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Yong-Jae Kim,Kyu Myung Lee,Masaya Watada 한국자기학회 2011 Journal of Magnetics Vol.16 No.3
The stationary discontinuous armatures that are used in permanent magnet linear synchronous motors (PMLSMs) have been proposed as a driving source for transportation systems. However, the stationary discontinuous armature PM-LSM contains the outlet edges which always exist as a result of the discontinuous arrangement of the armature. For this reason, the high alteration of the outlet edge cogging force produced between the armature’s core and the mover’s permanent magnet when a mover passes the boundary between the armature’s installation part and non-installation part has been indicated as a problem. Therefore, we have examined the outlet edge cogging force by installing the auxiliary teeth at the armature’s outlet edge in order to minimize the outlet edge cogging force generated when the armature is arranged discontinuously. Moreover, we obtained the calculation by analyzing the shape of the auxiliary teeth in which the outlet edge cogging force is minimized the most.
Expression mechanism of tryptophan hydroxylase 1 in mouse islets during pregnancy.
Iida, Hitoshi,Ogihara, Takeshi,Min, Mun-kyeong,Hara, Akemi,Kim, Yeong Gi,Fujimaki, Kyoko,Tamaki, Motoyuki,Fujitani, Yoshio,Kim, Hail,Watada, Hirotaka Journal of Endocrinology (Ltd. by Guarantee) 2015 Journal of molecular endocrinology Vol.55 No.1
<P>Serotonin signaling plays key roles in augmentation of pancreatic β-cell function during pregnancy. Increased expression of tryptophan hydroxylase 1 (Tph1), a rate-limiting enzyme for serotonin synthesis by lactogenic hormones, is involved in this phenomenon. To investigate its mechanisms, we here performed 5'-RACE and identified β-cell-specific transcription initiation sites for Tph1. Prolactin enhanced the expression of mRNA containing these exons; however, reporter gene plasmids containing the proximal 5'-flanking region of these exons did not show prolactin responsiveness in MIN6 cells. Prolactin-induced Tph1 expression was inhibited by a Jak2 inhibitor and was partially inhibited by an MEK1/2 or PI3K inhibitor. Therefore, we analyzed interferon γ-activated sequences (GAS) and found GAS-A about 9-kbp upstream of the transcription start site. The reporter gene plasmid containing the GAS-A region linked to a heterologous promoter showed increased promoter activity by prolactin, which was inhibited by the forced expression of a dominant-negative mutant form of Stat5A and a Jak2 inhibitor. Chromatin immunoprecipitation analysis showed that prolactin treatment augmented Stat5 binding to the GAS-A region in MIN6 cells, as well as in isolated mouse islets, and that Stat5 recognized the GAS-A region in pregnant mouse islets. In addition, the transactivation activity of Stat5 was enhanced by prolactin through the Erk and PI3K pathways in MIN6 cells. Finally, serotonin expression was attenuated in islets of β-cell-specific Stat5-deficient mice compared with that of control littermates during pregnancy. Our findings suggest that prolactin-induced Tph1 expression is mediated by the activation of Jak2/Stat5, Erk, and PI3K pathways in β cells.</P>