Jim,
What’s the latest update on the trial?
Jim,
What’s the latest update on the trial?
Ya, this thread has been pretty quiet on the news front, Whats up
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Maybe a setback happened?![]()
Incorrectomundo.
The IND, now 1,500 pages, will be submitted next week.
In other news, Dr. Young formed a company that will use new technology to collect and process cord blood. Currently, the entire world supply is only enough treat a small fraction of those with SCI, not to mention other disorders. Wise will donate his share of profits to fund SCI research and trials.
Jim,
Forgive me for not being up to date with regulations but, the fda has 90 days to respond correct? Also the fact that it took longer to write the paper is that a good or bad thing? Or maybe just SOP. Anyway good luck Dr. Young and team!
I'm incomplete ASIA C and this is how I walk, using the central pattern generator, I started walking this way on my own about 6 months after my accident. In a couple of months I'll be going to Kunming to give the 6.6.6 program a try, see what happens when someone with some connection does the intense locomotive training. I've been trying to get doctors to include us incompletes in such things, more data helps everyone and answers a lot of questions in the differences between connection.
I just found out that deep brain stimulation helps Asia C and D walk practically normal in mice, yet no human tests. WHY???????? if we can get a fraction of the SCI community back to walking why are we not doing it? https://www.ncbi.nlm.nih.gov/pubmed/24154600
https://www.youtube.com/watch?v=R3iCFyjhDRs
spoke too soon, currently in trial in Switzerland. concludes in a year. god I hope this works.
https://clinicaltrials.gov/ct2/show/NCT03053791
Lee, before I took medical leave the paper was 1,000 pages, now it's 1,500. Not good or bad.
Jennifer, the following was written by Dr. Young. (Our lab has been concentrating on therapies for lumbosacral injuries.)
The lumbosacral spinal cord is located at T11-L1. It contains the neurons (gray matter) that innervate the muscles of the leg. Damage to the lumbosacral cord results in loss of gray matter including the neurons responsible for innervating muscle and the circuitry for reflexes and programmed movements. When you have flaccid paralysis, you don't have spasticity.
I believe that restoring function to lumbosacral injuries will require neuronal replacement. Neural stem cells can make neurons and some animal studies suggest that they can also replace motoneurons. There are several sources of immune-compatible neural stem cells. One is induced pluripotent stem (iPS) which can be differentiated to neural stem cells. The other is autologous call pluripotent adult stem cells which can be differentiated into neural stem cells, including the MUSE cells described by Mari Dezawa.
Please note, however, that much research still needs to be done to find out the best kind of cells to transplant to replace motoneurons, to get these cells to send axons out of the spinal cord to innervate muscle, to regenerate sensory and descending axons to connect with these neurons to reform reflex circuits, and to program the spinal cord for micturition (urination), bowel movements, walking, and other programmed motor function.
People who have injuries to L2 or lower segments will have primarily spinal root (cauda equina) injuries. These roots need to be regenerated. Axons must be coaxed to grow into the spinal cord. Motor axons must be grown from the spinal cord into the muscle. If the injury is close to the spinal cord, motoneuronal replacement may be necessary.
Finally, flaccidity (complete loss of muscle tone) usually results in marked atrophy of muscles. For a long time, clinicians thought that denervated muscles could not be restored. However, a group in Vienna has reported that very intense electrical stimulation of muscle can not only maintain but restore denervated muscles.
I know that the reversal of flaccid paralysis sounds daunting but I think that we will be surprised by how flexible the spinal cord is.
Wise