http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Development of Flight Simulator for Human-Powered Aircraft
Yasuhiro Inaba,Yuzo Shimada,Kenji Uchiyama,Kenichi Abe,Yoshio Ishikawa,Takao Sugimoto,Yasuyuki Miyazaki,Yuzo Koyama,Shohei Onishi,Kazuo Matubara,Chikatoshi Satoh,Takao Minejima,Kaname Hirayanagi,Michi 제어로봇시스템학회 2006 제어로봇시스템학회 국제학술대회 논문집 Vol.2006 No.10
Yoshitaka Matsuda,Tsukasa Shimada,Takenao Sugi,Satoru Goto,Takafumi Morisaki,Yasuyuki Ikegami 제어로봇시스템학회 2015 제어로봇시스템학회 국제학술대회 논문집 Vol.2015 No.10
This research deals with the design of PI controller for the liquid level control of separator in an ocean thermal energy conversion (OTEC) plant with Uehara cycle by considering some kinds of disturbances. The PI controller is designed for a liquid level model under H∞ constraint. The effectiveness of the designed PI controllers is evaluated through simulations considering disturbances.
Jin-Yong Lee,Maki Tokumoto,Yuta Hattori,Yasuyuki Fujiwara,Akinori Shimada,Masahiko Satoh 한국독성학회 2016 Toxicological Research Vol.32 No.1
Chronic exposure to cadmium (Cd) is known to adversely affect renal function. Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells. In this study, the effects of Cd on protein expression of p53 and apoptotic signals in the kidney and liver of mice exposed to Cd for 12 months were examined, as well as the effects of Cd on p53 protein levels and gene expression of the Ube2d family in various cell lines. Results showed that in the kidney of mice exposed to 300 ppm Cd for 12 months, there was overaccumulation of p53 proteins in addition to the induction of apoptosis, which was triggered specifically in the proximal tubules. Interestingly, the site of apoptosis was the same as that of p53 accumulation in the proximal tubules. In the liver of mice chronically exposed to Cd, gene expression of the Ube2d family tended to be slightly decreased, together with slight apoptosis without the accumulation of p53 protein. In rat small intestine epithelial (IEC-6) cells, Cd decreased not only the p53 protein level but also gene expression of Ube2d1, Ube2d2 and Ube2d4. In human brain microvascular endothelial cells (HBMECs), Cd did not suppress gene expression of the Ube2d family, but increased the p53 protein level. In human brain astrocytes (HBASTs), Cd only increased gene expression of UBE2D3. These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.
Lee, Jin-Yong,Tokumoto, Maki,Hattori, Yuta,Fujiwara, Yasuyuki,Shimada, Akinori,Satoh, Masahiko Korean Society of ToxicologyKorea Environmental Mu 2016 Toxicological Research Vol.32 No.1
Chronic exposure to cadmium (Cd) is known to adversely affect renal function. Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells. In this study, the effects of Cd on protein expression of p53 and apoptotic signals in the kidney and liver of mice exposed to Cd for 12 months were examined, as well as the effects of Cd on p53 protein levels and gene expression of the Ube2d family in various cell lines. Results showed that in the kidney of mice exposed to 300 ppm Cd for 12 months, there was overaccumulation of p53 proteins in addition to the induction of apoptosis, which was triggered specifically in the proximal tubules. Interestingly, the site of apoptosis was the same as that of p53 accumulation in the proximal tubules. In the liver of mice chronically exposed to Cd, gene expression of the Ube2d family tended to be slightly decreased, together with slight apoptosis without the accumulation of p53 protein. In rat small intestine epithelial (IEC-6) cells, Cd decreased not only the p53 protein level but also gene expression of Ube2d1, Ube2d2 and Ube2d4. In human brain microvascular endothelial cells (HBMECs), Cd did not suppress gene expression of the Ube2d family, but increased the p53 protein level. In human brain astrocytes (HBASTs), Cd only increased gene expression of UBE2D3. These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.