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Dr. Young Video; 'Why Umbilical Cord Blood Stem Cells'

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  • #16
    Originally posted by GRAMMY View Post
    There are 25.4 mm in 1 inch.
    Therefore 30mm X (1"/25.4mm) = (30/25.4) inches = 1.18 inches
    304.8 mm in one foot.
    lol, thanks. much easier just to google, how many mm in 1 ft.
    so what is the rate at which the axons will grow? is it mm a day or mm a month? a mm a day puts us regenerating at about a year. pffft, sign me up.

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    • #17
      Originally posted by Christopher Paddon View Post
      that is just under one year if a mm a day is correct

      I wonder of the tracts that the axons originally resided in remain open - scientists must have an answer - you can imagine millions of long spaghetti like holes where the axons were before they died off above and below the injury - does the spinal cord collapse on them or are the pathways left vacant?
      good questions. also, do the axons die and disappear/dissolve or something? or are they dead and just laying there?

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      • #18
        Originally posted by Christopher Paddon View Post
        that is just under one year if a mm a day is correct

        I wonder of the tracts that the axons originally resided in remain open - scientists must have an answer - you can imagine millions of long spaghetti like holes where the axons were before they died off above and below the injury - does the spinal cord collapse on them or are the pathways left vacant?

        Nerve guidance conduit
        Because of the limited functionality received from autografts, the current gold standard for nerve regeneration and repair, recent neural tissue engineering research has focused on the development of bioartificial nerve guidance conduits in order to guide axonal regrowth. The creation of artificial nerve conduits is also known as entubulation because the nerve ends and intervening gap are enclosed within a tube composed of biological or synthetic materials.[22]

        This is the scaffolding and hydrogel that the biotechs are working on to help with the guidance such as the Invivo Technology...
        http://www.invivotherapeutics.com/ou...nology/#video3
        http://www.invivotherapeutics.com/ou...nology/#video1
        http://www.invivotherapeutics.com/ou...nology/#video2
        Last edited by GRAMMY; 08-10-2011, 01:31 AM.
        http://spinalcordresearchandadvocacy.wordpress.com/

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        • #19
          that looks like a conduit across the injury site so one assumes there are long tube like sheaths remaining open where the axons used to be above and below the injury otherwise this technique wouldn't work


          I maybe misunderstanding it

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          • #20
            It's my understanding that it is indeed a "new" conduit. The old injury site isn't known to be hospitable to new growth so they're developing something different.
            http://www.invivotherapeutics.com/about-us/research/ for additional information.
            Last edited by GRAMMY; 08-10-2011, 02:01 AM.
            http://spinalcordresearchandadvocacy.wordpress.com/

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            • #21
              Originally posted by Christopher Paddon View Post
              that is just under one year if a mm a day is correct

              I wonder of the tracts that the axons originally resided in remain open - scientists must have an answer - you can imagine millions of long spaghetti like holes where the axons were before they died off above and below the injury - does the spinal cord collapse on them or are the pathways left vacant?
              Christopher,

              In earlier posts I had addressed many of these questions but these questions are usually too advanced. Understanding the answers to these questions require an understanding of the slow rate of axonal growth, the long distance of axonal growth, and the concept of neuron survival above and below the injury site. Let me first go through these three concepts and then answer your question.

              1. Rate of axon growth. Axons grow slowly. In the peripheral nerve, regeneration occurs at 1 mm/day or less. So, if you crush your ulnar nerve at the elbow and lose sensation in the fourth and fifth fingers of your hand, the axons in the ulnar nerve will regenerate but the distance (at least for my arm) is 38-40 cm. At 1 mm/day, it may take more than a year before one regains sensation. Nobody really knows how fast spinal axons grow in human but I have suggested that the rate of growth spinal axons is no faster than peripheral nerve. It may well be slower than 1 mm/day, particularly if you are older. The other comparison is the rate of hair growth. Most of us grow hair at the rate of about a mm per day when we are young and slower when we are older.

