무선통신기반 열차제어시스템에서의 운전시격 계산과 간격제어 성능개선을 위한 열차간격제어 알고리즘

오세찬(Oh, Seh-Chan),김경희(Kim, Kyung-Hee),이성훈(Lee Seong-Hoon),김자영(Kim, Ja-Young),전종화(Quan, Zhong-Hua) 한국산학기술학회 2015 한국산학기술학회논문지 Vol.16 No.10

무선통신기반 열차제어시스템은 관할영역 내에 운행 중인 열차의 위치정보를 지상시스템에서 실시간으로 수신하고 다시 각각의 열차의 차상시스템에 새로운 이동권한을 제공함으로써 안전한 간격제어를 수행한다. 열차제어시스템의 성능은 최소 운전시격으로 평가되며 그것은 열차제어시스템의 간격제어 성능뿐만 아니라 운영특성 그리고 열차의 특성을 반영하여 계산된다. 본 논문은 무선통신기반 열차제어시스템의 운전시격 계산과 운전시격을 개선하기 위한 새로운 열차간격제어 알고 리즘을 제안한다. 제안된 운전시격 계산 방법은 열차제어시스템 간격제어 성능을 반영한 안전마진 추정을 통해 각각 역간 운전시격과 역 운전시격을 정의한다. 또한 제안된 열차간격제어 개선 알고리즘은 간격제어 개선을 위해 거리와 속도를 포함 하는 이동권한을 새롭게 정의하며 선행열차에서 필연적으로 발생하는 제동거리를 이용함으로써 열차의 운전시격을 향상시 킬 수 있다. 제안된 운전시격 계산방법을 한국형 무선통신기반 열차제어시스템의 간격제어 성능을 대상으로 시뮬레이션을 수행하며 개선된 열차간격제어 알고리즘과 비교분석 한다. 시뮬레이션 결과에 따르면 제안된 운전시격 계산방법은 향후 무 선통신기반 열차제어시스템의 성능 지표로 활용이 가능하며 제안된 간격제어 알고리즘은 기존의 무선통신기반 열차제어시 스템의 역 운전시격과 역간 운전시격을 개선할 수 있음을 확인한다. Radio based train control system performs train safe interval control by receiving in realtime the position information of trains driving in the control area of the wayside system and providing onboard system in each train with updated movement authority. The performance of the train control system is evaluated to calculate the minimum operation headway, which reflects the operation characteristics and the characteristics of the train as well as the interval control performance of the train control system. In this paper, we propose the operation headway calculation for radio based train control system and a new train interval control algorithm to improve the operation headway. The proposed headway calculation defines line headway and station headway by the estimation the safety margin distance reflecting the performance of the train control system. Furthermore the proposed Enhanced Train Interval Control(ETIC) algorithm defines a new movement authority including both distance and speed, and improves the train operation headway by using braking distance occurring inevitably in the preceding train. The proposed operation headway calculation is simulated with Korean Radio-based Train Control System(KRTCS) and the simulated result is compared to improved train interval control algorithm. According to the simulated results, the proposed operation headway calculation can be used as performance indicator for radio based train control system, and the improved train control algorithm can improve the line and station headway of the conventional radio based train control system.

Proliferation of Hepatic Oval Cells via Cyclooxygenase-2 and Extracellular Matrix Protein Signaling during Liver Regeneration Following 2-AAF/Partial Hepatectomy in Rats

Bae, Si Hyun,Oh, Seh Hoon,Yoon, Seung Kew,Park, Joung Ah,Kim, Gi Dae,Hur, Wonhee,Choi, Jong Young,Oh, Il Hoan,Yoon, Kun Ho The Korean Society of Gastroenterology; the Korean 2011 Gut and Liver Vol.5 No.3

