The Key Gold: Enhanced Platinum Catalysis for the Selective Hydrogenation of α,β-Unsaturated Ketone

AuPt alloy nanoparticles (NPs) were facilely synthesized with oleylamine as the stabilizing ligand and characterized by high-resolution transmission electron microscopy, powder X-ray diffraction, inductively coupled plasma-atomic emission spectrometer analysis, and so on. In addition, the AuPt alloys supported by the nano CeO₂ exhibit high selectivity and efficiency in hydrogenation of benzylidene acetone under ambient temperature and pressure. By analyzing the catalytic performance over the NPs with different Au:Pt compositions, we found that the TON_Pt values (based on the number of Pt atoms) vary in the same trend with the change of conversion. Despite that gold itself shows no catalytic activity, the improved conversion and TON_Pt with the alloy catalysts clearly show the promotion effect of gold on the catalytic activity of the platinum. The inactive metal significantly improves the catalytic activity of active metal, which shows that the AuPt alloy exhibits an interesting synergistic effect

Dexmedetomidine Acts via the JAK2/STAT3 Pathway to Attenuate Isoflurane-Induced Neurocognitive Deficits in Senile Mice

<div><p>Background</p><p>Previous studies showed that isoflurane-induced cognitive deficits could be alleviated by dexmedetomidine in young animal subjects. In the current study, we examine whether dexmedetomidine could also alleviate isoflurane-induced cognitive deficits in senile animals.</p><p>Methods</p><p>Senile male C57BL/6 mice (20 months) received dexmedetomidine (50 μg/kg, i.p.) or vehicle 30 minutes prior to isoflurane exposure (1.3% for 4 h). Cognitive function was assessed 19 days later using a 5-day testing regimen with Morris water maze. Some subjects also received pretreatment with α₂ adrenoreceptor antagonist atipamezole (250 μg/kg, i.p.), JAK2 inhibitor AG490 (15 mg/kg i.p.) or STAT3 inhibitor WP1066 (40 mg/kg i.p.) 30 minutes prior to dexmedetomidine.</p><p>Results</p><p>Isoflurane exposure increased and reduced the time spent in the quadrant containing the target platform in training sessions. The number of crossings over the original target quadrant was also decreased. Dexmedotomidine attenuated such effects. Effects of dexmedotomidine were reduced by pretreatment with atipamezole, AG490 and WP1066. Increased phosphorylation of JAK2 and STAT3 in the hippocampus induced by isoflurane was augmented by dexmedetomidine. Effects of dexmedetomidine on JAK2/STAT3 phosphorylation were attenuated by atipamezole, AG490 and WP1066. Isoflurane promoted neuronal apoptosis and increased the expression of cleaved caspase-3 and BAD, and reduced Bcl-2 expression. Attenuation of such effects by dexmedotomidine was partially blocked by atipamezole, AG490 and WP1066.</p><p>Conclusion</p><p>Dexmedetomidine could protect against isoflurane-induced spatial learning and memory impairment in senile mice by stimulating the JAK2/STAT3 signaling pathway. Such findings encourage the use of dexmedetomidine in geriatric patients receiving isoflurane anesthesia.</p></div

Effects of dexmedetomidine on p-CREB levels and JAK2/STAT3 pathway activation in hippocampus.

<p>Representative Western blots (A) showing levels of JAK2, p-JAK2, STAT3, p-STAT3, CREB, and p-CREB in hippocampus at 19d after animals were treated as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164763#pone.0164763.g002" target="_blank">Fig 2</a>. Densitometry was used to determine ratios of the levels of p-JAK2 to JAK2 (B), p-STAT3 to STAT3 (C), and p-CREB to CREB (D). Data are represented as mean ± SD (n = 8). *<i>P</i> < 0.05 vs. control group; ^#<i>P</i>< 0.05 vs. ISO group; ^&<i>P</i>< 0.05 vs. DEX group.</p

Effects of dexmedetomidine on isoflurane-induced changes in expression of apoptosis-related proteins.

<p>Representative Western blots (A) showing levels of cleaved caspase-3, BAD, Bcl-2 and BDNF in hippocampus at 19d after animals were treated as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0164763#pone.0164763.g002" target="_blank">Fig 2</a>. Levels of caspase-3 (B), BAD (C), Bcl-2 (D) and BDNF (E) were quantitated relative to that of β-actin. Data are represented as mean ± SD (n = 8). *<i>P</i> < 0.05 vs. control group; ^#<i>P</i>< 0.05 vs. ISO group; ^&<i>P</i>< 0.05 vs. DEX group.</p

Analysis of arterial blood gases and blood glucose in senile mice immediately after isoflurane exposure.

<p>Analysis of arterial blood gases and blood glucose in senile mice immediately after isoflurane exposure.</p