Browse the latest research summaries in the field of regenerative medicine & stem cells for spinal cord injury patients and caregivers.
Showing 261-270 of 2,317 results
PLoS ONE, 2011 • March 18, 2011
The study demonstrates that transplantation of SENAs overexpressing L1 enhances functional recovery after spinal cord injury in mice. L1 overexpression improves survival and migration of grafted SENAs...
KEY FINDING: L1 overexpressing SENAs improve locomotor function after transplantation into the lesioned spinal cord in mice.
The Journal of Spinal Cord Medicine, 2011 • January 1, 2011
This case report investigates the use of sustained release platelet-rich plasma (PRP) therapy for treating chronic stage IV pressure ulcers in three veterans with spinal cord injuries. The PRP treatme...
KEY FINDING: PRP treatment consistently resulted in the formation of granulation tissue, which is essential for wound healing.
Frontiers in Cell and Developmental Biology, 2015 • August 7, 2015
This review explores the neuroregenerative potential of G-CSF, highlighting its vasculogenic and neurogenic mechanisms in SCI and ALS. G-CSF promotes angiogenesis and arteriogenesis, creating a regene...
KEY FINDING: G-CSF stimulates neurogenesis, arteriogenesis in the CNS, and markedly improves long-term behavioral outcome after cortical ischemia or spinal cord injury.
Neural Regen Res, 2015 • July 1, 2015
This study investigated the distribution of PirB in the central and peripheral nervous systems of rats after unilateral lumbar spinal cord injury to understand nerve regeneration inability. The result...
KEY FINDING: PirB immunoreactivity increased in the dorsal root ganglia, sciatic nerves, and spinal cord segments following unilateral spinal cord injury.
Neurotherapeutics, 2016 • December 16, 2015
This review examines the role of axon guidance molecules, such as Wnts, semaphorins, and ephrins, in neural circuit remodeling after spinal cord injury (SCI). Following SCI, these molecules, which are...
KEY FINDING: Following SCI, the re-expression of axon guidance molecules like ephrins, semaphorins, and Wnts can inhibit neural circuit plasticity and functional recovery.
Cell Mol Neurobiol, 2012 • August 11, 2011
The study investigates the use of human neural stem cells (hNSC) to promote functional recovery and structural reconnection in a rat model of complete spinal cord transection. The transplantation of h...
KEY FINDING: Transplanted hNSCs can differentiate into astrocytes and neurons at the injury site in the spinal cord.
The Journal of Neuroscience, 2009 • April 29, 2009
This study demonstrates that α9 integrin expression promotes neurite outgrowth on tenascin-C (TN-C) both in vitro and in vivo, suggesting a potential therapeutic strategy for enhancing axon regenerati...
KEY FINDING: Expression of α9 integrin in PC12 cells and adult rat DRG neurons promotes extensive neurite outgrowth on tenascin-C in vitro.
The Journal of Immunology, 2017 • August 1, 2017
This study investigates the impact of innate immune components on human neural stem cell (hNSC) fate and migration. It was found that polymorphonuclear leukocytes (PMN) secrete factors that induce ast...
KEY FINDING: Conditioned media from polymorphonuclear leukocytes (PMN) selectively increased hNSC astrogliogenesis and promoted cell migration in vitro.
J Korean Neurosurg Soc, 2017 • July 1, 2017
This study examined the additive effects of GCSF on ADSC infusion in treating acute SCI in rats. The results indicated that ADSCs alone improved functional recovery, but the addition of GCSF did not s...
KEY FINDING: ADSC and ADSC+GCSF groups showed significantly higher Basso-Beattie-Bresnahan scores than the Sham group during 8 weeks.
American Journal of Pathology, 2018 • January 1, 2018
This review surveys the mechanisms leading to the formation of dystrophic growth cone at the injured axonal tip, the subsequent axonal dieback, and the molecular determinants of axon growth, plasticit...
KEY FINDING: Injured axons in the CNS often fail to regenerate and form dystrophic end bulbs, which persist at the lesion border.