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( Qifei Zhou ),( Na Ren ),( Changqing Zhu ),( Deyu Tong ) 한국인터넷정보학회 2018 KSII Transactions on Internet and Information Syst Vol.12 No.7
Most of current watermarking algorithms for GIS vector data embed copyright information by means of modifying the coordinate values, which will do harm to its quality and accuracy. To preserve the fidelity of vector line data and protect its copyright at the same time, a lossless watermarking algorithm is proposed based on storage feature in this paper. Firstly, the superiority of embedding watermark based on storage feature is demonstrated theoretically and technically. Then, the basic concepts and operations on storage feature have been defined including length and angle of the polyline feature. In the process of embedding watermark, the watermark information is embedded into directions of polyline feature by the quantitative mechanism, while the positions of embedding watermark are determined by the feature length. Hence, the watermark can be extracted by the same geometric features without original data or watermark. Finally, experiments have been conducted to show that coordinate values remain unchanged after embedding watermark. Moreover, experimental results are presented to illustrate the effectiveness of the method.
Xin Sun,Tao Zhang,Qifei Deng,Qirui Zhou,Xianchao Sun,Enlai Li,Dexin Yu,Caiyun Zhong 한국분자세포생물학회 2018 Molecules and cells Vol.41 No.3
Benzidine, a known carcinogen, is closely associated with the development of bladder cancer (BC). Epithelial–mesenchymal transition (EMT) is a critical pathophysiological process in BC progression. The underlying molecular mechanisms of mitogen-activated protein kinase (MAPK) pathway, especially extracellular regulated protein kinases 5 (ERK5), in regulating benzidine-induced EMT remains unclarified. Hence, two human bladder cell lines, T24 and EJ, were utilized in our study. Briefly, cell migration was assessed by wound healing assay, and cell invasion was determined by Transwell assay. Quantitative PCR and western blot were utilized to determine both gene expressions as well as protein levels of EMT and MAPK, respectively. Small interfering RNA (siRNA) was transfected to further determine ERK5 function. As a result, the migration and invasion abilities were enhanced, epithelial marker ex-pression was decreased while mesenchymal marker expression was increased in human BC cell lines. Meanwhile, benzidine administration led to activation of ERK5 and activator protein 1 (AP-1) proteins, without effective stimulation of the Jun N-terminal kinase (JNK) or p38 pathways. Moreover, Benzidine-induced EMT and ERK5 activation were completely suppressed by XMD8-92 and siRNAs specific to ERK5. Of note, ERK1/2 was acti-vated in benzidine-treated T24 cells, while benzidine-induced EMT could not be reversed by U0126, an ERK1/2 inhibitor, as indicated by further study. Collectively, our findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression, indicating the therapeutic significance of ERK5 in benzidine-related BC.
Sun, Xin,Zhang, Tao,Deng, Qifei,Zhou, Qirui,Sun, Xianchao,Li, Enlai,Yu, Dexin,Zhong, Caiyun Korean Society for Molecular and Cellular Biology 2018 Molecules and cells Vol.41 No.3
Benzidine, a known carcinogen, is closely associated with the development of bladder cancer (BC). Epithelial-mesenchymal transition (EMT) is a critical pathophysiological process in BC progression. The underlying molecular mechanisms of mitogen-activated protein kinase (MAPK) pathway, especially extracellular regulated protein kinases 5 (ERK5), in regulating benzidine-induced EMT remains unclarified. Hence, two human bladder cell lines, T24 and EJ, were utilized in our study. Briefly, cell migration was assessed by wound healing assay, and cell invasion was determined by Transwell assay. Quantitative PCR and western blot were utilized to determine both gene expressions as well as protein levels of EMT and MAPK, respectively. Small interfering RNA (siRNA) was transfected to further determine ERK5 function. As a result, the migration and invasion abilities were enhanced, epithelial marker expression was decreased while mesenchymal marker expression was increased in human BC cell lines. Meanwhile, benzidine administration led to activation of ERK5 and activator protein 1 (AP-1) proteins, without effective stimulation of the Jun N-terminal kinase (JNK) or p38 pathways. Moreover, Benzidine-induced EMT and ERK5 activation were completely suppressed by XMD8-92 and siRNAs specific to ERK5. Of note, ERK1/2 was activated in benzidine-treated T24 cells, while benzidine-induced EMT could not be reversed by U0126, an ERK1/2 inhibitor, as indicated by further study. Collectively, our findings revealed that ERK5-mediated EMT was critically involved in benzidine-correlated BC progression, indicating the therapeutic significance of ERK5 in benzidine-related BC.