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The phenomenon of frequency upconversion (UC) is observed in Er3+:Yb3+:SrAl2O4 powders prepared by combustion synthesis. Strong UC emission at the green (bands peaked at 521, 538, 547, and 562 nm) and weak UC emission at the red (bands peaked at 659 and 682 nm) corresponding to 4f–4f transitions of Er3+ were observed when the samples were irradiated with near-infrared laser excitation at ∼980 nm. Saturation of UC emission is observed for concentrations of 1.5 wt.% of Er3+ and 1.5 wt.% of Yb3+. The green-to-red intensity ratio, on the other hand, increases linearly with Er3+ concentration (Er3+ concentration varying from 0.5 to 1.5 wt.%) while keeping Yb3+ concentration fixed (at 1.5 wt.%). The green UC decay time was measured and Er3+–Er3+ interaction was suggested as a possible mechanism to explain the luminescence quenching effect observed. [ABSTRACT FROM AUTHOR]

The phenomenon of frequency upconversion (UC) is observed in Er3+:Yb3+:SrAl2O4 powders prepared by combustion synthesis. Strong UC emission at the green (bands peaked at 521, 538, 547, and 562 nm) and weak UC emission at the red (bands peaked at 659 and 682 nm) corresponding to 4f–4f transitions of Er3+ were observed when the samples were irradiated with near-infrared laser excitation at ∼980 nm. Saturation of UC emission is observed for concentrations of 1.5 wt.% of Er3+ and 1.5 wt.% of Yb3+. The green-to-red intensity ratio, on the other hand, increases linearly with Er3+ concentration (Er3+ concentration varying from 0.5 to 1.5 wt.%) while keeping Yb3+ concentration fixed (at 1.5 wt.%). The green UC decay time was measured and Er3+–Er3+ interaction was suggested as a possible mechanism to explain the luminescence quenching effect observed. [ABSTRACT FROM AUTHOR]

Aim/hypothesis. By acting in the brain, insulin suppresses food intake. However, little is known with regard to insulin signalling in the hypothalamus in insulin-resistant states. Methods. Western blotting, immunohistochemistry and polymerase chain reaction assays were combined to compare in vivo hypothalamic insulin signalling through the PI3-kinase and MAP kinase pathways between lean and obese Zucker rats. Results. Intracerebroventricular insulin infusion reduced food intake in lean rats to a greater extent than that observed in obese rats, and pre-treatment with PI3-kinase inhibitors prevented insulin-induced anorexia. The relative abundance of IRS-2 was considerably higher than that of IRS-1 in hypothalamus of both lean and obese rats. Insulin-stimulated phosphorylation of IR, IRS-1/2, the associations of PI 3-kinase to IRS-1/2 and phosphorylation of Akt in hypothalamus were decreased in obese rats compared to lean rats. These effects seem to be mediated by increased phosphoserine content of IR, IRS-1/2 and decreased protein levels of IRS-1/2 in obese rats. In contrast, insulin stimulated the phosphorylation of MAP kinase equally in lean and obese rats. Conclusion/interpretation. This study provides direct measurements of insulin signalling in hypothalamus, and documents selective resistance to insulin signalling in hypothalamus of Zucker rats. These findings provide support for the hypothesis that insulin could have anti-obesity actions mediated by the PI3-kinase pathway, and that impaired insulin signalling in hypothalamus could play a role in the development of obesity in this animal model of insulin-resistance. [ABSTRACT FROM AUTHOR]