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  • Peripheral Nerve Growth

    I was wondering if Dr. Wise or anyone else could help me understand peripheral nerve growth. When I had my accident they had to put a rod in my left humerus. They hit my radial nerve and my hand was limp and useless. They told me peripheral nerves like the one they damaged in my arm do grow back and function again. Well, they were right. I worked with a therapist to get my hand working again and I got back about 95% function and the spot on my thumb that went numb has almost all of the feeling back. My question is why are peripheral nerves capable of repairing themselves and functioning again but nerves of the spinal cord cannot. Also, is there anyone studying why this is possible and is anyone also trying to gather information from this to see if they can learn anything from this and use the information to find out ways to help with SCI research? Or, do they know enough about it to realize nothing can be done with it? Thanks.
    Ken

    Guns don't kill people. Daddys with cute daughters do!

  • #2
    I heard because if the spinal cord had a lot of regenerating functions that it would get too crowded and chaotic. Plus scar tissue grows around the area so the little regenerating affects teh spinal cord does has is cock blocked.

    Comment


    • #3
      Originally posted by BigK View Post
      I was wondering if Dr. Wise or anyone else could help me understand peripheral nerve growth. When I had my accident they had to put a rod in my left humerus. They hit my radial nerve and my hand was limp and useless. They told me peripheral nerves like the one they damaged in my arm do grow back and function again. Well, they were right. I worked with a therapist to get my hand working again and I got back about 95% function and the spot on my thumb that went numb has almost all of the feeling back. My question is why are peripheral nerves capable of repairing themselves and functioning again but nerves of the spinal cord cannot. Also, is there anyone studying why this is possible and is anyone also trying to gather information from this to see if they can learn anything from this and use the information to find out ways to help with SCI research? Or, do they know enough about it to realize nothing can be done with it? Thanks.
      BigK, very good question. Let me take three types of nervous tissue and describe the spontaneous axonal regeneration in these tissues. Let me first describe three anatomical aspects of the motor and sensory system. First, when I use the word regeneration, I am referring to regrowth of axons (or nerve fibers) which are extensions of neurons (or nerve cells). If a neuron is killed, regeneration cannot occur from that neuron. Second, the neurons for sensory axons reside in little groups called dorsal root ganglia (DRG) that are situated just outside of the spinal cord. The DRG neurons send one branch of their axon out the peripheral nerve to the skin, muscle, bone, etc. and the other branch into the spinal cord where they contact spinal neurons and also travel up the spinal cord to the brain. Third, the neurons for muscles reside in the spinal cord where they receive signals from the brain and they send their axons through the ventral or anterior roots into peripheral nerve to muscle.

      Peripheral nerves do regenerate, particularly after compression or crush accidents like what you describe. In general, they do not regenerate as well if the nerves have been cut and a gap is allowed to be present between the two cut ends of the nerve. When the two cut ends of the nerves were re-opposed together, regeneration of about 10% of the axons take place and some limited functional recovery may occur. Both motor and sensory axons will regenerate and thus one gets back both motor and sensory function.

      Spinal roots do not regenerate as well as peripheral nerves. For example, injury to the spinal roots can occur with herniated discs pressing on them or compression or crushing of the cauda equina (below L1 of the spine) where most of the lumbosacral spinal roots are located. Such injuries generally result in limited sensory recovery and partial motor recovery. The reason why little sensory improvement occurs is because the injury is occurring to the spinal root between the dorsal root ganglia. The sensory axon from the dorsal root ganglion has to grow into the spinal cord before it can make any connections and axons will stop at the edge of the peripheral and central nervous system, called the CNS/PNS interface. Motor axons will regenerate to some extent unless the injury is close enough to the spinal cord to damage the motoneurons in the spinal cord.

      Spinal cord does not regenerate well. This does not mean that the spinal cord does not regenerate at all. I suspect that the spinal cord (particularly incomplete injuries) may regenerate. Surviving axons certainly can sprout additional branches. Regeneration takes a long time (years) and the spinal cord (particularly the injury site) is not particularly hospitable to growing axons and have proteins like Nogo and chondroitin-6-sulfate proteoglycans that stop axonal growth. Therapy is necessary to provide long-term sustained growth factor support, cells are needed to bridge the injury site, and growth inhibitor blockers are necessary to allow axons to grow long-distances.