<P><B>Background/Aims</B></P><P>In the 2-acetylaminofluorene (2-AAF)/70% partial hepatectomy (PHx) model, the mechanism underlying the differentiation of activated hepatic oval cells (HOCs) into hepatocytes and bile ductile cells is unclear. We investigated the role of cyclooxygenase-2 (COX-2) in HOCs and the relationship between COX-2 and extracellular matrix proteins in cellular proliferation.</P><P><B>Methods</B></P><P>Reverse transcription-polymerase chain reaction, immunohistochemical staining, and Western blotting were used to assess COX-2 expression. The co-localization of COX-2 with Thy1, c-Met, epithelial cell adhesion molecule, and α-smooth muscle actin was also examined. Additionally, we investigated whether connective tissue growth factor (CTGF), fibronectin (FN), extracellular signal-regulated kinase 1/2 (P-ERK1/2), and AKT were expressed in HOCs.</P><P><B>Results</B></P><P>The expression of COX-2, prostaglandin E2 receptors, and c-Met was upregulated in HOCs. However, HOCs treated with the COX-2 inhibitor NS398 showed decreased COX-2, CTGF, FN, and AKT expression, whereas P-ERK1/2 was unaffected. Additionally, NS398 inhibited HOC proliferation, but not the proliferation of HOCs cultured on FN-coated dishes. Furthermore, the proliferative response of HOCs treated with NS398 was reversed by hepatic growth factor treatment.</P><P><B>Conclusions</B></P><P>These results suggest that HOC proliferation is mediated through COX-2, extracellular FN expression, and AKT activation. Thus, COX-2 plays an important role in HOC proliferation following acute injury.</P>

Proliferation of Hepatic Oval Cells via Cyclooxygenase-2 and Extracellular Matrix Protein Signaling during Liver Regeneration Following 2-AAF/Partial Hepatectomy in Rats

( Si Hyun Bae ),( Seh Hoon Oh ),( Seung Kew Yoon ),( Joung Ah Park ),( Gi Dae Kim ),( Wonhee Hur ),( Jong Young Choi ),( Il Hoan Oh ),( Kun Ho Yoon ) 대한소화기기능성질환·운동학회 2011 Gut and Liver Vol.5 No.3

Background/Aims: In the 2-acetylaminofluorene (2-AAF)/ 70% partial hepatectomy (PHx) model, the mechanism underlying the differentiation of activated hepatic oval cells (HOCs) into hepatocytes and bile ductile cells is unclear. We investigated the role of cyclooxygenase-2 (COX-2) in HOCs and the relationship between COX-2 and extracellular matrix proteins in cellular proliferation. Methods: Reverse transcription- polymerase chain reaction, immunohistochemical staining, and Western blotting were used to assess COX-2 expression. The co-localization of COX-2 with Thy1, c-Met, epithelial cell adhesion molecule, and a-smooth muscle actin was also examined. Additionally, we investigated whether connective tissue growth factor (CTGF), fibronectin (FN), extracellular signal-regulated kinase 1/2 (P-ERK1/2), and AKT were expressed in HOCs. Results: The expression of COX-2, prostaglandin E2 receptors, and c-Met was upregulated in HOCs. However, HOCs treated with the COX-2 inhibitor NS398 showed decreased COX-2, CTGF, FN, and AKT expression, whereas P-ERK1/2 was unaffected. Additionally, NS398 inhibited HOC proliferation, but not the proliferation of HOCs cultured on FN-coated dishes. Furthermore, the proliferative response of HOCs treated with NS398 was reversed by hepatic growth factor treatment. Conclusions: These results suggest that HOC proliferation is mediated through COX-2, extracellular FN expression, and AKT activation. Thus, COX-2 plays an important role in HOC proliferation following acute injury. (Gut Liver 2011;5:367-376)

Tumor necrosis factor-inducible gene 6 reprograms hepatic stellate cells into stem-like cells, which ameliorates liver damage in mouse

Wang, Sihyung,Kim, Jieun,Lee, Chanbin,Oh, Dayoung,Han, Jinsol,Kim, Tae-Jin,Kim, Sang-Woo,Seo, Young-Su,Oh, Seh-hoon,Jung, Youngmi Elsevier 2019 Biomaterials Vol.219 No.-

<P><B>Abstract</B></P> <P>Liver fibrosis is a major characteristic of liver disease. When the liver is damaged, quiescent hepatic stellate cells (HSCs) transdifferentiate into proliferative myofibroblastic/activated HSCs, which are the main contributors to liver fibrosis. Hence, a strategy for regulating HSC activation is important in the treatment of liver disease. Tumor necrosis factor-inducible gene 6 protein (TSG-6), a cytokine released from mesenchymal stem cells (MSCs), influences MSC stemness. Therefore, we investigated the biological effect of TSG-6 on HSCs. Human primary HSCs treated with TSG-6 showed significant downregulation of HSC activation markers and upregulation of senescence markers. TSG-6 promoted these cells to express stem cell markers and form spherical organoids, which exhibited elevated expression of stemness-related genes. These organoids differentiated into functional hepatocytic cells under specific culture conditions. Organoids derived from TSG-6-treated HSCs improved livers in organoid transplant mice subjected to CCl<SUB>4</SUB> treatment (which induces liver fibrosis). Furthermore, HSC transdifferentiation by TSG-6 was mediated by Yes-associated protein 1. These findings demonstrate that TSG-6 induces the conversion of HSCs into stem cell-like cells in vitro and that organoids derived from TSG-6-treated HSCs can restore fibrotic liver, suggesting that direct reprogramming of HSCs by TSG-6 can be a useful strategy to control liver disease.</P>

