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Osaka, Japan

Heian Jogakuin University also known at St. Agnes' University, is a private women's college with campuses in Kyoto, Kyoto and Takatsuki, Osaka in Japan. The university's foundation history can be traced through the establishment of St. Agnes' School to 1875. The university received its official charter as an accredited four year university in 2000. The university is an affiliated educational institution of the Nippon Sei Ko Kai, the province of the Anglican Communion in Japan. Wikipedia.

Nakamura K.,Heian Jogakuin University | Fusaoka A.,Ritsumeikan University
Proceedings of the SICE Annual Conference | Year: 2011

In this paper, we introduce a subclass of hybrid automaton called a symmetric hybrid automaton in which the continuous dynamics for each state is given by a transformation (diffeomorphism) from a core dynamics. Since the continuous dynamics is collapsed into the core dynamics in the symmetric hybrid automaton, we can deal with the properties of systems such as stability and reachability in the core dynamics. We focus on the discrete dynamics and the geometric properties, especially Zeno behavior, of a symmetric hybrid automaton. © 2011 SICE.

Nakamura K.,Heian Jogakuin University | Fusaoka A.,Ritsumeikan University
Proceedings of the IEEE International Conference on Control Applications | Year: 2010

In this paper, we introduce an enlargement of a standard hybrid automaton (HA) called a nonstandard hybrid automaton (NHA) which is another model of HA in the domain of *ℝ rather than ℝ. We define two kinds of almost periodic trajectories called the z-*cycle and p-*cycle on NHA, and we discuss a slightly extended Zeno (*Zeno) and a limit cycle in terms of these cycles. Moreover, we classify the ω-limit set of hybrid dynamics into 4 types and present an example of NHA for each type. © 2010 IEEE.

Nagao H.,Kyoto Prefectural University of Medicine | Nakajima K.-I.,Kyoto Prefectural University of Medicine | Niisato N.,Kyoto Prefectural University of Medicine | Niisato N.,Heian Jogakuin University | And 6 more authors.
Cellular Physiology and Biochemistry | Year: 2012

Potassium chloride cotransporters (KCCs) mediate electroneutrally-coupled transport of K+ and Cl-, and play crucial roles in various cell functions including regulation of cell volume and homeostasis of cellular Cl-content. Four isoforms of KCCs (KCC1, 2, 3, and 4) have been identified. KCC1 is ubiquitously expressed, whereas KCC2 is mainly expressed in neuronal cells of central nervous system. KCC3 is highly expressed in heart, skeletal muscle, kidney, lung and placenta. KCC4 is mainly expressed in epithelial cells. In this study, we investigated roles of KCCs in NGF-induced neurite outgrowth of rat pheochromocytoma PC12 cells. The most abundantly expressed isoform in PC12 cells was KCC1. Inhibition of KCCs using [(dihydronindenyl)oxy] alkanoic acid (DIOA), an inhibitor of KCCs, enhanced the NGF-induced neurite outgrowth of PC12 cells in a dose-dependent manner. Treatment of PC12 cells with NGF significantly decreased mRNA expression of KCC1, whereas other isoforms, KCC2-4, showed no changes in their mRNA expression in response to NGF treatment. Knockdown of KCC1 using small interfering RNA (siRNA) enhanced the NGF-induced neurite outgrowth. These results suggest that KCC1 negatively regulates the NGF-induced neurite outgrowth of PC12 cells. Copyright © 2012 S. Karger AG, Basel.

Nakajima K.-I.,Kyoto Prefectural University of Medicine | Niisato N.,Kyoto Prefectural University of Medicine | Niisato N.,Heian Jogakuin University | Marunaka Y.,Kyoto Prefectural University of Medicine | Marunaka Y.,Heian Jogakuin University
Biomedical Research | Year: 2011

In the present report, we studied if an isoflavone, genistein, enhances the nerve growth factor (NGF)-induced neurite outgrowth of PC12 cells. Application of genistein enhanced the NGFinduced neurite outgrowth. Knockdown of Na +/K +/2Cl - cotransporter isoform 1 (NKCC1) abolished the stimulatory effect of genistein on the neurite outgrowth. These observations indicate that NKCC1 is essential for genistein to stimulate the NGF-induced neurite outgrowth, although genistein had no effect on the protein expression of NKCC1. On the other hand, genistein activates NKCC1 as shown in our previous study. Taken together, these observations indicate that genistein enhanced the NGF-induced neurite outgrowth in PC12 cells via activation of NKCC1.

Niisato N.,Kyoto Prefectural University of Medicine | Niisato N.,Heian Jogakuin University | Ohta M.,Kyoto Prefectural University of Medicine | Eaton D.C.,Emory University | And 2 more authors.
American Journal of Physiology - Renal Physiology | Year: 2012

We investigated a physiological role for ERK, a member of the MAPK family, in the hypotonic stimulation of epithelial Na+ channel (ENaC)-mediated Na+ reabsorption in renal epithelial A6 cells. We show that hypotonic stress causes a major dephosphorylation of ERK following a rapid transient phosphorylation. PD98059 (a MEK inhibitor) increases dephosphorylated ERK and enhances the hypotonic-stress-stimulated Na+ reabsorption. ERK dephosphorylation is mediated by MAPK phosphatase (MKP). Hypotonic stress activates p38, which in turn induces MKP-1 and to a lesser extent MKP-3 mRNA expression. Inhibition of p38 suppresses MKP-1 induction, preventing hypotonic stress from dephosphorylating ERK. Inhibition of MKP-1 and -3 by the inhibitor NSC95397 also suppresses the hypotonicity-induced dephosphorylation of ERK. NSC95397 reduces both β- and γ-ENaC mRNA expression and ENaC-mediated Na+ reabsorption stimulated by hypotonic stress. In contrast, pretreatment with PD98059 significantly enhances mRNA and protein expression of β- and γ-ENaC even under isotonic conditions. However, PD98059 only stimulates Na+ reabsorption in response to hypotonic stress, suggesting that ERK inactivation by itself (i.e., under isotonic conditions) is not sufficient to stimulate Na+ reabsorption, even though ERK inactivation enhances β- and γ-ENaC expression. Based on these results, we conclude that hypotonic stress stimulates Na+ reabsorption through at least two signaling pathways: 1) induction of MKP-1 that suppresses ERK activity and induces β- and γ-ENaC expression, and 2) promotion of translocation of the newly synthesized ENaC to the apical membrane. © 2012 the American Physiological Society.

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