in New York .
Written in English
|Other titles||Proliferation in spinal cord grafts.|
|Statement||By Leona Ruth Zacharias.|
|LC Classifications||QL937 .Z3 1938|
|The Physical Object|
|Pagination||1 p. l., p. 135-157, 1 l.|
|Number of Pages||157|
|LC Control Number||38034937|
Download Citation | On Feb 2, , S. R. Detwiler published Further observations on proliferation of nerve cells in grafted units of spinal cord | Find, read and cite all the research you need on. Growth responses in caudally grafted brachial segments of the embryonic spinal cord of Amblystoma Article in Journal of Experimental Zoology 64(1) - May with 2 Reads. To understand spinal cord regeneration, it is necessary to understand spinal cord development. In humans, oligodendrocytes are found in cultures of fetal spinal cord at 7 and 12 weeks of gestation [28,29]. Myelination begins at 10 to 11 weeks of gestation [30,31] and continues throughout the second year of life [32,33]. Hypoxic-ischemic (HI) brain injury and spinal cord injury (SCI) lead to extensive tissue loss and axonal degeneration. The combined application of the polymer scaffold and neural progenitor cells.
Grafted hiPSC-NSs Survived, Migrated, and Differentiated into Three Neural Lineages. Contusive SCI was induced at the Th10 level in NOD-SCID mice, and 5 × 10 5 Venus + hiPSC-NSs or PBS was injected into the lesion epicenter, 9 d after injury. To examine the effects of grafted hiPSC-NSs in the injured spinal cord, histological analyses were performed 56 d after SCI [after functional . An analysis of cellular proliferation in grafted segments of embryonic spinal cord and differentiation within the embryonic spinal cord. These results, . Significance statement. The present study shows that application of hypoxia‐regulated basic fibroblast growth factor modified primary embryonic neural stem cells to specifically target the hypoxic loci resulted in a reversal of the hypoxic microenvironment after spinal cord injury (SCI), concomitant with decreased cellular autophagy, reduced CNS glial scar formation, and improved locomotor. The grafted ESC segments were well integrated with the parenchyma of the host tissue forming a seamless continuous spinal cord. There were no obvious glial boundaries at the host–graft interface (Fig. 1A).The grafted PN segments were also well fused with the host spinal cord, but a clear boundary consisting of a different cytoarchitecture was observed at the host–graft interface (Fig. 1B).
Preliminary experiments suggest that spinal cord neural cells derived from mouse embryonic stem cells can adhere and grow axons through the pores of collagen scaffolds (Supplementary Fig. 2f). ) to promote graft survival and retention in the lesion site. Cells were grafted into C5 spinal cord hemisection lesion sites (n = 7), 2 weeks after the original spinal cord injury. Control subjects (n = 5) underwent the same lesions and injections of the fibrin matrix containing the growth factor cocktail lacking neural stem cells. Embryonic spinal cord tissue has been used as a source of progenitors for spinal cord injury repair for more than 30 years. The earliest experimental studies successfully demonstrated that cells obtained from fetal spinal cord (FSC) tissue thrive and integrate anatomically and functionally with the surrounding neuropil of the injured adult host spinal cord. The molecular and cellular organization of spinal cord Neural induction occurs from polarized mesodermal structures. The spinal cord is populated by multiple distinct populations of neurons and glia born in different locations and times along both the rostral-caudal and dorsal–ventral axes of the spinal cord (Ramón y Cajal, ). These.