A distributed-feedback laser was demonstrated by using a fluorescent dye-doped polymer. The periodic structure of a one-dimensional photonic crystal was fabricated through spin coating and alternate stacking of high and low refractive-index polymers. The rhodamine-6G-doped multilayer showed a photonic band gap in the transmissivity spectrum at the fluorescent wavelength range. Laser emission from the surface of the multilayer was attained at the band edge for a pump of the second harmonic of a neodymium-doped yttrium aluminum garnet laser. Wavelength tuning was possible by spin coating a multilayer onto a concave substrate.

Although several autoimmune diseases are known to develop in postmenopausal women, the mechanisms by which estrogen defi ciency infl uences autoimmunity remain unclear. Recently, we found that retinoblastoma-associated protein 48 (RbAp48) induces tissuespecifi c apoptosis in the exocrine glands depending on the level of estrogen defi ciency. In this study, we report that transgenic (Tg) expression of RbAp48 resulted in the development of autoimmune exocrinopathy resembling Sj ö gren ' s syndrome. CD4 + T cell -mediated autoimmune lesions were aggravated with age, in association with autoantibody productions. Surprisingly, we obtained evidence that salivary and lacrimal epithelial cells can produce interferon-␥ (IFN-␥ ) in addition to interleukin-18, which activates IFN regulatory factor-1 and class II transactivator. Indeed, autoimmune lesions in Rag2 ؊ / ؊ mice were induced by the adoptive transfer of lymph node T cells from RbAp48 -Tg mice. These results indicate a novel immunocompetent role of epithelial cells that can produce IFN-␥ , resulting in loss of local tolerance before developing gender-based autoimmunity.

CD25+CD4+ regulatory T cells suppress T cell activation and regulate multiple immune reactions in in vitro and in vivo studies. To define the regulatory function of human CD25+CD4+ T cells at various stages of maturity, we investigated in detail the functional differences of CD25+CD4+ T cells from thymocytes, cord blood (CB), and adult peripheral blood (APB). CB CD25+CD4+ T cells displayed low-FOXP3 protein expression level and had no suppressive activity. In contrast, CD25+CD4+ T cells from thymocytes or APB expressed high expression level of FOXP3 protein associated with significant suppressive activity. Although CB CD25+CD4+ T cells exhibited no suppressive activity, striking suppressive activity was observed following expansion in culture associated with increased FOXP3 expression and a shift from the CD45RA+ to the CD45RA− phenotype. These functional differences in CD25+CD4+ T cells from Thy, CB, and APB hence suggest a pathway of maturation for Treg in the peripheral immune system.

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Recently, endoscopic ultrasonography-guided fine needle aspiration (EUS-FNA) has been applied for diagnosis of gastrointestinal submucosal tumors. There have been no definite criteria, however, for the adequate cytological diagnosis of gastrointestinal stromal tumor (GIST) in practice. To facilitate this a novel method is proposed that combines cytology and histology. For 49 cases of submucosal tumor of gastrointestinal tract, EUS-FNA was performed. The aspirated materials were processed for cytology and histology. Both cytological and histological findings were examined on immunocytochemical and immunohistochemical staining of c-kit. Of 49 cases, 40 (81.6%) proved adequate for cytological and/or histological examination. On cytology, cluster types were classified into type A (piled clusters with high cellularity showing a fascicular pattern), type B (thin layered clusters with high cellularity showing a fascicular pattern), and type C (mono-layered clusters or scattered cells). Types A and B were strongly associated with histological diagnosis of GIST. Type C clusters needed confirmation on c-kit positivity and histology. Thus, the combined cytology with newly defined features, and classification and histological diagnostic method for EUS-FNA materials can contribute to improved routine diagnosis for GIST.

Our findings indicate that human Müller cells can produce IL-6 when stimulated by IL-1beta or LPS. Müller cell IL-6 production may have an important role in various conditions involving ocular inflammation

Transcription factor Slug/SNAI2 (snail homolog 2) plays a key role in the induction of the epithelial mesenchymal transition in cancer cells; however, whether the overexpression of Slug mediates the malignant phenotype and alters drug sensitivity in lung cancer cells remains largely unclear. We investigated Slug focusing on its biological function and involvement in drug sensitivity in lung cancer cells. Stable Slug transfectants showed typical morphological changes compared with control cells. Slug overexpression did not change the cellular proliferations; however, migration activity and anchorage-independent growth activity with an antiapoptotic effect were increased. Interestingly, stable Slug overexpression increased drug sensitivity to tubulin-binding agents including vinorelbine, vincristine, and paclitaxel (5.8- to 8.9-fold increase) in several lung cancer cell lines but did not increase sensitivity to agents other than tubulin-binding agents. Real-time RT-PCR (polymerase chain reaction) and western blotting revealed that Slug overexpression downregulated the expression of βIII and βIVa-tubulin, which is considered to be a major factor determining sensitivity to tubulin-binding agents. A luciferase reporter assay confirmed that Slug suppressed the promoter activity of βIVa-tubulin at a transcriptional level. Slug overexpression enhanced tumor growth, whereas Slug overexpression increased drug sensitivity to vinorelbine with the downregulation of βIII and βIV-tubulin in vivo. Immunohistochemistry of Slug with clinical lung cancer samples showed that Slug overexpression tended to be involved in response to tubulin-binding agents. In conclusion, our data indicate that Slug mediates an aggressive phenotype including enhanced migration activity, anoikis suppression, and tumor growth, but increases sensitivity to tubulin-binding agents via the downregulation of βIII and βIVa-tubulin in lung cancer cells.

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