              2. Distance and barriers to axon growth. Axons usually die back to their first branch point before the injury site. This statement has multiple implications. First, most axons connect to many neurons. For example, a corticospinal neuron has branches that connects to the midbrain, the brainstem, the cervical spinal cord, and the lumbar spinal cord. So, an injury at the thoracic level will disconnect the axon from the lumbar spinal cord and the axon may die back to its first branch point in the cervical spinal cord. So, the regenerating axons must grow from the cervical spine down to the lumbar cord, in order to reconnect. On the other hand, in animal models, it is clear that most of the spinal axons will die back and then can and will grow from the first branch point to the edge of the injury site. This was one of the reasons by Jerry Silver (a very good scientist) once told me that this was why he did not believe in the Nogo theory of axon growth inhibition. After all, the axons that have died back and then regrow to the injury edge must have been growth amongst myelinated tracts and should have been inhibited. Jerry Silver showed and hypothesized that chondroitin-6-sulfate proteoglycans at the edge of the injury site stopped axonal growth. In experiments with treatments such as olfactory ensheathing glia, once axons cross the injury site, they seem to be able to keep growing, again suggesting that myelin inhibitors are not as important as originally thought. It is possible that axons grow slower in the presence of myelin growth inhibitors rather than stop altogether. Very recently, a former graduate student (Kai Liu) showed that if he shuts off a gene called PTEN in neurons, he could induce massive regeneration of the corticospinal tract in rats. This was the first time that anybody had demonstrated that the obstacles to axonal growth are not just axonal inhibitors but the presence of genes that hold back or prevent axonal growth. Finally, decades after spinal cord injury, one can see axons forming dystrophic terminals at the edge of the injury site. These terminals were once thought to be degenerating ends of terminals but is now thought of as "frustrated" growth comes. This indicates that axons are continuing to growing to the injury site and stopping at the edge, possibly due to chondroitin-6-sulfate-proteoglycans surrounding the injury site.

              3. Neuronal survival above and below the injury site. Trauma damages not only axons but neurons in the spinal cord. When the neurons are damaged, this means that axonal regeneration may not restore function. Thankfully, most of us have more neurons that we need and we continue to be able to function even if we lose 20-50% of the neurons in a given segment. Until recently, although axonal regeneration is considered to be possible, neuronal replacement was considered to be in the neverneverland of scientific fantasy. However, the discovery of neural stem cells in the late 1990's and the demonstration that they can create neurons that incorporate into the neural circuity of the brain changed this pessimism. Today, most scientists believe that neuronal replacement is also possible, although there have not been many clear examples of neuronal replacements leading to functional recovery.

              Given the above, you can perhaps understand why most neuroscientists are optimistic about the possibility of spinal cord regeneration and restoration of function. Please understand how new these are ideas are. In 1997, when I started Spinewire, we did not know the second two. In 2001, when we converted Spinewire to CareCure, we did not know the third point. IN fact, if you go back to my writings in the early days of CareCure, you will find that I was very pessimistic about neuronal replacement.

              So, back to your question concerning what happens to the places where axons have degenerated. Do the degenerated pathways "collapse"? Do regenerating axons have to make new pathways for growth? I don't know the answers to these questions but can provide some educated guesses based on what I have seen. First, degenerated tracts often remain for months after injury. Called "Wallerian" degeneration, after Waller who noted that degenerating tracts can be identified with silver stains for months or even years after injury, these tracts are very likely to remain available to axons to regrow into them. This may or may not be true years after injury but I suspect that the problem may not be loss of physical space for growth but the loss signals to tell the axon that it is growing on the right path and to keep on going.

              In the mid-1990's, I likened the journey of axons in the spinal cord to the journey of Odysseus back home. First, the Odyssesus is a long ways from home. Second, after he crosses the injury site where he had to combat a variety of monsters, including cyclops (macrophages), he has to sail past the syrens (neurons) along the way. Third, as he gets closer to home, he may stop at a place that is not his home (Circe's Island). Finally, when he gets home, he will find that many suitors have taken his place and he has to fight them off in order to get Penelope back.

