get a sense of their timeline. Their new delivery system of the enzyme should be completely proprietary to the inventors. The ISRT is my bet for the clinical future of chondroitinase.

                  Our peptide strategy has a ways to go. We need to move towards a therapy that works to restore function after chronic contusive injury and show efficacy and safety with a maximum tolerated dose study.

                  These challenging experiments are now in progress.
                  Anyone contacted the ISRT (Spinal Research) yet?

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

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                  • #69
                    Not here yet. They're on Twitter and Facebook though.
                    Roses are red. Tacos are enjoyable. Don't blame immigrants, because you're unemployable.

                    T-11 Flaccid Paraplegic due to TM July 1985 @ age 12

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                    • #70
                      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.
                      Last edited by 6 Shooter; 03-27-2016, 01:46 PM.

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                      • #71
                        intermittent hypoxic therapy

                        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!

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                        • #72
                          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?

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                          • #73
                            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.

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                            • #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.

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                              • #75
                                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.

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