IntroductionThe present study was aimed to test the role of endothelin-1 (ET-1) as a possible autocrine/paracrine growth factor for cardiac fibroblasts, and to examine its interaction with cardiac natriuretic hormones. Expression of preproET-1 (ppET-1) mRNA by cultured cardiac fibroblasts from neonatal rats was demonstrated by Northern blot analysis using cDNA for rat ppET-1 as a probe. Although cardiomyocytes occupy -75% of the structural space of the heart, they constitute only one third of the total cell population (1, 2). The remaining non-myocytes consist mainly of cardiac fibroblasts in the interstitium. It has been recently shown that growth of cardiac fibroblast associated with enhanced collagen accumulation in the myocardial interstitium is involved in the remodeling process of left ventricular hypertrophy (3, 4). Several recent in vivo studies have suggested that angiotensin II (ANG I) 1 is a critical growth factor for cardiac hypertrophy. Treatment with a subdepressor dose of angiotensin-converting enzyme inhibitors (5) and angiotensin receptor antagonists (6) prevent an increase in left ventricular mass. It has been also reported that chronic infusion of a subpressor dose of ANG II into rats causes left ventricular hypertrophy(6). Since ANG II stimulates cellular proliferation (7) and several extracellular matrix gene expressions in cardiac fibroblasts (8), and induces cardiomyocyte hypertrophy (9, 10), ANG II is considered to act directly on both cardiomyocytes and fibroblasts.We (11)

We have studied the impact of the Al2O3 inter-layer on interface properties of HfO2/InGaAs metal-oxide-semiconductor (MOS) interfaces. We have found that the insertion of the ultrathin Al2O3 inter-layer (2 cycle: 0.2 nm) can effectively improve the HfO2/InGaAs interface properties. The frequency dispersion and the stretch-out of C-V characteristics are improved, and the interface trap density (Dit) value is significantly decreased by the 2 cycle Al2O3 inter-layer. Finally, we have demonstrated the 1-nm-thick capacitance equivalent thickness in the HfO2/Al2O3/InGaAs MOS capacitors with good interface properties and low gate leakage of 2.4 × 10−2 A/cm2.

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We report that a Ni–InGaAs alloy can be used as a source/drain (S/D) metal for InGaAs metal–oxide–semiconductor field-effect transistors (MOSFETs), allowing us to employ the salicide-like self-align S/D formation. We also introduce Schottky barrier height (SBH) engineering process by increasing the indium content of InxGa1-xAs channels, which successfully reduces SBH down to zero. We propose a fabrication process for self-aligned metal S/D MOSFETs using Ni–InGaAs and demonstrate successful operation of the metal S/D InxGa1-xAs MOSFETs. The In0.7Ga0.3As MOSFETs exhibit an S/D resistance (RSD) that is 1/5 lower than that in P–N junction devices and a high peak mobility of 2000 cm2 V-1 s-1.

Neuropeptide Y (NPY) is a potent feeding stimulant. The orexigenic effect of NPY might be caused in part by the action of Y1 receptors. However, the existence of multiple NPY receptors including a possible novel feeding receptor has made it difficult to determine the relative importance of the Y1 receptor in feeding regulation. Herein we certified that the Y1 receptor is a major feeding receptor of NPY by using the potent and selective Y1 antagonist (-)-2-[1-(3-chloro-5-isopropyloxycarbonylaminophenyl)ethylamino]-6-[2-(5-ethyl-4-methyl-1,3-thiazol-2-yl)ethyl]-4-morpholinopyridine (J-115814) and Y1 receptor-deficient (Y1-/-) mice. J-115814 displaced (125)I-peptide YY binding to cell membranes expressing cloned human, rat, and murine Y(1) receptors with K(i) values of 1.4, 1.8, and 1.9 nM, respectively, and inhibited NPY (10 nM)-induced increases in intracellular calcium levels via human Y1 receptors (IC(50) = 6.8 nM). In contrast, J-115814 showed low affinities for human Y2 (K(i) > 10 microM), Y4 (K(i) = 640 nM) and Y5 receptors (K(i) = 6000 nM). Intracerebroventricular (ICV) (10-100 microg) and intravenous (IV) (0.3-30 mg/kg) administration of J-115814 significantly and dose-dependently suppressed feeding induced by ICV NPY (5 microg) in satiated Sprague-Dawley rats. Intraperitoneal (IP) administration of J-115814 (3-30 mg/kg) significantly attenuated spontaneous feeding in db/db and C57BL6 mice. Feeding induced by ICV NPY (5 microg) was unaffected by IP-injected J-115814 (30 mg/kg) in Y1-/- mice and was suppressed in wild-type and Y5-/- mice. These findings clearly suggest that J-115814 inhibits feeding behaviors through the inhibition of the typical Y1 receptor. We conclude that the Y1 receptor plays a key role in regulating food intake.