Therapeutic Potential of Human Mesenchymal Stem Cells Derived from Amnion and Bone Marrow in a Rat Model of Acute Liver Injury and Fibrosis

( Joung Ah Park ),( Gi Dae Kim ),( Jung Hoon Cha ),( Hye Lim Kim ),( Eun Suk Choi ),( Eun Sun Jung ),( Seung Kew Yoon ),( Seh Hoon Oh ),( Si Hyun Bae ) 한국조직공학·재생의학회 2011 조직공학과 재생의학 Vol.8 No.4

Mesenchymal stem cells (MSCs) derived from various human tissues, including amnion (AM) from the placenta and bone marrow (BM), have been known to differentiate into multi-lineages and mesodermal cell lines. Few comparative studies have reported their potential for hepatogenic differentiation using an in vitro culture system and it remains unclear if their therapeutic potential in an animal model also depends on this differentiation. The pur-pose of this study was to compare the hepatogenic differentiation capacity of AM- and BM-derived MSCs, and toevaluate their antifibrotic efficacy after direct transplantation into a bile duct-ligated rat model of liver fibrosis. The proliferation of AM-MSCs derived from placenta was higher than that of BM-MSCs. Differentiated hepatocyte-like cells changed in morphology, expressed hepatocyte-specific genes, and demonstrated functional activities. Differ-entiated AM- and BM-derived hepatocyte-like cells were directly transplanted into rat livers suffering from hepaticfibrosis due to bile duct ligation. Liver tissues were analyzed at one and two weeks post-transplantation. Albumin expression was increased in rats one week after transplanting AM- and BM-derived hepatocyte-like cells. And, col-lagen deposition decreased compared with the control group. These results contribute to our understanding of the antifibrotic effects of AM- and BM-derived hepatocyte-like cells on liver disease and their ability to undergo hepato-genic differentiation. AM- and BM-derived MSCs may be a source of cells for liver regeneration and may providea foundation for the development of novel cell therapies.

열차간격제어를 위한 정적속도프로파일 생성 연구

윤용기(Yong-Ki Yoon),오세찬(Seh-Chan Oh),김창훈(Chang-Hoon Kim),김용규(Yong-Kyu Kim) 한국철도학회 2010 한국철도학회 학술발표대회논문집 Vol.2010 No.10

한국 청년층의 UVB에 의한 최소홍반량에 따른 광피부형의 분류

윤재일 ( Jai Il Youn ),오준규 ( Jun Gyu Oh ),김병국 ( Byoung Kook Kim ),정진호 ( Jin Ho Chung ),오선진 ( Sun Jin Oh ),김진준 ( Jin Jun Kim ),강세훈 ( Seh Hoon Kang ) 대한피부과학회 1996 대한피부과학회지 Vol.34 No.6

Background: We predicted that t.he self reporting questionnaire proposed by Fitzpatrick might not be appropriate for classifyin~v; the skin phoiotype in Korean people. Objective : We classified the skin phototypes in Korean people by measuring the minimal erythema dose (MED) of UVB on t.he basis of MEDs of skin type proposed by Pathak and Fitzpatrick. Methods : Two hundred and eighty-four male Korean rnedical students participated in this study. We irradiated UVB with Waldmann UV 800 and measured MEDs after 24 hours. Results : The mean MED was 70.1+21.3 mJ/cm2. Most of the MEDs were 70, 60, 50 mJ/cm in the order of frequency. On the basis of the skin type proposed by Pathak and Fitzpatrick, the most frequent phototype was the skin type V(56.3%) by MED. 20.8% and 13.8% of the subjects eorresponded to the skin types UV and III, respectively. 9.1% of the subjects fell into the UV sensitive group, skin type l and II. Conclusion : Using these results as groundwork, simple and precisely applicable classification of skin phototype in Korean people needs to be established. (Kor J Dermatol 1996;34(6): 893-897)

