We increased the light-extraction efficiency (LEE) of AlGaN-based deep-ultraviolet light-emitting diodes (DUV LEDs) by introducing a highly reflective photonic crystal (HR-PhC) into the surface of the p-AlGaN contact layer, thereby achieving a high external quantum efficiency (EQE). A low-damage HR-PhC with a lattice period of approximately 250 nm was fabricated using nanoimprinting and dry etching. A reflective Ni/Mg p-type electrode was deposited on the HR-PhC layer using a tilted-evaporation method. The EQE of a conventional DUV LED with emission around 283 nm was increased from 4.8 to 10% by introducing the HR-PhC and the reflective Ni/Mg electrode. A simple estimation of the effective reflectance of the HR-PhC p-AlGaN contact layer with the Ni/Mg electrode indicated a value exceeding 90%.
Straight single-line defect optical waveguides in photonic crystal slabs are designed by the finite difference time-domain method and fabricated into a silicon-on-insulator (SOI) wafer. By employing an airbridge structure, clear light propagation for both polarizations is observed without any leakage along the waveguide. This experimental result is well explained by photonic bands of pure guided modes. Minimum propagation loss is estimated to be 11 dB/mm. This value is lower than that reported so far for threeline-defect waveguides with an SOI slab structure and almost comparable to that for an index confinement waveguide with a rectangular Si core. This propagation loss is dominated by the scattering loss by some irregularities. However, photonic crystal waveguides have the possibility of an essential lower scattering loss than in the index confinement waveguide because of the inhibition of radiation modes by the photonic bandgap.Index Terms-FDTD, photonic bandgap, photonic crystal, SOI, waveguide.
1 A possible mechanism for the action of the K ATP channel opener diazoxide on the improvement of energy metabolism of ischaemic/reperfused hearts was examined. 2 Isolated, perfused rat hearts were subjected to 40 min ischaemia followed by 60 min reperfusion. Diazoxide at concentrations of 3 to 30 mM was present in the perfusion bu er for the last 15 min of pre-ischaemia. 3 Treatment of the perfused heart with diazoxide enhanced the post-ischaemic recovery of ratepressure product, attenuated the post-ischaemic rise in left ventricular end-diastolic pressure, and suppressed the release of creatine kinase and purine nucleosides and bases from the reperfused heart. Treatment of the heart with diazoxide also restored myocardial ATP and creatine phosphate and attenuated the decrease in mitochondrial oxygen consumption rate after reperfusion. This attenuation was maintained at the end of ischaemia as well as at the end of reperfusion. 4 In another set of experiments, myocardial skinned bundles were incubated for 30 min under hypoxic conditions in the presence and absence of diazoxide, and then the mitochondrial oxygen consumption rate was determined. Hypoxia induced a decrease in the mitochondrial oxygen consumption rate of the skinned bundles to approximately 40% of the pre-hypoxic value. In contrast, treatment of the bundles with 30 mM diazoxide preserved the normal mitochondrial oxygen consumption rate during hypoxia. This e ect was abolished concentration-dependently by the combined treatment with either the K ATP channel blocker glibenclamide or 5-hydroxydecanoate. 5 These results suggest that diazoxide is capable of attenuating ischaemia/reperfusion injury of isolated perfused hearts due to preservation of mitochondrial function during ischaemia.
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