Fabrication of wafer-scale nanoporous AlGaN-based deep ultraviolet distributed Bragg reflectors via one-step selective wet etching

Abstract In this paper, we reported on wafer-scale nanoporous (NP) AlGaN-based deep ultraviolet (DUV) distributed Bragg reflectors (DBRs) with 95% reflectivity at 280 nm, using epitaxial periodically stacked n-Al0.62Ga0.38N/u-Al0.62Ga0.38N structures grown on AlN/sapphire templates via metal–organic chemical vapor deposition (MOCVD). The DBRs were fabricated by a simple one-step selective wet etching in heated KOH aqueous solution. To study the influence of the temperature of KOH electrolyte on the nanopores formation, the amount of charge consumed during etching process was counted, and the surface and cross-sectional morphology of DBRs were characterized by Scanning electron microscopy (SEM) and atomic force microscopy (AFM). As the electrolyte temperature increased, the nanopores became larger while the amount of charge reduced, which revealed that the etching process was a combination of electrochemical and chemical etching. The triangular nanopores and hexagonal pits further confirmed the chemical etching processes. Our work demonstrated a simple wet etching to fabricate high reflective DBRs, which would be useful for AlGaN based DUV devices with microcavity structures

Deep UV Laser at 249 nm Based on GaN Quantum Wells

Deep UV Laser at 249 nm Based on GaN Quantum Well

Cigarette smoke induces C/EBP-β-mediated activation of miR-31 in normal human respiratory epithelia and lung cancer cells.

BACKGROUND: Limited information is available regarding mechanisms by which miRNAs contribute to pulmonary carcinogenesis. The present study was undertaken to examine expression and function of miRNAs induced by cigarette smoke condensate (CSC) in normal human respiratory epithelia and lung cancer cells. METHODOLOGY: Micro-array and quantitative RT-PCR (qRT-PCR) techniques were used to assess miRNA and host gene expression in cultured cells, and surgical specimens. Software-guided analysis, RNA cross-link immunoprecipitation (CLIP), 3' UTR luciferase reporter assays, qRT-PCR, focused super-arrays and western blot techniques were used to identify and confirm targets of miR-31. Chromatin immunoprecipitation (ChIP) techniques were used to evaluate histone marks and transcription factors within the LOC554202 promoter. Cell count and xenograft experiments were used to assess effects of miR-31 on proliferation and tumorigenicity of lung cancer cells. RESULTS: CSC significantly increased miR-31 expression and activated LOC554202 in normal respiratory epithelia and lung cancer cells; miR-31 and LOC554202 expression persisted following discontinuation of CSC exposure. miR-31 and LOC554202 expression levels were significantly elevated in lung cancer specimens relative to adjacent normal lung tissues. CLIP and reporter assays demonstrated direct interaction of miR-31 with Dickkopf-1 (Dkk-1) and DACT-3. Over-expression of miR-31 markedly diminished Dkk-1 and DACT3 expression levels in normal respiratory epithelia and lung cancer cells. Knock-down of miR-31 increased Dkk-1 and DACT3 levels, and abrogated CSC-mediated decreases in Dkk-1 and DACT-3 expression. Furthermore, over-expression of miR-31 diminished SFRP1, SFRP4, and WIF-1, and increased Wnt-5a expression. CSC increased H3K4Me3, H3K9/14Ac and C/EBP-β levels within the LOC554202 promoter. Knock-down of C/EBP-β abrogated CSC-mediated activation of LOC554202. Over-expression of miR-31 significantly enhanced proliferation and tumorigenicity of lung cancer cells; knock-down of miR-31 inhibited growth of these cells. CONCLUSIONS: Cigarette smoke induces expression of miR-31 targeting several antagonists of cancer stem cell signaling in normal respiratory epithelia and lung cancer cells. miR-31 functions as an oncomir during human pulmonary carcinogenesis