      For many years, the reason why peripheral nerve was believed to be able to regenerate was because of the Schwann cells that myelinate axons in the peripheral nerve. In the central nervous system, the cells that myelinate axons are oligodendroglia. Each Schwann cell wraps around one segment of one axon. Each oligodendroglia may provide myelin segments to as many as 20 axons. Oligodendroglia myelin express a protein called Nogo, which stop axonal growth. For many years, scientists through that Nogo expression is the difference between peripheral and central nervous nerve growth. However, as it turns out Schwann cell myelin also expresses Nogo.

      The important difference between Schwann cell and oligodendroglial myelin is that Schwann cells in injured peripheral nerves transform into cells that look by macrophages and that scavenge myelin fragments. Oligodendroglia do not. Because they myelinate multiple axons, as long as some of the axons are still alive, the oligodendroglia myelin is still present. At the injury site, there are macrophages (mostly from blood or microglia in the spinal cord) that eat myelin fragments, although some recent studies by a colleague in my laboratory showed that microglial macrophages stop taking up myelin debris after a while because they cannot process them. In any case, in the central nervous system, the cleanup of the myelin debris is slow and inefficient. In the peripheral nerve, the myelin is cleared out and the axons are able to regenerate in the nerve.

      Finally, there is now growing evidence that certain spinal tracts do not grow as well as others. In particular, the corticospinal tract is the main spinal tract that goes from the brain to the spinal cord. A former student of mine has found out the reason why corticospinal neurons do not regenerate well and has discovered a treatment that can make them do so. This is quite exciting and I am very hopeful that this will be part of the therapies that we will be able to take to clinical trials in the coming years.

      Wise.

      Comment


      • #4
        Originally posted by Wise Young View Post
        BigK, very good question. Let me take three types of nervous tissue and describe the spontaneous axonal regeneration in these tissues. Let me first describe three anatomical aspects of the motor and sensory system. First, when I use the word regeneration, I am referring to regrowth of axons (or nerve fibers) which are extensions of neurons (or nerve cells). If a neuron is killed, regeneration cannot occur from that neuron. Second, the neurons for sensory axons reside in little groups called dorsal root ganglia (DRG) that are situated just outside of the spinal cord. The DRG neurons send one branch of their axon out the peripheral nerve to the skin, muscle, bone, etc. and the other branch into the spinal cord where they contact spinal neurons and also travel up the spinal cord to the brain. Third, the neurons for muscles reside in the spinal cord where they receive signals from the brain and they send their axons through the ventral or anterior roots into peripheral nerve to muscle.

        Peripheral nerves do regenerate, particularly after compression or crush accidents like what you describe. In general, they do not regenerate as well if the nerves have been cut and a gap is allowed to be present between the two cut ends of the nerve. When the two cut ends of the nerves were re-opposed together, regeneration of about 10% of the axons take place and some limited functional recovery may occur. Both motor and sensory axons will regenerate and thus one gets back both motor and sensory function.

        Spinal roots do not regenerate as well as peripheral nerves. For example, injury to the spinal roots can occur with herniated discs pressing on them or compression or crushing of the cauda equina (below L1 of the spine) where most of the lumbosacral spinal roots are located. Such injuries generally result in limited sensory recovery and partial motor recovery. The reason why little sensory improvement occurs is because the injury is occurring to the spinal root between the dorsal root ganglia. The sensory axon from the dorsal root ganglion has to grow into the spinal cord before it can make any connections and axons will stop at the edge of the peripheral and central nervous system, called the CNS/PNS interface. Motor axons will regenerate to some extent unless the injury is close enough to the spinal cord to damage the motoneurons in the spinal cord.

        Spinal cord does not regenerate well. This does not mean that the spinal cord does not regenerate at all. I suspect that the spinal cord (particularly incomplete injuries) may regenerate. Surviving axons certainly can sprout additional branches. Regeneration takes a long time (years) and the spinal cord (particularly the injury site) is not particularly hospitable to growing axons and have proteins like Nogo and chondroitin-6-sulfate proteoglycans that stop axonal growth. Therapy is necessary to provide long-term sustained growth factor support, cells are needed to bridge the injury site, and growth inhibitor blockers are necessary to allow axons to grow long-distances.

        For many years, the reason why peripheral nerve was believed to be able to regenerate was because of the Schwann cells that myelinate axons in the peripheral nerve. In the central nervous system, the cells that myelinate axons are oligodendroglia. Each Schwann cell wraps around one segment of one axon. Each oligodendroglia may provide myelin segments to as many as 20 axons. Oligodendroglia myelin express a protein called Nogo, which stop axonal growth. For many years, scientists through that Nogo expression is the difference between peripheral and central nervous nerve growth. However, as it turns out Schwann cell myelin also expresses Nogo.

