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The depth profiles of Ni-coated copper substrates polished by different mesh size sandpapers were measured by the glow discharge optical emission spectroscopy (GDOES) depth profiling technique. The measured depth profiles were well fitted by the MRI-CRAS model developed recently on the basis of the Mixing-Roughness-Information depth (MRI) model and the CRAter-Simulation (CRAS) model, taking into account the pronounced crater effect upon GDOES depth profiling. The crater effect upon depth profiling was characterized quantitatively and the interface roughness values between the coated Ni layer and the Cu substrates were determined and compared with the ones measured by AFM.

The potential combined effect and mechanism of calcium channel blockers (CCB) and angiotensin II type 1 receptor blockers (ARB) to improve insulin resistance were investigated in type 2 diabetic KK-Ay mice, focusing on their antioxidative action. Treatment of KK-Ay mice with a CCB, azelnidipine (3 mg/kg/day), or with an ARB, olmesartan (3 mg/kg/day), for 2 weeks lowered the plasma concentrations of glucose and insulin in the fed state, attenuated the increase in plasma glucose in the oral glucose tolerance test (OGTT), and increased 2-[(3)H]deoxy-d-glucose (2-[(3)H]DG) uptake into skeletal muscle with the increase in translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Both blockers also decreased the in situ superoxide production in skeletal muscle. The decrease in plasma concentrations of glucose and insulin in the fed state and superoxide production in skeletal muscle, as well as GLUT4 translocation to the plasma membrane, after azelnidipine administration was not significantly affected by coadministration of an antioxidant, 2,2,6,6-tetramethyl-1-piperidinyloxy (tempol). However, those changes caused by olmesartan were further improved by tempol. Moreover, olmesartan enhanced the insulin-induced tyrosine phosphorylation of insulin receptor substrate-1 induced in skeletal muscle, whereas azelnidipine did not change it. Coadministration of azelnidipine and olmesartan further decreased the plasma concentrations of glucose and insulin, improved OGTT, and increased 2-[(3)H]DG uptake in skeletal muscle. These results suggest that azelnidipine improved glucose intolerance mainly through inhibition of oxidative stress and enhanced the inhibitory effects of olmesartan on glucose intolerance, as well as the clinical possibility that the combination of CCB and ARB could be more effective than monotherapy in the treatment of insulin resistance.

Abstracts— The present study explored the possibility that estrogen enhances the inhibitory effect of an angiotensin II type-1 (AT 1 ) receptor blocker (ARB), olmesartan, on atherosclerosis, focusing on oxidative stress using apolipoprotein E knockout mice (ApoEKO). After 6 weeks on a high-cholesterol diet, marked atherosclerotic lesion formation with an increase in oxidative stress, such as superoxide production, NAD(P)H oxidase activity and expression of p47 phox mRNA and rac-1 mRNA, were observed in the proximal aorta in both male and female ApoEKO mice, whereas these changes were less marked in female mice. Ovariectomy enhanced these parameters, the changes of which were reversed by 17β-estradiol (80 μg/kg per day) replacement. Treatment with olmesartan (3 mg/kg per day) significantly inhibited oxidative stress and atherosclerosis, whereas its inhibitory effects were more marked in female than in male or ovariectomized mice. Smaller doses of olmesartan (0.5 mg/kg per day) or 17β-estradiol (20 μg/kg per day) did not influence atherosclerosis and oxidative stress in ovariectomized mice, whereas co-administration of olmesartan and 17β-estradiol at these doses attenuated these parameters. An angiotensin-converting enzyme (ACE) inhibitor, temocapril, also inhibited atherosclerotic changes similarly to olmesartan. Moreover, angiotensin II–mediated activation of NAD(P)H oxidase in cultured vascular smooth muscle cells was attenuated by 17β-estradiol. These results indicate that estrogen and an ARB synergistically attenuate atherosclerosis at least partly via inhibition of oxidative stress.

Angiotensin II has been shown to contribute to the pathogenesis of insulin resistance; however, the mechanism is not well understood. The present study was undertaken to investigate the potential effect of an angiotensin II type-1 (AT 1 ) receptor blocker, valsartan, to improve insulin resistance and to explore the signaling basis of cross-talk of the AT 1 receptor- and insulin-mediated signaling in type 2 diabetic KK-Ay mice. Treatment of KK-Ay mice with valsartan at a dose of 1 mg/kg per day, which did not influence systolic blood pressure, significantly increased insulin-mediated 2-[ 3 H]deoxy- d -glucose (2-[ 3 H]DG) uptake into skeletal muscle and attenuated the increase in plasma glucose concentration after a glucose load and plasma concentrations of glucose and insulin. In contrast, insulin-mediated 2-[ 3 H]DG uptake into skeletal muscle was not influenced in AT 2 receptor null mice, and an AT 2 receptor blocker, PD123319, did not affect 2-[ 3 H]DG uptake and superoxide production in skeletal muscle of KK-Ay mice. Moreover, we observed that valsartan treatment exaggerated the insulin-induced phosphorylation of IRS-1, the association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3 kinase (PI 3-K), PI 3-K activity, and translocation of GLUT4 to the plasma membrane. It also reduced tumor necrosis factor-α (TNF-α) expression and superoxide production in skeletal muscle of KK-Ay mice. Specific AT 1 receptor blockade increases insulin sensitivity and glucose uptake in skeletal muscle of KK-Ay mice via stimulating the insulin signaling cascade and consequent enhancement of GLUT4 translocation to the plasma membrane.

Low-density parity-check (LDPC) codes have been widely considered as error-correcting codes for next generation communication systems. A good LDPC decoder design requires both implementation friendly LDPC codes and efficient decoder architectures. The quality of LDPC code is crucial in determining the coding gain and implementation complexity of LDPC hardware decoders. This paper presented a genetic algorithm (GA) based LDPC code search algorithm with hardware considerations. Regular quasi-cyclic LDPC codes are used due to its friendliness to hardware implementation. Our hardware architecture design schedules pipeline LDPC decoding operation to boost the hardware utilization efficiency (HUE) of LDPC decoder. A LDPC decoder with a block size of 12288 is implemented in FPGA to validate our code and architecture design.