No abstract

Electronic degeneracy to express metallic conduction in Al-rich AlGaN for the electron injection layer enhances the efficiencies of deep ultraviolet light emitters. This study systematically demonstrates the Si doping range and conditions to realize degenerate n-type Al0.6Ga0.4N layers based on the electron compensation effect. The temperature-independent electron concentrations resulting from the degenerate band appear in high Si doping conditions to overcome the electron compensation due to carbon on nitrogen sites (CN). However, excessive Si doping of over 4.0 × 1019 cm−3 leads to the collapse of the electronic degeneracy and a switch to the temperature-dependent electron transport via the impurity bands, where the luminescence bands originating from III vacancy-Si complexes (VIII-nSi) are dominant. The key parameter is the effective donor concentration, Nd − Na, based on the reduction in electron concentrations via acceptor-like deep levels such as CN and VIII-nSi. The Hall-effect analyses for n-type Al0.6Ga0.4N layers with various Si concentrations yielded an Nd − Na value of (9.5 ± 2.9) × 1018 cm−3 to vanish the ionization energy of Si donors, which is approximately six times higher than that in GaN. The results suggest not only the optimal doping range to obtain an Al-rich AlGaN layer with metallic conduction but also the necessity of the growth condition to minimize electron compensation.

We reduced the operating voltage of AlGaN homojunction tunnel junction (TJ) deep-ultraviolet (UV) light-emitting diodes (LEDs) by two approaches: the suppression of carbon incorporation and the doping of a high concentration of silicon in an n + -AlGaN layer. The AlGaN homojunction TJ deep-UV LEDs had a significantly reduced forward voltage upon suppressing the incorporation of carbon in the n + -AlGaN layer. The suppression of electron compensation by carbon in nitrogen sites and the doping of a high concentration of silicon in an n + -AlGaN layer are important for reducing the operating voltage of AlGaN homojunction TJ deep-UV LEDs.

In order to elucidate the causal relationship between (Na(+)-K+)ATPase and diabetic nephropathy, we studied the erythrocyte (Na(+)-K+)ATPase activity in Type 2 diabetic patients, 20 with microalbuminuria and 27 without microalbuminuria and in 16 control subjects. (Na(+)-K+)ATPase activities in microalbuminuric patients (0.273 +/- 0.012 mumol Pi/mg protein/h, mean +/- SE) were significantly reduced compared with those without microalbuminuric patients (0.308 +/- 0.011 mumol Pi/mg protein/h, p < 0.05) and control subjects (0.330 +/- 0.011 mumol Pi/mg protein/h, p < 0.01). Microalbuminuric patients had higher systolic blood pressure (133 +/- 3 vs 124 +/- 3 mmHg, p < 0.05) and greater frequency of parental hypertension (50% vs 19%, p < 0.05) than those without microalbuminuria. (Na(+)-K+)ATPase activities in diabetic patients with hypertension were significantly reduced compared with those in diabetic patients without hypertension. Moreover, (Na(+)-K+)ATPase activities in diabetic patients with parental hypertension were significantly reduced compared with those in patients without parental hypertension. There was no difference in erythrocyte Na+ content between with and without microalbuminuria or hypertension or parental hypertension in diabetic patients. Erythrocyte Na+ content was significantly negatively correlated with (Na(+)-K+)ATPase activity in control subjects (r = -0.619, p < 0.05), but not in diabetic patients (r = -0.194). Plasma digitalis-like substances showed no correlation with (Na(+)-K+)ATPase activities in diabetic patients with microalbuminuria or hypertension or parental hypertension. We concluded that the reduction of erythrocyte (Na(+)-K+)ATPase activity may be related to a familial predisposition to arterial hypertension and may partly be responsible for the development of diabetic nephropathy in Type 2 diabetic patients.