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A plasmonic array, consisting of metallic nanocylinders periodically arranged with a pitch comparable to the optical wavelength, is a system in which both the localized surface plasmon polaritons (SPPs) and diffraction in the plane of the array are simultaneously excitable. When combined with a phosphor film, the array acts as a photoluminescence (PL) director and enhancer. Since the array can modify both excitation and emission processes, the overall modification mechanism is generally complex and difficult to understand. Here, we examined the mechanism by simplifying the discussion using an emitter with a high quantum yield, large Stokes shift, and long PL lifetime. Directional PL enhancement as large as five-fold occurred, which is mainly caused by outcoupling, i.e., the PL trapped in the emitter film by total internal reflection is extracted into free space through the SPPs and diffraction. The present scheme is robust and applicable to arbitrary emitters, and it is useful for designing compact and efficient directional illumination devices.

The Wilms' tumor gene WT1 is overexpressed in leukemia and solid tumors and has an oncogenic role in leukemogenesis and tumorigenesis. However, precise regulatory mechanisms of WT1 overexpression remain undetermined. In the present study, microRNA-125a (miR-125a) was identified as a miRNA that suppressed WT1 expression via binding to the WT1-3'UTR. MiR-125a knockout mice overexpressed WT1, developed myeloproliferative disorder (MPD) characterized by expansion of myeloid cells in bone marrow (BM), spleen and peripheral blood, and displayed urogenital abnormalities. Silencing of WT1 expression in hematopoietic stem/progenitor cells of miR-125a knockout MPD mice by short-hairpin RNA inhibited myeloid colony formation in vitro. Furthermore, the incidence and severity of MPD were lower in miR-125a (-/-) mice than in miR-125a (+/-) mice, indicating the operation of compensatory mechanisms for the complete loss of miR-125a. To elucidate the compensatory mechanisms, miRNA array was performed. MiR-486 was occasionally induced in compete loss of miR-125a and inhibited WT1 expression instead of miR-125a, resulting in the cancellation of MPD occurrence. These results showed for the first time the post-transcriptional regulatory mechanisms of WT1 by both miR-125a and miR-486 and should contribute to the elucidation of mechanisms of normal hematopoiesis and kidney development.

When photothermally superheated liquid is on a high thermal conductive substrate, the liquid temperature stays constant for a certain range of incident laser power before bubbles are formed.

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