        The important difference between Schwann cell and oligodendroglial myelin is that Schwann cells in injured peripheral nerves transform into cells that look by macrophages and that scavenge myelin fragments. Oligodendroglia do not. Because they myelinate multiple axons, as long as some of the axons are still alive, the oligodendroglia myelin is still present. At the injury site, there are macrophages (mostly from blood or microglia in the spinal cord) that eat myelin fragments, although some recent studies by a colleague in my laboratory showed that microglial macrophages stop taking up myelin debris after a while because they cannot process them. In any case, in the central nervous system, the cleanup of the myelin debris is slow and inefficient. In the peripheral nerve, the myelin is cleared out and the axons are able to regenerate in the nerve.

        Finally, there is now growing evidence that certain spinal tracts do not grow as well as others. In particular, the corticospinal tract is the main spinal tract that goes from the brain to the spinal cord. A former student of mine has found out the reason why corticospinal neurons do not regenerate well and has discovered a treatment that can make them do so. This is quite exciting and I am very hopeful that this will be part of the therapies that we will be able to take to clinical trials in the coming years.

        Wise.
        So all the theories that so far are used to explain why CNS does not rigenerate are becoming obsolete or even completly wrong.

        I have been thinking for a while that researcher probably have been shooting just at the shadow of the real target so far.
        I guess the CNS is full of shadows that make it difficult to understand what the target should be.


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

        Comment


        • #5
          Originally posted by paolocipolla View Post
          So all the theories that so far are used to explain why CNS does not rigenerate are becoming obsolete or even completly wrong.

          I have been thinking for a while that researcher probably have been shooting just at the shadow of the real target so far.
          I guess the CNS is full of shadows that make it difficult to understand what the target should be.


          Paolo
          Paolo,

          It is very important to separate out what various scientists believe and what the evidence shows. Some scientists who proposed and advocate certain theories, such as Martin Schwab and Nogo, will do experiments to prove their theories and argue against the other theories. Other scientists, such as Jerry Silver, advocate a central role for chondroitin-6-sulfate-proteoglycans and will point out data against the Nogo theory. Some believe that certain types of astrocytes are bad, i.e. Stephen Davies.

          In many cases, the evidence is incomplete and the story turns out to be more complex than the simplistic pictures depicted by early papers. Early papers by Martin Schwab in 1991 suggested that myelin is the main and perhaps only inhibitor of axonal growth in the spinal cord. In 1994, Saburo Kawaguchi showed that sharply transected neonatal rats spinal cords can regenerate. Kawaguchi believed that immature astrocytes are critical for regeneration (similar to what Stephen Davies is proposing) but he was never able to show regeneration in sharply transected adult rat cords.

          Others tried to show that animals that don't express Nogo, i.e. Nogo-knockout mice, can regenerate but these mice don't regenerate well either, suggesting that other factors besides Nogo may prevent regeneration. So, at the present, most scientists in the field believe that at least two factors inhibit axonal regeneration in the adult spinal cord: Nogo and chondroitin-6-sulfate-proteoglycans (CSPG). There is evidence that blockade of Nogo will stimulate regeneration. Likewise, there is evidence that chondroitinase, which breaks down CSPG, will stimulate regeneration.

          it is not true that the theories (such as the Nogo and CSPG theories) are wrong. They just don't account for all the factors in the central nervous system that regulate axonal growth. This is not surprising. Early scientists had the hubris to assume that they had the one and only factor that regulates regeneration. They should know better. Nothing in our bodies or central nervous system is controlled by only one factor. Multiple factors play a role, especially when it is a phenomenon as important as regeneration of the spinal cord.

          The science is much stronger and better than the impression that you are giving, i.e. that we are shooting at shadows. It is also not surprising that multiple mechanisms affect regeneration and growth of axons. There are other factors. Marie Filbin and Mary Bunge have shown that axons that are expressing high levels of cAMP ignore whatever inhibitors might be present. Likewise, a former student of mine will be coming out with a beautiful story suggest that certain spinal tracts express factors that make them less likely to regenerate than others. These aren't shadows but real evidence-based mechanisms that will lead to definitive regenerative therapies.

          Wise.

