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To explore resonance phenomena in the nonlinear region, we show by experimental measurements and theoretical analyses that resonance happens in modulation instability (MI) from non-instantaneous nonlinearities in photorefractive crystals. With a temporally periodic modulation in the external bias voltage, corresponding to a modulation in the nonlinear strength, an enhancement in the visibility of MI at resonant frequency is reported through spontaneous optical pattern formations. Modeled by such temporally periodic nonlinear driving force to the system, theoretical curves obtained from a nonlinear non-instantaneous Schr\"{o}dinger equation give good agreement to experimental data. As MI is a universal signature of symmetry-breaking phenomena, our observation on the resonance in MI may provide a control on chaotic, solitary, and turbulence waves., Comment: 5 pages, 4 figures

Aims FHL2, a member of the four and a half LIM domain (FHL) family of proteins, may play an important role in the circulatory system and in particular atherosclerosis. Main methods To investigate the role of FHL2 in atherogenesis, FHL2-null and wild-type control male mice were fed either a normal chow (NC) or a cholesterol-enriched diet (CED). Key findings At 3 months post CED, aortic atherosclerotic plaques were observed in both control and FHL2-null mice. Lesions in control mice increased dramatically by 6 months of CED. In contrast, lesion size did not increase during this time in CED-fed FHL2-null mice. Relative to control mice on a normal chow of diet (NCD), control mice on a CED exhibited lower circulating nitric oxide (NO) levels, and decreased expression of connexin37 (Cx37) and Cx40 in aortic endothelium. In contrast, FHL2-null mice on a CED maintained similar levels of circulating NO as FHL2-null mice fed a NCD. Cxs levels in aortic endothelium of FHL2-null mutants on a NCD were lower relative to control mice on a NCD, and did not decrease with CED. Significance Our data demonstrate a role for FHL2 in atherogenesis, the regulation of circular NO release, and expression of gap junctions within aortic endothelium.

With measured optical images in spontaneous pattern formations, we observe the phase boundaries in the phase diagram, defining by the degree of coherence and biased voltage. Pattern transitions in the form of stripes, reoriented stripes, hexagons, and spots are revealed experimentally and theoretically for incoherent beams in noninstantaneous anisotropic photorefractive crystals, with demonstrations in the boundary of mixed-phase states.

We report experimental observation of lasing on surface states, in the form of standing waves at the termination of a defect-free photonic crystal on top of vertical-cavity surface-emission lasers. Direct images of lasing modes at the truncated periodic potential, along one side of a square lattice, are demonstrated by collecting near-field radiation patterns, as well as in numerical simulations. Our results provide a step toward realizing surface and edge states in optical cavities.

Objective— We sought to clarify the response of endothelial connexins to hyperlipidemia and lipid-lowering therapy. Methods and Results— Aortic endothelial gap junctions were analyzed by en face immunoconfocal microscopy and electron microscopy in C57BL/6 mice subjected to the following regimens: (1) normal chow (NC) for 3 months (3 mo), (2) NC for 9 mo, (3) NC for 3 mo, followed by a cholesterol-enriched diet (CED) for 6 mo, (4) NC for 3 mo and CED for 6 mo, with simvastatin in the final week, and (5) (in apoprotein E [apoE]-deficient mice) NC and examined at 3 mo and 7 to 9 mo. In wild-type mice, connexin37 (Cx37) and Cx40 were markedly downregulated in the CED-fed animals compared with those fed NC (CED vs 9-mo NC, 77% reduction in Cx37 and 65% reduction in Cx40; both P P P Conclusions— Mouse aortic endothelial gap junctions and connexins are downregulated during long-term hyperlipidemia. Short-term treatment with simvastatin leads to recovery of Cx37 expression but not Cx40 expression.

We show by experimental measurements and theoretical analyses that there exists a pattern transition from optical modulation instability to transverse instability in nonlinear media. An input coherent beam propagating in the photorefractive crystals is observed to break up into stripe filaments at a first threshold voltage. By modeling the periodic strip filaments as cnoidal waves, we demonstrate that a second threshold voltage for forming dot filaments comes from the transverse instability, resulting in a good agreement with the experimental data.

We show by experimental measurements there exists an intensity dependent pattern transition from optical modulation instability to transverse instability in nonlinear media which is explained by our model of periodic strip-filamens on cnoidal waves.

By experimental measurements and theoretical analyses, we demonstrate the control of modulation instability in photorefractive crystals though the intensity ratio of coherent background to signal fields. Appearance, suppression, and disappearance of modulated stripes are observed in a series of spontaneous optical pattern formations, as the intensity of input coherent beam increases. Theoretical curves based on the band transport model give good agreement to experimental data, both for different bias voltages and different intensity ratios.

We compared the behavior of endothelial cells grown on stent materials. Human umbilical vein endothelial cells (HUVEC) were seeded (200 or 800 cells/mm(2)) onto different metallic sheets, including 316 stainless steel (low carbon; 316LSS), nitinol, and 316LSS coated with TiN or TiO(2). Cells seeded onto tissue culture-treated polystyrene dish coated with gelatin were used as controls. Forty-eight hours later, the cells were examined by Western blotting, immunofluorescence microscopy, and scanning electron microscopy (SEM). The results showed that for either seeding values, the levels of cellularity on TiN and TiO(2) are comparable or higher, and those on 316LSS and nitinol are lower compared to the controls (p < 0.05). SEM demonstrated that cells are well-attached on the metallic surface with various amount of cellular processes. In metals seeded with 800 cells/mm(2), Western blotting showed that the overlying cells expressed less amounts of endothelial nitric oxide synthase (eNOS), Von Willebrand factor (VWF), and connexin43 protein compared to the controls (p < 0.05). Immunofluorescence microscopy confirmed the results of immunoblotting. In conclusion, stent materials affect HUVEC's growth and protein expression profile. Down-regulation of eNOS, VWF, and connexin43 gap junctions is a common phenomenon in the cells growing on the examined metallic materials, suggesting the existence of endothelial dysfunction in the arterial segments containing the stents made of such materials.

Background Long-term heavy alcohol drinkers are prone to the development of cardiac arrhythmia. To understand the mechanisms, we evaluated the cardiac structural and electrophysiological changes in mice chronically drinking excessive alcohol. Results Male C57BL/6J mice were given 36% alcohol in the drinking water. Those given blank water were used as control. Twelve weeks later, the phenotypic characteristics of the heart, including gap junctions and electrical properties were examined. In the alcohol group the ventricles contained a smaller size of cardiomyocytes and a higher density of capillary networks, compared to the control. Western blots showed that, after drinking alcohol, the content of connexin43 (Cx43) protein in the left ventricle was increased by 18% (p < 0.05). Consistently, immunoconfocal microscopy demonstrated that Cx43 gap junctions were up-regulated in the alcohol group with a disorganized distribution, compared to the control. Optical mapping showed that the alcohol group had a reduced conduction velocity (40 ± 18 vs 60 ± 7 cm/sec, p < 0.05) and a higher incidence of ventricular tachyarrhythmia (62% vs 30%, p < 0.05). Conclusion Long-term excessive alcohol intake resulted in extensive cardiac remodeling, including changes in expression and distribution of gap junctions, growth of capillary network, reduction of cardiomyocyte size, and decrease of myocardial conduction.