The influence of oxidation aperture on the output characteristics of the circularly symmetric vertical-cavity-surface-emitting laser (VCSEL) structure is investigated. To do so, VCSELs with different oxide aperture sizes are simulated by the finite-difference time-domain (FDTD) method. The relationships among the field distribution of mode superposition, mode wavelength, output spectra, and far-field divergence with different oxide apertures are obtained. Further, VCSELs respectively with oxide aperture sizes of 2.7 μm, 4.4 μm, 5.9 μm, 7 μm, 8 μm, 9 μm, and 18.7 μm are fabricated and characterized. The maximum output power increases from 2.4 mW to 5.7 mW with oxide aperture increasing from 5.9 μm to 9 μm. Meanwhile, the wavelength tuning rate decreases from 0.93 nm/mA to 0.375 nm/mA when the oxide aperture increases from 2.7 μm to 9 μm. The thermal resistance decreases from 2.815 °C/mW to 1.015 °C/mW when the oxide aperture increases from 4.4 μm to 18.7 μm. It is demonstrated theoretically and experimentally that the wavelength spacing between adjacent modes increases with the augment of the injection current and the spacing becomes smaller with the oxide aperture increasing. Thus it can be reported that the aperture size can effectively reduce the mode overlaying but at the cost of the power decreasing and the wavelength tuning rate and thermal resistance increasing.
The in-depth study of melanoma pathogenesis has revealed that epigenetic modifications, particularly DNA methylation, is a universal inherent feature of the development and progression of melanoma. In the present study, the analysis of the tumor suppressor gene growth arrest-specific transcript 5 (GAS5) demonstrated that its expression was downregulated in melanoma, and its expression level had a certain negative association with its methylation modification level. The promoter of GAS5 presented with detectable CpG islands, and methylation-specific polymerase chain reaction analysis demonstrated that GAS5 was actually modified by methylation in melanoma tissues and cells; however, no methylation modification of GAS5 was detected in normal tissues. Following the treatment of melanoma cells with 5-Aza-2'-deoxycytidine (5-Aza-dC), GAS5 methylation was significantly reversed. The analysis of melanoma cell proliferation revealed that 5-Aza-dC inhibited A375 and SK-MEL-110 cell proliferation in a time-dependent manner. Further analysis of apoptosis demonstrated that 5-Aza-dC significantly increased the apoptosis level of the two cell lines. Moreover, migration analysis of melanoma cells revealed that 5-Aza-dC significantly reduced cell migration. Furthermore, 5-Aza-dC significantly decreased the invasive ability of the two cell lines. However, when the expression of GAS5 was silenced, the effects of 5-Aza-dC on cell proliferation, apoptosis, invasion and migration were not significant. Furthermore, the subcutaneous injection of A375 cells in nude mice successfully resulted in xenograft tumor formation. However, following an intraperitoneal injection of 5-Aza-dC, the volume and weight of xenograft tumors and Ki-67 expression were significantly reduced, and caspase-3 activity and GAS5 expression were enhanced; following the silencing of GAS5, the antitumor effect of 5-Aza-dC was significantly blocked. On the whole, the present study demonstrates that 5-Aza-dC inhibits the growth of melanoma, and its function may be related to the methylation modification of GAS5.
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