          Comment


          • #6
            Originally posted by Wise Young View Post
            Paolo,

            It is very important to separate out what various scientists believe and what the evidence shows. Some scientists who proposed and advocate certain theories, such as Martin Schwab and Nogo, will do experiments to prove their theories and argue against the other theories. Other scientists, such as Jerry Silver, advocate a central role for chondroitin-6-sulfate-proteoglycans and will point out data against the Nogo theory. Some believe that certain types of astrocytes are bad, i.e. Stephen Davies.

            In many cases, the evidence is incomplete and the story turns out to be more complex than the simplistic pictures depicted by early papers. Early papers by Martin Schwab in 1991 suggested that myelin is the main and perhaps only inhibitor of axonal growth in the spinal cord. In 1994, Saburo Kawaguchi showed that sharply transected neonatal rats spinal cords can regenerate. Kawaguchi believed that immature astrocytes are critical for regeneration (similar to what Stephen Davies is proposing) but he was never able to show regeneration in sharply transected adult rat cords.

            Others tried to show that animals that don't express Nogo, i.e. Nogo-knockout mice, can regenerate but these mice don't regenerate well either, suggesting that other factors besides Nogo may prevent regeneration. So, at the present, most scientists in the field believe that at least two factors inhibit axonal regeneration in the adult spinal cord: Nogo and chondroitin-6-sulfate-proteoglycans (CSPG). There is evidence that blockade of Nogo will stimulate regeneration. Likewise, there is evidence that chondroitinase, which breaks down CSPG, will stimulate regeneration.

            it is not true that the theories (such as the Nogo and CSPG theories) are wrong. They just don't account for all the factors in the central nervous system that regulate axonal growth. This is not surprising. Early scientists had the hubris to assume that they had the one and only factor that regulates regeneration. They should know better. Nothing in our bodies or central nervous system is controlled by only one factor. Multiple factors play a role, especially when it is a phenomenon as important as regeneration of the spinal cord.

            The science is much stronger and better than the impression that you are giving, i.e. that we are shooting at shadows. It is also not surprising that multiple mechanisms affect regeneration and growth of axons. There are other factors. Marie Filbin and Mary Bunge have shown that axons that are expressing high levels of cAMP ignore whatever inhibitors might be present. Likewise, a former student of mine will be coming out with a beautiful story suggest that certain spinal tracts express factors that make them less likely to regenerate than others. These aren't shadows but real evidence-based mechanisms that will lead to definitive regenerative therapies.

            Wise.
            Thanks for this clarification, that gives me a much better picture of the present situation.

            I think it is ok that a researcher goes on with his line of research until the bottom, but sometimes it just look like once they get to the bottom a few wants to go deeper and deeper to get nowhere.
            In God we trust; all others bring data. - Edwards Deming

            Comment


            • #7
              When God or whoever you believe in made our extraordinary bodies, he did a great job with everything except our central nervous sytem. Why would the body fight itself like that when it has so many life saving mechanisms? Thanks for your response doc.
              Ken

              Guns don't kill people. Daddys with cute daughters do!

              Comment


              • #8
                Originally posted by BigK View Post
                When God or whoever you believe in made our extraordinary bodies, he did a great job with everything except our central nervous sytem. Why would the body fight itself like that when it has so many life saving mechanisms? Thanks for your response doc.
                BigK,

                Regeneration of the spinal cord is one of those goals that is similar to getting to the moon. For almost all of human history, doctors have believed that the spinal cord cannot regenerate. Some 3000 thousand years ago, an anonymous Egyptian physician (in the Edwin-Smith papyrus) described spinal cord injury in warriors (including the priapism) and recommended that water should be withheld and not to treat the condition. In the early 1900's, the father of neuroanatomy, Santiago Ramon y Cajal proposed the neuron theory and described the frustrated efforts of axons to grow across a cut in the spinal cord.

                Cutting the spinal cord is perhaps the most difficult challenge that one can present to growing axons. When the spinal cord is cut and no repair of the dura or pia is done, fibroblasts from surrounding tissues invade into the injury site and astrocytes from the spinal cord proliferate in response to form a "glial scar". Axons will not grow across such scars. I have pointed on this forum and elsewhere that such cuts of the spinal cord are abnormal and unusual spinal cord injury. A vast majority of spinal cord injuries involve contusion and compression of the spinal cord, without a penetrating wound.

