Large electron capture-cross-section of the major nonradiative recombination centers in Mg-doped GaN epilayers grown on a GaN substrateThe nonradiative lifetime (s NR ) of the near-band-edge emission in various quality GaN samples is compared with the results of positron annihilation measurement, in order to identify the origin and to determine the capture-cross-section of the major intrinsic nonradiative recombination centers (NRCs). The room-temperature s NR of various n-type GaN samples increased with decreasing the concentration of divacancies composed of a Ga vacancy (V Ga ) and a N vacancy (V N ), namely, V Ga V N . The s NR value also increased with increasing the diffusion length of positrons, which is almost proportional to the inverse third root of the gross concentration of all point defects. The results indicate that major intrinsic NRC in n-type GaN is V Ga V N . From the relationship between its concentration and s NR , its hole capture-cross-section is estimated to be about 7 Â 10 À14 cm 2 . Different from the case of 4H-SiC, the major NRCs in p-type and n-type GaN are different: the major NRCs in Mg-doped p-type GaN epilayers are assigned to multiple vacancies containing a V Ga and two (or three) V N s, namely, V Ga (V N ) n (n ¼ 2 or 3). The ion-implanted Mgdoped GaN films are found to contain larger size vacancy complexes such as (V Ga ) 3 (V N ) 3 . In analogy with GaN, major NRCs in Al 0.6 Ga 0.4 N alloys are assigned to vacancy complexes containing an Al vacancy or a V Ga . Published by AIP Publishing. https://doi.
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Several studies have documented an association between serum uric acid (SUA) concentration and cardiac hypertrophy in hypertensive patients; however, the association remains unclear in chronic kidney disease (CKD) patients. If there is an association between SUA and hypertrophy in these patients, it is unknown whether the association is different between men and women. Our aim in this study is to determine whether SUA is associated with cardiac hypertrophy in CKD patients, focusing on any sex differences. Two hundred sixteen CKD patients (117 men and 99 women) were enrolled in this cross-sectional study. Patients prescribed uric acid-lowering agents and those with congestive heart failure, valvular heart disease, or ischemic heart disease were excluded from this study. Left ventricular mass index (LVMI) and left ventricular hypertrophy (LVH) were assessed using echocardiography. The prevalence of LVH was 58% in men and 47% in women. In multivariate linear regression analysis, SUA levels did not correlate with LVMI in men, whereas SUA was independently associated with LVMI in women (β=0.27, P=0.02). Multivariate logistic regression analysis also revealed that diabetes mellitus (odds ratio (OR), 4.41; P=0.01) was associated with LVH in men, whereas age (OR, 1.13; P<0.01), hypertension (OR, 7.38; P=0.03) and SUA (OR, 1.91; P=0.03) were associated with LVH in women. In female CKD patients, SUA levels were associated with LVMI and LVH, whereas there was no association in male patients. These observations suggest that an association between SUA levels and the development of cardiac hypertrophy is more likely in women than in men.
Chronic inhibition of nitric oxide synthase by N(omega)-nitro- L-arginine methyl ester (L-NAME) causes progressive renal injury with systemic hypertension and interstitial macrophage infiltration. We have previously shown that there is local activation of the renin-angiotensin-aldosterone system in the renal cortex as a major pathogenic feature of macrophage infiltration. In this study, we measured the effects of the aldosterone antagonist, spironolactone, on renal injury in L-NAME-treated male Wistar rats. After 12 weeks of L-NAME-treatment, rats had increased systolic blood pressure, urinary protein excretion, and serum creatinine and histological analysis showed glomerulosclerosis, interstitial fibrosis, and macrophage infiltration. Treatment with spironolactone significantly prevented these renal changes, whereas treatment with hydralazine had no effect. The cortical expression of osteopontin was significantly elevated in L-NAME-treated rats, and expression of its mRNA significantly correlated with the number of infiltrating macrophages and degree of interstitial fibrosis. Spironolactone treatment markedly suppressed osteopontin expression. Our results suggest that reduced nitric oxide bioavailability caused renal inflammation and fibrosis through an aldosterone receptor-dependent mechanism associated with osteopontin expression independent of its systemic hemodynamic effects.
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