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환승 및 노선우회를 고려한 광역도시철도 경로선택모형 구축
양수정(Sujeong Yang),우연식(Yeonsik Woo),이장호(Jang-Ho Lee) 한국철도학회 2017 한국철도학회 학술발표대회논문집 Vol.2017 No.05
본 연구는 광역·도시철도 네트워크에서 환승과 노선우회를 고려한 경로선택 모형을 구축하였다. 이용경로의 우회에 따른 영향을 반영하기 위해서 우회비용(angular cost)을 변수로 반영하였으며, 수도권 교통카드 이력자료를 활용하여 이항로짓모형을 구축하였다. 분석결과, 경로선택의 영향요인으로는 통행시간과 환승횟수, 환승통로의 총 환산거리 등이 나타났으며, 우회비용은 통계적 유의성이 높지 않게 나타났다. 모수추정결과로부터 통행시간대비 환승역 총 환산거리와 환승횟수에 대한 한계대체율을 분석하였는데, 실질적인 환승시간 이외에 환승 자체만으로 평균 약 8~13분 정도를 환승저항으로 인지하는 것으로 분석되었다. 이를 통해 광역도시철도 이용자의 경로선택행태를 모사할 수 있을 뿐만 아니라, 최적경로에 대한 정보제공에 활용할 수 있을 것으로 기대된다. The goal of this study is establish a route choice model considering transfer penalty and angular cost in rapid transit networks. In order to take the transfer penalty into account, horizontal distance, the number of stairs, the presence of escalators, and the total scaled distance were used as independent variables. Simultaneously, we also have considered the angular cost to reflect the effect of line alignment. As a result of the analysis, factors affecting the route choice such as the total travel time, the number of transfers, and the total scaled distance of the transfer station were statistically significant. However, the angular cost did not have a significant effect on the route choice. This study allows simulating the route choice behavior in the rapid transit network, it is also expected that the suggested model may be applied to provide information on the optimal route, referring to the marginal rate of substitution among the variables mentioned above.
Yang, Ji Seon,Jeon, Sujeong,Yoon, Kee Dong,Yoon, Shin Hee The Korean Society of Pharmacology 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.6
Increasing evidence implicates changes in $[Ca^{2+}]_i$ and oxidative stress as causative factors in amyloid beta ($A{\beta}$)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting $Ca^{2+}$ and $Zn^{2+}$ signaling. The present study aimed to determine whether C3G exerts a protective effect against $A{\beta}_{25-35}$-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for $Ca^{2+}$, $Zn^{2+}$, MMP and ROS. Treatment with $A{\beta}_{25-35}$ ($20{\mu}M$) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited $A{\beta}_{25-35}$-induced $[Zn^{2+}]_i$ increases as well as $[Ca^{2+}]_i$ increases in the cultured rat hippocampal neurons. C3G also significantly inhibited $A{\beta}_{25-35}$-induced mitochondrial depolarization. C3G also blocked the $A{\beta}_{25-35}$-induced formation of ROS. In addition, C3G significantly inhibited the $A{\beta}_{25-35}$-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid ${\beta}$-induced neuronal cell death by reducing multiple apoptotic signals.
