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发布于:2019-12-8 09:04:48  访问:18 次 回复:0 篇
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L loss was detected at 6 weeks (data not shown). Wild-type (black
Scale bar =15 m.Dissecting out a single cytokine from a complex map of signaling pathways by genetic deletion is MedChemExpress Irinotecan (hydrochloride) likely an oversimplification of any disease pathology. Journal of Neuroinflammation 2014, 11:194 http://www.jneuroinflammation.com/content/11/1/Page 7 ofFigure 3 Mice deficient for Tnf have GSK2141795 web greater retinal ganglion cell loss from crush than wild-type mice. Approximately 40 of the neurons in the GCL stain for BRN3A in control retinas of both wild-type (B) and Bax-/- (D) mice [53,55]. Retinas exposed to a single injection of TNF, 8 weeks prior, exhibit a complete absence of BRN3A staining (wild-type mice in C, and Bax-deficient mice in E). Scale bar =15 m.Dissecting out a single cytokine from a complex map of signaling pathways by genetic deletion is likely an oversimplification of any disease pathology. It is more plausible that TNF is part of a larger orchestrated injury response, and without auxiliary injury signals this cytokine may be limited in its effectiveness. We therefore tested the effect of TNF when delivered in conjunction with injury to RGCs by optic nerve crush. We tested two conditions: first, the PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26563313 cytokine was delivered prior to optic nerve crush to pre-activate the TNF signaling network, which is expectedly enhanced following crush injury. When an intraocular injection of 100 ng TNF was delivered 5 days prior to crush injury, RGC loss was reduced by almost 50 1 week after crush, compared to PBS-injected crushed mice (Figure 4A, P <0.001). This protective effect PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/24737349 persisted, relative to PBS-injected eyes, to 14 days post-crush, although cell density decreased in both cohorts of mice (P <0.001). A second condition was also tested in which 100 ng TNF was delivered 7 days after optic nerve crush; however, there was no statistically significant difference in cell survival between any of the groups subjected to crush (Figure 4B, P >0.05). These results support our findings above that TNF may protect RGCs from optic nerve injury and, importantly, will not exacerbate damage when applied after the initial insult to the optic nerve.Mac Nair et al. Journal of Neuroinflammation 2014, 11:194 http://www.jneuroinflammation.com/content/11/1/Page 7 ofFigure 3 Mice deficient for Tnf have greater retinal ganglion cell loss from crush than wild-type mice. (A) Wild-type and Tnf-/- mice were subjected to optic nerve crush and analyzed for total retinal ganglion cell layer neuronal cells remaining at 7, 14, and 21 days after injury. The decline in cell numbers was not statistically significant between the two genotypes at 7 days, but at 14 and 21 days Tnf-/- mice had significantly more cell loss (*P <0.001 for both time points). (B,C) Retinal whole mounts from wild-type and Tnf-/- mice were analyzed for Caspase 3 (CASP3) activation 3 and 5 days after optic nerve crush. At 3 days, Tnf-/- mice has a significantly greater number of CASP3+ cells (*P <0.05), but by 5 days the difference between the two genotypes was no longer significant.
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