                In contused and compressed cords, there is astrocytosis (proliferation of astrocytes or glial cells) but no invasion of fibroblasts. Unlike cut spinal cords, most contused spinal cords have a loose matrix of tissue at the injury site and not always a cyst. In a 1997 paper by the Multicenter Animal Spinal Cord Injury Study, we reported histological studies of several rat spinal cords injured with a standardized contusion. We found many axons growing into the loose tissue matrix at the injury site. So, while the injury site is a barrier to axonal growth in cut spinal cords, it is not an absolute barrier in contused cords.

                Having watched many people with spinal cord injury recover over the years, I believe that the human spinal cord does regenerate spontaneously to some extent. For example, many people with incomplete spinal cord injuries do continue to recover over many years. The timing of such recovery is consistent with regrowth of axons at 1 mm a day. Some of the recovery is a result of surviving axons sprouting but there is also a descent of the sensory level by 4-5 segments.

                Our goal is to help the contused and compressed spinal cord regenerate better. Much of the pessimism surrounding the inability of the spinal cord to regenerate comes from the transection model of spinal cord injury that many researchers have been using. A transection the spinal cord without dural repair is very rarely seen clinically. It is not representative of spinal cord injury in humans. It is one of the reasons why I have spent the past two decades developing and training now over 600 laboratories around the world to do the contusion model of rat spinal cord injury. In my opinion, we should be studying regeneration in the contused or compressed spinal cord, rather than the sharply transected spinal cord.

                Wise.

                Comment


                • #9
                  Wise. Could we cheat the CNS and make it believe it is peripheral?

                  Comment


                  • #10
                    Wise, understanding that "atraumatic" (sez who?) injuries to the cns are markedly different than the average SCI resulting from trauma, many of us with congenital causes of paralysis still see SCI research as the most accessible way to gain insight into our paralysis.

                    You have differentiated between cut and crush injuries. How would you describe the CNS damage created by a tethered cord?
                    Foolish

                    "We have met the enemy and he is us."-POGO.

                    "I have great faith in fools; self-confidence my friends call it."~Edgar Allan Poe

                    "Dream big, you might never wake up!"- Snoop Dogg

                    Comment


                    • #11
                      I have a condition called critical care polyneuropathy, which is caused by damage to the peripheral nerves, that occured after a severe illness.

                      When I was first in hospital I couldn't move any of my muscles but gradually I regained movement in all body parts but still lack strength in my legs, hands and lower arms in particular.

                      I was told to 'wait and see' by the doctors and was informed that nerves regrow 1mm a day. Unfortunately, although I have improved alot, I'm still technically a quad.

                      In my experience the recovery of the peripheral nerves has been far from full and the damage has been as debilitating as an SCI.

                      Comment


                      • #12
                        Originally posted by Foolish Old View Post
                        Wise, understanding that "atraumatic" (sez who?) injuries to the cns are markedly different than the average SCI resulting from trauma, many of us with congenital causes of paralysis still see SCI research as the most accessible way to gain insight into our paralysis.

                        You have differentiated between cut and crush injuries. How would you describe the CNS damage created by a tethered cord?
                        Or my problem, that being spinal cord ischemia? I lost a lot of blood/oxygen to my cord from blunt aortic trauma and my tissue is necrotic.
                        Ken

                        Guns don't kill people. Daddys with cute daughters do!

                        Comment


                        • #13
                          Originally posted by Foolish Old View Post
                          Wise, understanding that "atraumatic" (sez who?) injuries to the cns are markedly different than the average SCI resulting from trauma, many of us with congenital causes of paralysis still see SCI research as the most accessible way to gain insight into our paralysis.

                          You have differentiated between cut and crush injuries. How would you describe the CNS damage created by a tethered cord?
                          FO, as you know, spina bifida is not one condition but many different conditions that related by their cause but not necessarily the consequence. In some cases, there is failure of parts of the spinal cord and roots to develop. In other cases, there is a cyst that has grown. In many, tethering or spine malformation is the problem. Each one of these have to be investigated and individual solutions have to be developed for each. These include peripheral nerve grafting, neuronal replacement, and regenerative therapies. Let me address the issue of how tethering and ischemia damages the spinal cord separately.

                          Wise.

                          Comment


                          • #14
                            New article on peripheral nerve growth

                            J Plast Reconstr Aesthet Surg. 2009 Oct 12.

                            Adipose-derived stem cells enhance peripheral nerve regeneration.

                            di Summa PG, Kingham PJ, Raffoul W, Wiberg M, Terenghi G, Kalbermatten DF.

