Efficient Cadmium-Free Inverted Red Quantum Dot Light-Emitting Diodes.

Here, we report an efficient inverted red indium phosphide (InP) comprising QD (InP/ZnSe/ZnS, core/shell structure) light-emitting diode (QLED) by modulating an interfacial contact between the electron transport layer and emissive InP-QDs and applying self-aging approach. The red InP-QLED with optimized interfacial contact exhibits a significant improvement in maximum external quantum efficiency and current efficiency from 4.42 to 10.2% and 4.70 to 10.8 cd/A, respectively, after 69 days of self-aging, which is an almost 2.3-fold improvement compared to the fresh device. The analysis indicates the consecutive reduction in electron injection and accumulation in the emissive QD due to changes in the conduction band minimum of ZnMgO (0.1 eV after 10 days of storage) through a downward vacuum-level shift according to the aging times. During the device aging periods, the oxygen vacancy of ZnMgO reduces, which leads to lower the conductivity of ZnMgO. As a result, charge balance of the device is improved with the suppression of exciton quenching at the interface of ZnMgO and InP-QD.

Decreased Expression and Induced Nucleocytoplasmic Translocation of Pancreatic and Duodenal Homeobox 1 in INS-1 Cells Exposed to High Glucose and Palmitate.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is often accompanied by increased levels of circulating fatty acid. Elevations in fatty acids and glucose for prolonged periods of time have been suggested to cause progressive dysfunction or apoptosis of pancreatic beta cells in T2DM. However, the precise mechanism of this adverse effect is not well understood. METHODS: INS-1 rat-derived insulin-secreting cells were exposed to 30 mM glucose and 0.25 mM palmitate for 48 hours. RESULTS: The production of reactive oxygen species increased significantly. Pancreatic and duodenal homeobox 1 (Pdx1) expression was down-regulated, as assessed by reverse transcription-polymerase chain reaction and Western blot analyses. The promoter activities of insulin and Pdx1 were also diminished. Of note, there was nucleocytoplasmic translocation of Pdx1, which was partially prevented by treatment with an antioxidant, N-acetyl-L-cysteine. CONCLUSION: Our data suggest that prolonged exposure of beta cells to elevated levels of glucose and palmitate negatively affects Pdx1 expression via oxidative stress.