Yellow Luminescence of Polar and Nonpolar GaN Nanowires on <i>r</i>‑Plane Sapphire by Metal Organic Chemical Vapor Deposition

We have grown horizontal oriented, high growth rate, well-aligned polar (0001) single crystalline GaN nanowires and high-density and highly aligned GaN nonpolar (11–20) nanowires on <i>r</i>-plane substrates by metal organic chemical vapor deposition. It can be found that the polar nanowires showed a strong yellow luminescence (YL) intensity compared with the nonpolar nanowires. The different trends of the incorporation of carbon in the polar, nonpolar, and semipolar GaN associated with the atom bonding structure were discussed and proved by energy-dispersive X-ray spectroscopy, suggesting that C-involved defects are the origin responsible for the YL in GaN nanowires

Inhibition of Autophagy Contributes to Ischemic Postconditioning-Induced Neuroprotection against Focal Cerebral Ischemia in Rats

<div><h3>Background</h3><p>Ischemic postconditioning (IPOC), or relief of ischemia in a stuttered manner, has emerged as an innovative treatment strategy to reduce programmed cell death, attenuate ischemic injuries, and improve neurological outcomes. However, the mechanisms involved have not been completely elucidated. Recent studies indicate that autophagy is a type of programmed cell death that plays elusive roles in controlling neuronal damage and metabolic homeostasis. This study aims to determine the role of autophagy in IPOC-induced neuroprotection against focal cerebral ischemia in rats.</p> <h3>Methodology/Principal Findings</h3><p>A focal cerebral ischemic model with permanent middle cerebral artery (MCA) occlusion plus transient common carotid artery (CCA) occlusion was established. The autophagosomes and the expressions of LC3/Beclin 1/p62 were evaluated for their contribution to the activation of autophagy. We found that autophagy was markedly induced with the upregulation of LC3/Beclin 1 and downregulation of p62 in the penumbra at various time intervals following ischemia. IPOC, performed at the onset of reperfusion, reduced infarct size, mitigated brain edema, inhibited the induction of LC3/Beclin 1 and reversed the reduction of p62 simultaneously. Rapamycin, an inducer of autophagy, partially reversed all the aforementioned effects induced by IPOC. Conversely, autophagy inhibitor 3-methyladenine (3-MA) attenuated the ischemic insults, inhibited the activation of autophagy, and elevated the expression of anti-apoptotic protein Bcl-2, to an extent comparable to IPOC.</p> <h3>Conclusions/Significance</h3><p>The present study suggests that inhibition of the autophagic pathway plays a key role in IPOC-induced neuroprotection against focal cerebral ischemia. Thus, pharmacological inhibition of autophagy may provide a novel therapeutic strategy for the treatment of stroke.</p> </div

Identification of neuronal apoptosis by the TUNEL-assay in rat hippocampus at different time-point after SE.

<p>(<b>A–E</b>) Representative photo of TUNEL-staining in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. Scale bars: 500 µm. (<b>F–J</b>) Representative photo of TUNEL-staining in the CA1 region of rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. Scale bars: 50 µm. (<b>H–O</b>) Representative photo of TUNEL-staining in the CA3 region of rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. Scale bars: 50 µm. (<b>P</b>) Apoptosis index (%) at different time-point after SE in the CA1 region. (<b>Q</b>) Apoptosis index (%) in the CA3 region at different time-point after SE. Data are presented as the mean ± S.D.; * <i>P</i><0.05 versus control group; n = 6 per group.</p

Distribution of the sequencing reads and classification of small RNAs.

<p>(<b>A</b>) Distribution of the non-redundant sequencing reads from the experimental group (at 24 hours after SE). (<b>B</b>) Distribution of the non-redundant sequencing reads from control group. (<b>C</b>) Classification of the sequenced small RNA tags from the experimental group (at 24 hours after SE). (<b>D</b>) Classification of the sequenced small RNA tags from control group.</p

Correlations between levels of miR-365-5p and miR-99b-3p and apoptosis index.

<p>(<b>A,B</b>) The correlation between miRNA-365-5p and apoptosis index in the CA1 and CA3 regions after SE. (<b>C, D</b>) The correlation between miRNA-99b-3p and apoptosis index in the CA1 and CA3 regions after SE.</p

Identification of neuronal survival by Nissl-staining in rat hippocampus at different time-point after SE.

<p>(<b>A–E</b>) Representative photo of Nissl-staining in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. Scale bars: 500 µm. (<b>F–J</b>) Representative photo of Nissl-staining in the CA1 region of rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. Scale bars: 50 µm. (<b>H–O</b>) Representative photo of Nissl-staining in the CA3 region of rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. (<b>P</b>) Survival index in the CA1 region at different time-point after SE. (<b>Q</b>) Survival index (%) in the CA3 region at different time-point after SE. Data are presented as the mean ± S.D.; * <i>P</i><0.05 versus control group; n = 6 per group.</p

Validation of six differentially expressed miRNAs using qRT-PCR at 24 hours after SE.

<p>The levels of six differentially expressed miRNAs (miR-874-3p, miR-20a-5p, miR-345-3p, miR-365-5p, miR-764-3p and miR-99b-3p) in the rat hippocampus at 24 hours after SE were confirmed using qRT-PCR. The expression of all genes was normalized to the levels of U6 snoRNA. Data are presented as the mean ± S.D.; *<i>P</i><0.05 versus control group; n = 6 per group</p

The dynamic alterations of six differentially expressed miRNAs at different time-point after SE.

<p>(<b>A</b>) Measurement of miR-874-3p expression in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. (<b>B</b>) Measurement of miR-20a-5p expression in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. (<b>C</b>) Measurement of miR-345-3p expression in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. (<b>D</b>) Measurement of miR-365-5p expression in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. (<b>E</b>) Measurement of miR-764-3p expression in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. (<b>F</b>) Measurement of miR-99b-3p expression in rat hippocampus at 4 hours, 24 hours, 1 week and 3 weeks after SE. The expression of all genes was normalized to the levels of U6 snoRNA. Data are presented as the mean ± S.D.; *<i>P</i><0.05 versus control group; n = 6 per group.</p

Genes potentially targeted by six differentially expressed miRNAs.

<p>Boxes in yellow represent miRNAs, whereas cycles in red represent mRNAs.</p

TTC staining and brain edema measurement from rat brains in different groups.

<p>Rats were treated with an i.c.v. injection of 35 pmol rapamycin 15 min before postconditioning, and then followed by 24 h reperfusion. (A) Representative infarcts stained with TTC in the Sham, I/R-24 h, IPOC-24 h, IPOC+rapa and IPOC+Veh groups 24 h after stroke. (B) Quantification of infarct size from each group at 24 h after ischemia. (C) Quantification of water content from each group at 24 h after ischemia. IPOC reduced infarct size and mitigated brain edema after stroke, whereas rapamycin partially eliminated the neuroprotection of IPOC. n = 8 for each group. *<i>p</i><0.05 vs. the Sham group; ^#<i>p</i><0.05 vs. I/R-24 h group; ^$<i>p</i><0.05 vs. IPOC+rapa group.</p