Decreased C-reactive protein induces abnormal vascular structure in a rat model of liver dysfunction induced by bile duct ligation

( Ji Hye Jun ),( Jong Ho Choi ),( Si Hyun Bae ),( Seh Hoon Oh ),( Gi Jin Kim ) 대한간학회 2016 Clinical and Molecular Hepatology(대한간학회지) Vol.22 No.3

Background/Aims: Chronic liver disease leads to liver fibrosis, and although the liver does have a certain regenerative capacity, this disease is associated with dysfunction of the liver vessels. C-reactive protein (CRP) is produced in the liver and circulated from there for metabolism. CRP was recently shown to inhibit angiogenesis by inducing endothelial cell dysfunction. The objective of this study was to determine the effect of CRP levels on angiogenesis in a rat model of liver dysfunction induced by bile duct ligation (BDL). Methods: The diameter of the hepatic vein was analyzed in rat liver tissues using hematoxylin and eosin (H&E) staining. The expression levels of angiogenic factors, albumin, and CRP were analyzed by real-time PCR and Western blotting. A tube formation assay was performed to confirm the effect of CRP on angiogenesis in human umbilical vein endothelial cells (HUVECs) treated with lithocholic acid (LCA) and siRNA-CRP. Results: The diameter of the hepatic portal vein increased significantly with the progression of cirrhosis. The expression levels of angiogenic factors were increased in the cirrhotic liver. In contrast, the expression levels of albumin and CRP were significantly lower in the liver tissue obtained from the BDL rat model than in the normal liver. The CRP level was correlated with the expression of albumin in hepatocytes treated with LCA and siRNA-CRP. Tube formation was significantly decreased in HUVECs when they were treated with LCA or a combination of LCA and siRNA-CRP. Conclusions: CRP seems to be involved in the abnormal formation of vessels in hepatic disease, and so it could be a useful diagnostic marker for hepatic disease. (Clin Mol Hepatol 2016;22:372-381)

폐수술환자에 있어서 운동적성검사에 관한 연구

장운삼 ( Woon Sam Chang ),이현우 ( Hyeon Woo Lee ),송세훈 ( Seh Hoon Song ),오장근 ( Chang Kun Oh ) 대한내과학회 1965 대한내과학회지 Vol.8 No.5

RNA Binding Proteins Control Transdifferentiation of Hepatic Stellate Cells into Myofibroblasts

Wang, Sihyung,Jung, Youngmi,Hyun, Jeongeun,Friedersdorf, Matthew,Oh, Seh-Hoon,Kim, Jieun,Premont, Richard T.,Keene, Jack D.,Diehl, Anna Mae S. Karger AG 2018 CELLULAR PHYSIOLOGY AND BIOCHEMISTRY Vol.48 No.3

<P><B><I>Background/Aims:</I></B> Myofibroblasts (MF) derived from quiescent nonfibrogenic hepatic stellate cells (HSC) are the major sources of fibrous matrix in cirrhosis. Because many factors interact to regulate expansion and regression of MF-HSC populations, efforts to prevent cirrhosis by targeting any one factor have had limited success, motivating research to identify mechanisms that integrate these diverse inputs. As key components of RNA regulons, RNA binding proteins (RBPs) may fulfill this function by orchestrating changes in the expression of multiple genes that must be coordinately regulated to affect the complex phenotypic modifications required for HSC transdifferentiation. <B><I>Methods:</I></B> We profiled the transcriptomes of quiescent and MF-HSC to identify RBPs that were differentially-expressed during HSC transdifferentiation, manipulated the expression of the most significantly induced RBP, insulin like growth factor 2 binding protein 3 (Igf2bp3), and evaluated transcriptomic and phenotypic effects. <B><I>Results:</I></B> Depleting Igf2bp3 changed the expression of thousands of HSC genes, including multiple targets of TGF-β signaling, and caused HSCs to reacquire a less proliferative, less myofibroblastic phenotype. RNA immunoprecipitation assays demonstrated that some of these effects were mediated by direct physical interactions between Igf2bp3 and mRNAs that control proliferative activity and mesenchymal traits. Inhibiting TGF-β receptor-1 signaling revealed a microRNA-dependent mechanism that induces Igf2bp3. <B><I>Conclusions:</I></B> The aggregate results indicate that HSC transdifferentiation is ultimately dictated by Igf2bp3-dependent RNA regulons and thus, can be controlled simply by manipulating Igf2bp3.</P>