ϭ 3 ϫ 10 7 S/m, and the input modulated Gaussian pulse is V 0 ϭ 1.0 V, ϭ 16.68 ps, and t 0 ϭ 66.68 ps.As in Figure 4, the attenuation of the propagating sinusoidally modulated Gaussian pulse is due mainly to the ohmic loss of both the center strip and ground planes. Also, the attenuation is more rapid at the start of the pulse propagation distance. CONCLUSIONSBased on an improved empirical formula to calculate the ohmic loss of CPWs, the lossy effects in coplanar waveguides on the pulse propagation have been studied. These CPWs are assumed to be fabricated on single-layer, low-dispersion and low-loss LTCC. For normal LTCC CPWs, it is shown that the total loss is contributed mainly by the ohmic loss of the conductive planes in the frequency range up to 40 GHz. The ohmic loss can lead to nearly 50% pulse magnitude attenuation at the start of the propagation distance of less than several millimeters.

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The diet-induced atherosclerotic rabbit is an ideal model for atherosclerosis study, but temporal changes in atherosclerotic development in hypercholesterolemic rabbits are poorly understood. Japanese white rabbits were fed a high-cholesterol diet to induce sustained hypercholesterolemia, and each group of 10–12 animals was then sacrificed at 6, 12, 16, or 28 weeks. The rabbit aortas were harvested, and the sizes of the gross and intima atherosclerotic lesions were quantified. The cellular component of macrophages (Mφs) and smooth muscle cells (SMCs) in aortic intimal lesions was also quantified by immunohistochemical staining, and the correlation between plasma cholesterol levels and the progress of atherosclerotic lesions was studied. The ultrastructure of the atherosclerotic lesions was observed by transmission electron microscopy (TEM). Widely variable atherosclerotic plaques were found from 6 weeks to 28 weeks, and the lesional progress was closely correlated with cholesterol exposure. Interestingly, a relatively reduced accumulation of Mφ, an increased numbers of SMCs, and a damaged endothelial layer were presented in advanced lesions. Moreover, SMCs were closely correlated with cholesterol exposure and lesional progress for the whole period. Cholesterol exposure directly determines atherosclerotic progress in a rabbit model, and the changes in the cellular component of advanced lesions may affect plaque stability in an atherosclerotic rabbit model.

We found that the PB group and the PB+CZ group exhibited a reduction in the lesion areas (70% in the PB+CZ group, 56% in the PB group) compared with the vehicle group. However, although PB alone and PB+CZ led to a reduction in the lesion size, the histological analysis revealed that only PB+CZ significantly decreased the macrophage accumulation and smooth muscle cell proliferation in the lesions compared with the vehicle group. The plasma levels of total cholesterol in the PB+CZ group were decreased compared with the vehicle group, Moreover, PB+CZ exerted obvious anti-oxidant and anti-inflammatory effects. Interestingly, the PB+CZ treatment led to a marked increase in the levels of plasma NO. The in vitro experiments showed that the combinatorial treatment up-regulated the levels of NO and protein S-nitrosylation in endothelial cells treated with oxidized LDL. In summary, these results suggest that PB and CZ exert combinatorial anti-atherogenic effects.

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