              I think that we have tools to start Odysseus on his journey. Getting him home is another matter. On the other hand, much evidence suggests that the nervous system is much more plastic than we had ever thought and that intensive exercise helps strengthen desirable connections and eliminates undesirable connections. Therefore, if we get a lot of sailors (axons) growing home and they connect, they can do the job but it will require a lot of learning and practice before things work again.

              Wise.

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              • #22
                beautiful Greek mythology,Although the road ahead is still bumpy , but we have exposure to the great journey , and everyone is witness to the creation of a great part,thanks, DR.Wise

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                • #23
                  [QUOTE=Wise Young;1407537 This was one of the reasons by Jerry Silver (a very good scientist) once told me that this was why he did not believe in the Nogo theory of axon growth inhibition. After all, the axons that have died back and then regrow to the injury edge must have been growth amongst myelinated tracts and should have been inhibited. Jerry Silver showed and hypothesized that chondroitin-6-sulfate proteoglycans at the edge of the injury site stopped axonal growth. In experiments with treatments such as olfactory ensheathing glia, once axons cross the injury site, they seem to be able to keep growing, again suggesting that myelin inhibitors are not as important as originally thought. It is possible that axons grow slower in the presence of myelin growth inhibitors rather than stop altogether.

                  Finally, decades after spinal cord injury, one can see axons forming dystrophic terminals at the edge of the injury site. These terminals were once thought to be degenerating ends of terminals but is now thought of as "frustrated" growth comes. This indicates that axons are continuing to growing to the injury site and stopping at the edge, possibly due to chondroitin-6-sulfate-proteoglycans surrounding the injury site. [/QUOTE]

                  This why I think Jerry Silver's nerve graft and work with chondroitin in restoring breathing is so remarkable. I really wish this work would be taken into clinical trial and utilized.
                  http://spinalcordresearchandadvocacy.wordpress.com/

                  Comment


                  • #24
                    Dr Young if you have anwsered this question before sorry but i cant seem to find it but, how much return and function will your therapies have to show to become accepted and used in the USA. Thank You

                    Or anyone with the anwser. Thanks

                    Comment


                    • #25
                      Originally posted by #LHB# View Post
                      Dr Young if you have anwsered this question before sorry but i cant seem to find it but, how much return and function will your therapies have to show to become accepted and used in the USA. Thank You

                      Or anyone with the anwser. Thanks
                      LHB,

                      I think that almost any statistically significant effect shown in two trials (one in China and the other in the U.S.) will be sufficient as long as the treatment turns out to be safe. First, there is no other therapy known to restore function after spinal cord injury. Almost any positive benefit:risk ratio would argue for approval. Second, a statistically significant average improvement will mean that some patients will get a lot more than other patients. So, even if the average improvement may not be all that great, there will likely be individuals who will get substantial function back. Third, there is no controversy about this therapy.

                      Wise.

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                      • #26
                        Thank you and I didn't mean there was a controversy about the therapy sorry it came out wrong. At the end of the trials in the US if they prove safe and effective how long will it take to get to the public?

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                        • #27
                          Nice video. Truly moving. Thank you.
                          Dennis Tesolat
                          www.StemCellsandAtomBombs.blogspot.com

                          "Change does not roll in on the wheels of inevitability, but comes through continuous struggle. And so we must straighten our backs and work for our freedom."
                          Martin Luther King

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                          • #28
                            I hope the treatment is reasonably consistent across patients. It is such an unfair injury that it would be more injustice if the cure restored some to near normal and others gained little.

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                            • #29
                              I suppose it's the older, longer injured people who will most likely get the least back so the chances of walking again are slim

                              Comment


                              • #30
                                Originally posted by #LHB# View Post
                                Thank you and I didn't mean there was a controversy about the therapy sorry it came out wrong. At the end of the trials in the US if they prove safe and effective how long will it take to get to the public?
                                Because both umbilical cord blood and lithium are available, it should be available relatively quickly after the treatment has been approved. It would be far quicker if there were doctors in the United States who are already experienced with doing the procedure. This is of course the goal of doing the trials in the SCINetUSA, so that doctors are ready and able to implement the treatment as soon as the trials show that the treatment works.

                                Wise.

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