Jang, Sujeong,Park, Seokho,Cho, Hyong-Ho,Yang, Ung,Kang, Maru,Park, Jong-Seong,Park, Sah-Hoon,Jeong, Han-Seong The Basic Science Institute Chosun University 2019 조선자연과학논문집 Vol.12 No.4
Mesenchymal stem cells (MSCs) are known to differentiate into multiple lineages, making neurogenic differentiation an important target in the clinical field. In the present study, we induced the neurogenic differentiation of cells using histone deacetylase (HDAC) inhibitors and studied their mechanisms for further differentiation in vitro. We treated cells with the HDAC inhibitors, MS-275 and NaB; and found that the cells had neuron-like features such as distinct bipolar or multipolar morphologies with branched processes. The mRNA expressions encoding for NEFL, MAP2, TUJ1, OLIG2, and SYT was significantly increased following HDAC inhibitors treatment compared to without HDAC inhibitors; high protein levels of MAP2 and Tuj1 were detected by immunofluorescence staining. We examined the mechanisms of differentiation and found that the Wnt signaling pathway and downstream mitogen-activate protein kinase were involved in neurogenic differentiation of MSCs. Importantly, Wnt4, Wnt5a/b, and Wnt11 protein levels were highly increased after treatment with NaB; signals were activated through the regulation of Dvl2 and Dvl3. Interestingly, NaB treatment increased the levels of JNK and upregulated JNK phosphorylation. After MS-275 treatment, Wnt protein levels were decreased and GSK-3β was phosphorylated. In this cell, HDAC inhibitors controlled the non-canonical Wnt expression by activating JNK phosphorylation and the canonical Wnt signaling by targeting GSK-3β.
Improved Pure Pursuit Method for Unmanned Autonomous Vehicles
Jaepil Yang(양재필),Youngha Shin(신영하),Sungeun Jo(조성은),Jihyun Ryu(류지현),Hyeonsu Lim(임현수),Joohyeong Park(박주형),Minkyung Kim(김민경),Yongrae Choi(최용래),Hyungjun Hwnag(황형준),Sujeong Kim(김수정),Nahyun Lee(이나현),Dongwoo 대한전자공학회 2019 대한전자공학회 학술대회 Vol.2019 No.11
Non‐transcriptional regulation of NLRP3 inflammasome signaling by IL‐4
Hwang, Inhwa,Yang, Jungmin,Hong, Sujeong,Ju Lee, Eun,Lee, Seung‐,Hyo,Fernandes‐,Alnemri, Teresa,Alnemri, Emad S,Yu, Je‐,Wook Nature Publishing Group 2015 Immunology and Cell Biology Vol.93 No.6
<P>Th2 cytokine IL‐4 has been previously shown to suppress the production of proinflammatory cytokines in monocytes. However, the underlying molecular mechanism by which IL‐4 signaling antagonizes proinflammatory responses is poorly characterized. In particular, whether IL‐4 can modulate inflammasome signaling remains unknown. Here, we provide evidence that IL‐4 suppresses NLRP3‐dependent caspase‐1 activation and the subsequent IL‐1β secretion but does not inhibit absent in melanoma 2 (AIM2)‐ or NLRC4 (NOD‐like receptor family, CARD domain‐containing 4)‐dependent caspase‐1 activation in THP‐1 and mouse bone marrow‐derived macrophages. Upon lipopolysaccharide (LPS) or LPS/ATP stimulation, IL‐4 markedly inhibited the assembly of NLRP3 inflammasome, including NLRP3‐dependent ASC (apoptosis‐associated speck‐like protein containing a caspase recruitment domain) oligomerization, NLRP3‐ASC interaction and NLRP3 speck‐like oligomeric structure formation. The negative regulation of NLRP3 inflammasome by IL‐4 was not due to the impaired mRNA or protein production of NLRP3 and proinflammatory cytokines. Supporting this observation, IL‐4 attenuated NLRP3 inflammasome activation even in reconstituted NLRP3‐expressing macrophages in which NLRP3 expression is not transcriptionally regulated by TLR‐NF‐κB signaling. Furthermore, the IL‐4‐mediated suppression of NLRP3 inflammasome was independent of STAT6‐dependent transcription and mitochondrial reactive oxygen species (ROS). Instead, IL‐4 inhibited subcellular redistribution of NLRP3 into mitochondria and microtubule polymerization upon NLRP3‐activating stimulation. Our results collectively suggest that IL‐4 could suppress NLRP3 inflammasome activation in a transcription‐independent manner, thus providing an endogenous regulatory machinery to prevent excessive inflammasome activation.</P>