NSPCSNational School Psychology Certification System
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Univariate metaregression analysis was carried out according to 12 variables, including (1) timing of NSPC intervention after stroke onset, (2) NSPC dose, (3) ischemic stroke models (transient, permanent), (4) graft sites (focal or global), (5) degree of NSPC immunogenicity (allogeneic or xenogeneic), (6) species of NSPC recipients, (7) species of NSPC donors, (8) state of donor NSPCs (pluripotent stem cell derivatives or primary cells), (9) administration of immunosuppressive drugs, (10) design in blindness, (11) randomization, and (12) study quality score.
This study suggests that intraparenchymal delivery of NSPCs is a promising candidate for ischemic stroke therapy, improving the functional deficits and histopathology in animal models of ischemic stroke.
We conducted a meta-analysis to determine whether intraparenchymal NSPC transplantation is beneficial in preclinical studies based on neurobehavioral tests (mNSS, rotarod test, and cylinder test) and histological outcome (infarct volume).
In the SGZ, the main cellular components are astrocytes, endothelial cells, pericytes, oligodendrocytes, microglia, different types of neurons present in the DG, and the aforementioned NSPCs [65].
For example, astrocytes negatively influence the differentiation of NSPCs after the activation of jagged1-mediated Notch pathway by cell-cell contact [70] or by the secretion of growth factors such as insulin-like growth factor binding protein 6 (IGFBP6) and decorin [71].
FGF2, the protein encoded by Fgf2, is a potent and necessary proliferative factor in adult NSPCs [92].
NSPCs were cultured from a gestational day 14 mouse embryo to study hypoxia-inducible factor-^ (HIF-1[alpha]).
Understanding the role of human embryonic-derived NSPCs has been investigated for improving stroke outcomes.
The fate of endogenous NSPC is quite complex and depends on many factors but takes on four general processes including proliferation, migration, cell survival, and neuronal differentiation [18].
In this review, we focus on the effects of lipid nutrition in embryonic and adult NSPCs, mainly in rodents.
During early neural development, NSPCs emerge in the neural tissue at embryonic day (E) 8 in the mouse (or E10 in the rat).
During late neural development, astrocytes are differentiated from NSPCs, and their production has its peak just after birth.