IntroductionWe previously demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone mainly produced in the ventricle, while the major production site of atrial natriuretic peptide (ANP) is the atrium. 1. Abbreviations used in this paper: ANP, atrial natriuretic peptide; BNP, brain NP; ET-1, endothelin-1; HP-GPC, high performance gel permeation chromatography; -LI, like immunoreactivity; MLC-2, myosin light chain-2; PKC, protein kinase C.The identification of atrial natriuretic peptide (ANP)' in the cardiac atrium (1, 2) uncovered a new functional role of the heart as an endocrine organ regulating body fluid homeostasis and blood pressure control (3-5). ANP is mainly produced in and released from the atrium, and the plasma ANP concentration elevates in volume-overloaded states including congestive heart failure (6-8). In addition, the gene expression of ANP in the ventricle is markedly induced during the process of cardiac hypertrophy upon ventricular overload, and significantly contributes to the increase in the plasma ANP concentration in various cardiovascular disorders (9-11).Brain natriuretic peptide (BNP), originally isolated from the porcine brain (12), is a second member of natriuretic peptide family (3-5). We previously demonstrated that BNP is predominantly synthesized in and secreted from the cardiac ventricle (13-15). We have further shown that the ventricular gene expression of BNP is substantially augmented in response to ventricular overload in congestive heart failure, idiopathic cardiomyopathy, or hypertensive heart disease with cardiac hypertrophy (14-17). Although the plasma BNP concentration is approximately one-sixth of the plasma ANP concentration in healthy men, it markedly elevates in patients with congestive heart failure in parallel with its severity and surpasses the plasma ANP concentration in severe cases (14,(18)(19)(20). Furthermore, we have recently demonstrated that the plasma BNP concentration increases rapidly and tremendously, in contrast to the modest change of the plasma ANP concentration, in the early clinical course of acute myocardial infarction (21,22). These findings indicate that the biosynthesis and secretion of BNP are distinctly regulated from those of ANP in response to ventricular overload, and suggest that BNP may have a discrete pathophysiological role in the maintenance of cardiovascular homeostasis.The augmented productions of BNP and ANP in the hypertrophied myocardium can be considered as a compensation mechanism against ventricular overload, since BNP and ANP serve to reduce both cardiac preload and afterload by their natriuretic, diuretic, and vasodilatory actions (23)(24)(25). It will be of great importance to characterize the gene expressions of BNP and ANP during the development of cardiac hypertrophy, which also constitutes one of the principal adapting mechanisms against increased ventricular workload (26). The cellular mechanisms of the cardiac adaptations to ventricular overload, especially the expressions of various cardiac-spe...

Plan-view transmission electron microscopy (TEM) and cathodoluminescence (CL) images were taken for the same sample at exactly the same location in n-type GaN grown on sapphire substrate by metalorganic chemical vapor deposition (MOCVD). There was a clear one to one correspondence between the dark spots observed in CL images and the dislocations in TEM foils, indicating that the dislocations are non-radiative recombination centers. The hole diffusion length in n-type GaN was estimated to be neighboring 50 nm by comparing the diameters of the dark spots in thick samples used for CL and samples that were thinned for TEM observation. The efficiency of light emission is high as long as the minority carrier diffusion length is shorter than the dislocation spacing.

The role of dislocation for luminescence in InGaN grown on sapphire substrate by metal organic chemical vapor deposition (MOCVD) method was investigated by cathodoluminescence (CL) and atomic force microscopy (AFM). The CL emission area and dark spots between InGaN and GaN layers in InGaN/GaN single quantum well (SQW) and multiple quantum well (MQW) structures showed completely one to one correspondence. These results indicate that dislocations in InGaN work as non-radiative recombination centers. Furthermore it was confirmed that the phase separation in InGaN is caused by spiral growth due to mixed dislocations, and such a growth mechanism is discussed.

Crystal growth of cubic silicon carbide (3C-SiC) on α-SiC (6H- and 15R-SiC) substrates was carried out by chemical vapor deposition. 3C-SiC (111) can be epitaxially grown on 6H- and 15R-SiC (0001) substrates. Due to the peculiar stacking sequence of α-SiC, double positioning boundaries (DPBs) appear in the 3C-SiC (111) layers. The layer on 15R-SiC has far fewer DPBs than that on 6H-SiC. Successive etching of a thick grown layer and successive observation of a growing surface revealed that the DPBs decreased anisotropically as crystal growth proceeded. Facets formed along DPBs were analyzed by atomic force microscopy. The angles between the facets and the grown surface (111) varied with the crystallographic orientation of DPBs. DPBs may decrease due to the lateral growth from the facets. The difference in the velocities of the anisotropic decrease in DPBs was discussed on the basis of the number of dangling bonds on the facets.

The dislocation distribution and emission profile of sublimation lateral overgrowth GaN and metalorganic chemical vapor deposition films have been studied using transmission electron microscopy and cathodoluminescence. A close relationship between the emission profile and the dislocation distribution has been observed. The results show that the dislocations not only affect the band edge emission, but also the yellow emission. It is observed that the dislocations propagate laterally in the overgrowth region. The mechanism of the change in the propagation direction of dislocations has been discussed.