Highly efficient blue InGaN nanoscale light-emitting diodes.

Indium gallium nitride (InGaN)-based micro-LEDs (µLEDs) are suitable for meeting ever-increasing demands for high-performance displays owing to their high efficiency, brightness and stability1-5. However, µLEDs have a large problem in that the external quantum efficiency (EQE) decreases with the size reduction6-9. Here we demonstrate a blue InGaN/GaN multiple quantum well (MQW) nanorod-LED (nLED) with high EQE. To overcome the size-dependent EQE reduction problem8,9, we studied the interaction between the GaN surface and the sidewall passivation layer through various analyses. Minimizing the point defects created during the passivation process is crucial to manufacturing high-performance nLEDs. Notably, the sol-gel method is advantageous for the passivation because SiO2 nanoparticles are adsorbed on the GaN surface, thereby minimizing its atomic interactions. The fabricated nLEDs showed an EQE of 20.2 ± 0.6%, the highest EQE value ever reported for the LED in the nanoscale. This work opens the way for manufacturing self-emissive nLED displays that can become an enabling technology for next-generation displays.

Kv3.1 and Kv3.4, Are Involved in Cancer Cell Migration and Invasion.

Voltage-gated potassium (Kv) channels, including Kv3.1 and Kv3.4, are known as oxygen sensors, and their function in hypoxia has been well investigated. However, the relationship between Kv channels and tumor hypoxia has yet to be investigated. This study demonstrates that Kv3.1 and Kv3.4 are tumor hypoxia-related Kv channels involved in cancer cell migration and invasion. Kv3.1 and Kv3.4 protein expression in A549 and MDA-MB-231 cells increased in a cell density-dependent manner, and the pattern was similar to the expression patterns of hypoxia-inducible factor-1α (HIF-1α) and reactive oxygen species (ROS) according to cell density, whereas Kv3.3 protein expression did not change in A549 cells with an increase in cell density. The Kv3.1 and Kv3.4 blocker blood depressing substance (BDS) did not affect cell proliferation; instead, BDS inhibited cell migration and invasion. We found that BDS inhibited intracellular pH regulation and extracellular signal-regulated kinase (ERK) activation in A549 cells cultured at a high density, potentially resulting in BDS-induced inhibition of cell migration and invasion. Our data suggest that Kv3.1 and Kv3.4 might be new therapeutic targets for cancer metastasis.