Read e-book online Distribution and Phenotype of Proliferating Cells in the PDF

By A.B. Tonchev, T. Yamashima, G.N. Chaldakov

ISBN-10: 3540396136

ISBN-13: 9783540396130

ISBN-10: 3540396179

ISBN-13: 9783540396178

The authors' effects express that ischemia differentially prompts endogenous neural precursors dwelling in diversified destinations of the grownup primate valuable apprehensive method. A constrained endogenous strength for postischemic neuronal fix exists in neocortex and striatum, yet no longer within the hippocampus right of the grownup macaque monkey mind. The presence of putative parenchymal progenitors and of sustained progenitors in germinative facilities opens novel chances for precursor cellphone recruitment to websites of damage. The molecular manipulation of this procedure may well advance the skill to successfully practice mind progenitor cells within the remedy of human neurological ailments.

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Read or Download Distribution and Phenotype of Proliferating Cells in the Forebrain of Adult Macaque Monkeys after Transient Global Cerebral Ischemia (Advances in Anatomy, Embryology and Cell Biology) PDF

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Extra resources for Distribution and Phenotype of Proliferating Cells in the Forebrain of Adult Macaque Monkeys after Transient Global Cerebral Ischemia (Advances in Anatomy, Embryology and Cell Biology)

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1 Dentate Gyrus Within DG, most BrdU+ cells in all monkeys were localized to SGZ (Fig. 6). Ischemia led to a visible increase of BrdU+ cells in DG, on postischemic days 9 and 15 (Fig. 6A). Quantitative analysis of the monkeys with short-term survival after BrdU showed that in either DG as a whole or separately within SGZ or DGL, the density of proliferating cells had a peak on day 9 (Fig. 7A). , on postischemic days 23, 44, or 79 (Fig. 6B). Quantitative analysis of this monkey group showed that—similar to the short-term survival group—the density of BrdU+ cells in postischemic monkeys was significantly greater than the density in respective control DG, DGL, or SGZ (Fig.

Evaluation of the BrdU+ cells co-staining with the microglial marker Iba1 or the astrocytic marker S100β in the short-term survival group revealed that in control and postischemic day 4 CA1, only microglia but not astrocytes incorporated BrdU (Fig. 21A). However, in postischemic day 9 CA1 and at subsequent time-points, BrdU+ astroglia were detected (Fig. 21B; arrowheads), although such cells were fewer than the BrdU+ /Iba1+ microglia (Fig. 21B; arrows). Quantitative analysis revealed that the percentages of BrdU+ cells expressing either Iba1 or S100β were significantly increased after ischemia at all time-points (Table 5).

2002). Ki67 immunohistochemistry confirmed that proliferation was increased on day 9 (Fig. 9B) as compared to control (Fig. 9A), and subsequently declined (Fig. 9C). The Ki67+ cells were frequently grouped similarly to the BrdU+ cells, in clusters or “doublets” (Fig. 9D, E). Double-labeling for BrdU and Ki67 demonstrated they stain the same cells (Fig. 9F). BrdU also colabeled with the mitotic marker phosphohistone H3 (Fig. 9G). After observing the distribution and density of BrdU+ cells in DG, we started evaluating their phenotype by combining BrdU with markers for progenitor cells or more mature cell types.

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Distribution and Phenotype of Proliferating Cells in the Forebrain of Adult Macaque Monkeys after Transient Global Cerebral Ischemia (Advances in Anatomy, Embryology and Cell Biology) by A.B. Tonchev, T. Yamashima, G.N. Chaldakov

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