Browse our collection of 12,052 research summaries, all carefully curated and simplified for the spinal cord injury community.
Showing 11,941-11,950 of 12,052 results
Cellular and Molecular Neurobiology, 2006 • July 29, 2006
This study investigates the therapeutic potential of human mesenchymal stem cells (hMSCs) for spinal cord injury (SCI) in rats. hMSCs were intravenously injected into rats seven days after SCI, and fu...
KEY FINDING: Transplanted rats showed statistically significant improvement in locomotor function at 21 and 28 days after spinal cord injury compared to the control group.
Phil. Trans. R. Soc. B, 2006 • July 28, 2006
The adult mammalian CNS does not spontaneously regenerate after injury due to an inhibitory environment and changes in the neurons themselves. This contrasts with the neonatal CNS, which can regenerat...
KEY FINDING: The glial scar, formed by reactive astrocytes, is a major component of the inhibitory environment in the adult CNS. These astrocytes express inhibitory chondroitin sulphate proteoglycans (CSPGs).
The Journal of Neuroscience, 2006 • July 26, 2006
This study aimed to determine if the absence of Tenascin-R (TNR) has beneficial effects on recovery from spinal cord injury (SCI) in adult mice. The researchers used TNR-deficient mice and wild-type l...
KEY FINDING: TNR-deficient mice showed better recovery in open-field locomotion compared to wild-type mice after spinal cord compression.
PNAS, 2006 • July 18, 2006
The injured CNS limits functional recovery due to axon regeneration inhibitors (ARIs). Reversing ARI action may enhance axon outgrowth and recovery after CNS injury. Sialidase or chondroitinase ABC en...
KEY FINDING: Infusion of Clostridium perfringens sialidase to the injury site markedly increased the number of spinal axons that grew into the graft.
The Journal of Neuroscience, 2006 • July 12, 2006
The study demonstrates that modulation of extracellular matrix components promotes significant axonal regeneration beyond a PN bridge back into the spinal cord. Regenerating axons can mediate the retu...
KEY FINDING: ChABC treatment enhanced axonal regrowth from the PN graft into the spinal cord.
TheScientificWorldJOURNAL, 2006 • July 7, 2006
Newts possess remarkable regenerative abilities due to dedifferentiation, a process where cells revert to a multipotent state. Molecular pathways, including FGFs, MMPs, and Hox genes, control regenera...
KEY FINDING: Dedifferentiation is crucial for limb regeneration in newts, allowing specialized cells to revert to a pluripotent state.
Muscle Nerve, 2006 • July 1, 2006
This study investigated muscle fatigue in paralyzed soleus muscles after spinal cord injury (SCI) using a modified Burke fatigue protocol. The protocol demonstrated high between-day reliability. The s...
KEY FINDING: The between-day reliability of the modified Burke fatigue protocol was high (ICC = 0.96), indicating consistent measurements of muscle fatigue.
J Neurotrauma, 2006 • July 1, 2006
The study aimed to assess the feasibility of bladder reinnervation in a canine model by transecting and immediately repairing ventral roots. Results showed that five of eight nerve transected and repa...
KEY FINDING: Transected ventral and dorsal roots in the sacral spine can be repaired and are capable of functionally reinnervating the urinary bladder.
Cellular and Molecular Neurobiology, 2006 • June 16, 2006
This study investigates the potential of using transdifferentiated mesenchymal stem cells (MSCs) to promote nerve regeneration and myelination. Demyelination is a critical factor in various neurologic...
KEY FINDING: Transdifferentiated MSCs can myelinate PC12 cells in vitro, similar to Schwann cells, but the degree of myelination depends on the culture medium used.
The Journal of Neuroscience, 2006 • May 24, 2006
This study investigates the impact of Nogo-A deletion on axonal regeneration in two different mouse strains, 129X1/SvJ and C57BL/6, following spinal cord injury. The findings demonstrate that Nogo-A d...
KEY FINDING: Nogo-A-deficient mice displayed enhanced regeneration of the corticospinal tract after injury, confirming Nogo-A's role as an inhibitor of axonal regeneration.