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Fferent parts of the spinal cord (front, 7 to 10 mm cranial; middle front, 3 to 6 mm cranial; center, between 2 mm cranial and caudal to the injury epicenter; middle back, 3 to 6 mm caudal; back, 7 to -10 mm caudal) (B).Amemori et al. Stem Cell Research Therapy 2013, 4:68 http://stemcellres.com/content/4/3/Page 9 ofFigure 4 The survival and trophic effect of SPC-01 cells 8 weeks after transplantation. The robust engraftment (MTCO2, green) of SPC-01 cells in a lesioned rat spinal cord was observed 8 weeks after transplantation (A). At the site of contact with the intact tissue, SPC-01 cells migrated out of the graft (A1, higher magnification of A). The processes of only a few host cells entered the implant (A2). qPCR analysis revealed that the level of expression of the rat genes Ngf and Nt-3 was D(+)-Galactosamine (hydrochloride) increased in the spinal cords of both control and grafted rats compared with healthy rats; the increase was significant only in the spinal cord tissue of animals grafted with SPC-01 cells (B) (*P PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/16989806 the spinal cord tissue of transplanted rats (Figure 5A) than in sections from control animals (Figure 5B). The number of GAP43+ axonal fibers per section was significantly increased in grafted animals (176.55 ?18.26) compared with control rats (8.41 ?3.35) (Figure 5D). The grafted cells were not GAP43+, indicating that all sprouting came from endogenous host axons. To examine the ability of SPC-01 cells to differentiate toward motor neurons after transplantation into the injured rat spinal cord, we investigated the expression of motor neuron-specific markers. Immunohistochemical staining revealed that 8 weeks after transplantation, 25.31 ?2.15 of SPC-01 cells wereAmemori et al. Stem Cell Research Therapy 2013, 4:68 http://stemcellres.com/content/4/3/Page 10 ofFigure 5 Axonal sprouting in the injured spinal cords of control rats and rats transpla.