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Background: Pigment epithelium-derived factor (PEDF) is an anti-angiogenic factor. The purpose of this study is to examine the involvement of PEDF in the angiogenesis and biological behavior of bladder transitional cell carcinoma (TCC). Methods: We examined the expression of PEDF in 99 bladder TCCs and ten non-neoplastic tissues, and evaluated microvessel density (MVD). Results: The positive immunoreactivity for PEDF was seen in normal urothelium in 60% (6/10) and TCC in 13% (13/99). The PEDF expression had a significant correlation with MVD, i.e., a low MVD in 42% (5/12), a middle MVD in 11% (8/76) and a high MVD 0% (0/11) of tumors. The PEDF expression was not significantly correlated with the differentiation and invasion of TCC, but the degree of MVD was significantly higher in both high grade TCC and the pT2 tumors. Conclusions: The degree of PEDF expression is significantly higher in normal bladder urothelium than bladder TCC; it is inversely correlated with the angiogenesis; and it is not related to the differentiation and progression of TCC. It can therefore be concluded that bladder TCC would initially occur if there is a lack of the PEDF expression.
Carcinsarcoma is an uncommon pulmonary malignancy characterized by carcinmatous parenchyma and sarcomatous stroma. The cytologic, immunohistochemical and ultrastructural features of a case of pulmonary carcinosarcoma suspected by fine needle aspiration cytology is presented. Only bizarre spindle cells arranged in loose groups, in microtissue fragments and in a dissociate fashion were present on the aspiration smears. They were markedly positive for vimentin. The epithelial component was not found, which was probably due to marked paucity of carcinomatous component that was proved by histologic examination of the resected tumor. The diagnosis of pulmonary carcinosarcoma should be conidered whenever poorly differentiated epithelial ceil groups with a malignant mesenchymal component set in a myxoid background are seen in a pulmonary cytology specimen.
Background: We examined the distribution of CD8+ T cells and regulatory T cells (Tregs), measured the CD8+ T cell/Tregs ratio, investigated the relationship between Tregs and cyclooxygenase-2 (COX-2) expression during colorectal cancer (CRC) development. Methods: We performed immunohistochemical staining for CD8, forkhead box P3, E-cadherin, and COX-2 in 32 cases of invasive CRC, 10 cases of intramucosal CRC, 27 cases of high-grade tubular adenoma, 22 cases of low-grade tubular adenoma, and 32 cases of non-neoplastic conditions. Results: We observed a progressive increase in Tregs, and a decrease in CD8+ T cells and the CD8+ T cells/Tregs ratio during CRC development. The alterations were most severe in high-grade tubular adenoma and CRC. COX-2 expression was positively associated with Tregs infiltration. The degree of T cell infiltration differed among tumor compartment and the ratio in the tumor center was the lowest of all areas. The ratio and number of CD8+ T cells in the tumor center and the invasive front of invasive CRC were associated with gender, differentiation, node metastasis and tumor budding. Conclusions: Alteration in the distribution of both CD8+T cells and Tregs may contribute to the generation of an immune environment suitable for the development and progression of CRC.
Background : Nonsteroidal anti-inflammatory drug activated gene (NAG-1) has proapoptotic activities in the colon and also in gastric cancer cells that lack any endogenous COX-2 expression. Recent studies have suggested that the proa- poptotic activity of NAG-1 is cell type specific. I investigated the cell proliferation, invasiveness and apoptosis in Hep3B cells and SNU719 cells by determining the different expression levels of NAG-1. In addition, I examined the gene profile in the Hep3B cells that have a stable expression of NAG-1. Methods : SNU719 cells and several clones of Hep3B cells with a stable expression of NAG-1 were used. I reduced the expression level of NAG-1 via the RNAi method. An Agilent Human 22k microarray was used for studying the gene profile in Hep3B cells that had a stable expression of NAG-1. Results : The expression level of NAG-1 did not influence apoptosis, cell proliferation and invasiveness in Hep3B cells. There was no correlation between the reduction of the endogenous NAG-1 expression and cell proliferation, including invasiveness, in the SNU719 cells. However, a knocked-down NAG-1 expression protected against apoptosis in the SNU719 cells. The microarray analysis results showed that 0.25% (58/22,575) of the genes were induced or repressed more than three fold in the Hep3B cells that had a stable expression of NAG-1. Conclusions : Proapoptotic activity of NAG-1 is found in gastric cancer cells, but not in hepatocellular cancer cells.