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Fumihiro Inoue,Satoru Doi,Tatsuya Ishizaki,Yasuhiro Ikeda,Yutaka Ohta 제어로봇시스템학회 2010 제어로봇시스템학회 국제학술대회 논문집 Vol.2010 No.10
This paper describes an automated inspection robot for detecting tile exfoliation and a new diagnostic method for determining its existence and extent. The robot moves quickly along a vertical wall and stops to detect a tile’s inner condition using a hammering sound. Tile separation commonly comprises outer exfoliation where the tile separates from the mortar concrete and inner exfoliation where the space between the substrate and the mortar concrete deteriorates. In order to detect these two exfoliations, we focused attention on wavelet analysis, which enables us to analyze the frequency element of the sound waveform on time phase continuously. By comparing the wavelet volume rate expressing the characteristics of tile deterioration for several scale tiles and striking hammers, the quantitative detection and its scale effects of visually distinguishing the two exfoliation modes was established. The automated robot and the diagnostics method were used to perform a fast and highly accurate inspection of the outer tile wall.
Toshikazu Araoka,Hideharu Abe,Tatsuya Tominaga,Akira Mima,Takeshi Matsubara,Taichi Murakami,Seiji Kishi,Kojiro Nagai,Toshio Doi 한국분자세포생물학회 2010 Molecules and cells Vol.30 No.3
Smad1 has previously been shown to play a key role in the development of diabetic nephropathy (DN), by increasing synthesis of extracellular matrix. However, the regulatory mechanism of Smad1 in DN is still unclear. This study aims to elucidate molecular interactions between activin receptor-like kinase 1 (ALK1)/Smad1 signaling pathway and transcription factor 7-like 2 (TCF7L2) in the progression of DN in vitro and in vivo. The expressions of TCF7L2and ALK1 were induced by advanced glycation end products (AGEs) in parallel with Smad1, phosphorylated Smad1 (pSmad1), and alpha-smooth muscle actin (α-SMA)through TGF-β1 in cultured mesangial cells. Constitutively active ALK1 increased pSmad1 and α-SMA expressions. The binding of TCF7L2 to ALK1 promoter was confirmed by chromatin immunoprecipitation assay. Furthermore,TCF7L2 induced promoter activity of ALK1. AGEs and TGF-β1 induced a marked increase in TCF7L2 expression in parallel with ALK1. Overexpression of TCF7L2 increased the expressions of ALK1 and Smad1. Inversely, TCF7L2knockdown by siRNA suppressed α-SMA expression as well as ALK1 and Smad1. The iNOS transgenic mice (iNOS-Tgm), which developed diabetic glomerulosclerosis resembling human diabetic nephropathy, exhibited markedly increased expressions of ALK1, TCF7L2, Smad1,pSmad1, and α-SMA in glomeruli in association with mesangial matrix expansion. These results provide a new evidence that the TCF7L2/ALK1/Smad1 pathway plays a key role in the development of DN.
Araoka, Toshikazu,Abe, Hideharu,Tominaga, Tatsuya,Mima, Akira,Matsubara, Takeshi,Murakami, Taichi,Kishi, Seiji,Nagai, Kojiro,Doi, Toshio Korean Society for Molecular and Cellular Biology 2010 Molecules and cells Vol.30 No.3
Smad1 has previously been shown to play a key role in the development of diabetic nephropathy (DN), by increasing synthesis of extracellular matrix. However, the regulatory mechanism of Smad1 in DN is still unclear. This study aims to elucidate molecular interactions between activin receptor-like kinase 1 (ALK1)/Smad1 signaling pathway and transcription factor 7-like 2 (TCF7L2) in the progression of DN in vitro and in vivo. The expressions of TCF7L2 and ALK1 were induced by advanced glycation end products (AGEs) in parallel with Smad1, phosphorylated Smad1 (pSmad1), and alpha-smooth muscle actin (${\alpha}$-SMA) through TGF-${\beta}$1 in cultured mesangial cells. Constitutively active ALK1 increased pSmad1 and ${\alpha}$-SMA expressions. The binding of TCF7L2 to ALK1 promoter was confirmed by chromatin immunoprecipitation assay. Furthermore, TCF7L2 induced promoter activity of ALK1. AGEs and TGF-${\beta}$1 induced a marked increase in TCF7L2 expression in parallel with ALK1. Overexpression of TCF7L2 increased the expressions of ALK1 and Smad1. Inversely, TCF7L2 knockdown by siRNA suppressed ${\alpha}$-SMA expression as well as ALK1 and Smad1. The iNOS transgenic mice (iNOS-Tgm), which developed diabetic glomerulosclerosis resembling human diabetic nephropathy, exhibited markedly increased expressions of ALK1, TCF7L2, Smad1, pSmad1, and ${\alpha}$-SMA in glomeruli in association with mesangial matrix expansion. These results provide a new evidence that the TCF7L2/ALK1/Smad1 pathway plays a key role in the development of DN.