                            Chirurgie Plastique et Reconstructive CHUV, Université de Lausanne, Rue de Bugnon 46, 1005 Lausanne, CH, Switzerland; Blond McIndoe Research Laboratories. The University of Manchester, Manchester, UK.

                            Traumatic injuries resulting in peripheral nerve lesions often require a graft to bridge the gap. Although autologous nerve auto-graft is still the first-choice strategy in reconstructions, it has the severe disadvantage of the sacrifice of a functional nerve. Cell transplantation in a bioartificial conduit is an alternative strategy to create a favourable environment for nerve regeneration. We decided to test new fibrin nerve conduits seeded with various cell types (primary Schwann cells and adult stem cells differentiated to a Schwann cell-like phenotype) for repair of sciatic nerve injury. Two weeks after implantation, the conduits were removed and examined by immunohistochemistry for axonal regeneration (evaluated by PGP 9.5 expression) and Schwann cell presence (detected by S100 expression). The results show a significant increase in axonal regeneration in the group of fibrin seeded with Schwann cells compared with the empty fibrin conduit. Differentiated adipose-derived stem cells also enhanced regeneration distance in a similar manner to differentiated bone marrow mesenchymal stem cells. These observations suggest that adipose-derived stem cells may provide an effective cell population, without the limitations of the donor-site morbidity associated with isolation of Schwann cells, and could be a clinically translatable route towards new methods to enhance peripheral nerve repair.

                            http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum




                            J Neurosurg. 2009 Oct 9.

                            Enhancement of regeneration with glia cell line-derived neurotrophic factor-transduced human amniotic fluid mesenchymal stem cells after sciatic nerve crush injury.

                            Cheng FC, Tai MH, Sheu ML, Chen CJ, Yang DY, Su HL, Ho SP, Lai SZ, Pan HC.

                            Stem Cell Center, Department of Medical Research, and.

                            Object Human amniotic fluid-derived mesenchymal stem cells (AFMSCs) have been shown to promote peripheral nerve regeneration, and the local delivery of neurotrophic factors may additionally enhance nerve regeneration capacity. The present study evaluates whether the transplantation of glia cell line-derived neurotrophic factor (GDNF)-modified human AFMSCs may enhance regeneration of sciatic nerve after a crush injury. Methods Peripheral nerve injury was produced in Sprague-Dawley rats by crushing the left sciatic nerve using a vessel clamp. Either GDNF-modified human AFMSCs or human AFMSCs were embedded in Matrigel and delivered to the injured nerve. Motor function and electrophysiological studies were conducted after 1 and 4 weeks. Early or later nerve regeneration markers were used to evaluate nerve regeneration. The expression of GDNF in the transplanted human AFMSCs and GDNF-modified human AFMSCs was monitored at 7-day intervals. Results Human AFMSCs were successfully transfected with adenovirus, and a significant amount of GDNF was detected in human AFMSCs or the culture medium supernatant. Increases in the sciatic nerve function index, the compound muscle action potential ratio, conduction latency, and muscle weight were found in the groups treated with human AFMSCs or GDNF-modified human AFMSCs. Importantly, the GDNF-modified human AFMSCs induced the greatest improvement. Expression of markers of early nerve regeneration, such as increased expression of neurofilament and BrdU and reduced Schwann cell apoptosis, as well as late regeneration markers, consisting of reduced vacuole counts, increased expression of Luxol fast blue and S100 protein, paralleled the results of motor function. The expression of GDNF in GDNF-modified human AFMSCs was demonstrated up to 4 weeks; however, the expression decreased over time. Conclusions The GDNF-modified human AFMSCs appeared to promote nerve regeneration. The consecutive expression of GDNF was demonstrated in GDNF-modified human AFMSCs up to 4 weeks. These findings support a nerve regeneration scenario involving cell transplantation with additional neurotrophic factor secretion.

                            http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
                            Last edited by wildwilly; 10-22-2009, 04:30 AM.
                            “As the cast of villains in SCI is vast and collaborative, so too must be the chorus of hero's that rise to meet them” Ramer et al 2005

                            Comment


                            • #15
                              Dr. Wise may I ask your opinion...I had surgery to remove a maglignant tumour that had wrapped around my spinal cord and severely compressed/crushed it.T6-T9..during surgery would i be correct in thinking that my nerve ends were cut ...its just no one has ever explained this to me...and if so could you explain how and if they heal. Thank You

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