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외국인의 한국 재방문율 증진을 위한 디바이스 및 어플리케이션 개발
이종성(Jongsung Lee),이가람(Garam Lee),이지연(Jiyeon Lee),이정훈(Jeonghoon Rhee),조준동(Jundong Cho) 한국HCI학회 2017 한국HCI학회 학술대회 Vol.2017 No.2
최근 한류에 영향으로 많은 외국인 관광객들이 한국을 방문한다. 하지만 서울권의 관광 행태는 명동, 동대문시장 등에 편중되어 관광하고 있다. 관광의 65%이상이 쇼핑과 자연 풍경이고, 음식 탐방은 5.6%, 역사문화 유적 탐방은 6.2%로 낮은 비율을 차지하고 있다. 이러한 편중된 관광을 해결하고 다양한 콘텐츠와 새로운 관광지의 소개를 통해 재방문율을 높일 수 있는 서비스를 제안하고자 한다. 외국인들에게 소개해주고 싶은 관광지의 GPS 값을 애플리케이션에 미리 등록해 다양한 관광지를 관광할 수 있도록 하였다. 또한, 관광지 특정 위치에 RFID 카드를 설치해 RFID 수신기가 있는 디바이스를 이용해 TAG 를 하는 재미 요소를 추가하였다. TAG 된 사실을 관광에 따라(음식, 문화재, 등) 각기 다른 LED 의 색을 이용해 표시해주었으며, 블루투스를 이용해 TAG 한 정보를 애플리케이션으로 전송하여 습득한 관광지 정보를 확인할 수 있도록 하였다. 홍보가 필요한 곳에 본 서비스를 통해 관광객을 유치 및 유도할 수 있을 것으로 기대하며, 한국을 방문한 외국인들의 새로운 관광 아이템으로써 기존의 한국의 이미지와 더불어 한국에 대한 생각을 확장할 수 있는 계기가 될 것이다.
Melanogenesis inhibition activity of floralginsenoside A from Panax ginseng berry
Lee, Dae Young,Lee, Jongsung,Jeong, Yong Tae,Byun, Geon Hee,Kim, Jin Hee The Korean Society of Ginseng 2017 Journal of Ginseng Research Vol.41 No.4
Background: Panax ginseng is a traditional herb used for medicinal purposes in eastern Asia. P. ginseng contains various ginsenosides with pharmacological effects. In this study, floralginsenoside A (FGA), ginsenoside Rd (GRD), and ginsenoside Re (GRE) were purified from P. ginseng berry. Methods: Chemical structures of FGA, GRD, and GRE were determined based on spectroscopic methods, including fast atom bombardment mass spectroscopy, ID-nuclear magnetic resonance, and infrared spectroscopy. Inhibitory activities of these compounds on melanogenesis were studied by measuring the expression of protein and melanin content in the melan-a cell line. This inhibitory activity was confirmed by observing pigmentation and tyrosinase activities of zebrafish. Results: GRD, GRE, and FGA were not cytotoxic at concentrations less than $20{\mu}M$, $80{\mu}M$, and $160{\mu}M$ in melan-a cells, respectively. GRD, GRE, and FGA inhibited melanin biosynthesis in melan-a cells by 15.2%, 22.9%, and 23.9% at $20{\mu}M$, $80{\mu}M$, and $160{\mu}M$, respectively. FGA was observed to display the most potent inhibitory effect. In addition, FGA decreased microphthalmia-associated transcription factor protein expression in a dose-dependent manner. Moreover, FGA induced extracellular signal-regulated kinase phosphorylation level in melan-a cells. In addition, melanin pigment content and tyrosinase activity in zebrafish treated with FGA at $160{\mu}M$ were reduced. Conclusion: FGA showed the most potent inhibition of melanogenesis in both in vitro and in vivo studies. This study suggests that FGA purified from P. ginseng may be an effective melanogenesis inhibitor.
Artemisinic acid is a regulator of adipocyte differentiation and C/EBP δ expression
Lee, Jongsung,Kim, Moo‐,Han,Lee, Jin‐,Hyuck,Jung, Eunsun,Yoo, Eun‐,Sook,Park, Deokhoon Wiley Subscription Services, Inc., A Wiley Company 2012 Journal of cellular biochemistry Vol.113 No.7
<P><B>Abstract</B></P><P>Adipocyte dysfunction is associated with the development of obesity. In this study, artemisinic acid, which was isolated from <I>Artemisia annua L.</I>, inhibited adipogenic differentiation of human adipose tissue‐derived mesenchymal stem cells (hAMSCs) and its mechanism of action was determined. The mRNA levels of peroxidase proliferation‐activated receptor (PPAR) γ and CCAAT/enhancer binding protein (C/EBP) α, late adipogenic factors, were reduced by artemisinic acid. Moreover, the mRNA levels of the PPAR γ target genes lipoprotein lipase, CD36, adipocyte protein, and liver X receptor were down‐regulated by artemisinic acid. Artemisinic acid reduced expression of the C/EBP δ gene without impacting C/EBP β. In addition, attempts to elucidate a possible mechanism underlying the artemisinic acid‐mediated effects revealed that reduced expression of the C/EBP δ gene was mediated by inhibiting Jun N‐terminal kinase (JNK). Additionally, artemisinic acid also reduced the expression of the adipogenesis‐associated genes glucose transporter‐4 and vascular endothelial growth factor. In addition to the interference of artemisinic acid with adipogenesis, artemisinic acid significantly attenuated tumor necrosis factor‐α‐induced secretion of interleukin‐6 by undifferentiated hAMSCs, thus influencing insulin resistance and the inflammatory state characterizing obesity. Taken together, these findings indicate that inhibiting adipogenic differentiation of hAMSCs by artemisinic acid occurs primarily through reduced expression of C/EBP δ, which is mediated by the inhibition of JNK and suggest that aremisinic acid may be used as a complementary treatment option for obesity associated with metabolic syndrome. J. Cell. Biochem. 113: 2488–2499, 2012. © 2012 Wiley Periodicals, Inc.</P>
Indole-3-Carbinol Induces Apoptosis in Human Osteosarcoma MG-63 and U2OS Cells
Lee, Chang Min,Lee, Jongsung,Nam, Myeong Jin,Park, See-Hyoung Hindawi 2018 BioMed research international Vol.2018 No.-
<P>This study was focused on investigating the anticancer potential of indole-3-carbinol (I3C) against osteosarcoma MG-63 and U2OS cells. A wound healing assay indicated that IC3 inhibited migration of MG-63 and U2OS cells. MTT, WST-1, and colony formation assays revealed that treatment of MG-63 and U2OS cells with I3C decreased cell viability. Fluorescence-activated cell sorting (FACS) analysis showed that I3C induced apoptosis in a dose- and time-dependent manner in MG-63 and U2OS cells. Moreover, via terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP-biotin nick-end labeling (TUNEL) assay, we detected that I3C induced DNA fragmentation. Western blotting demonstrated that activated forms of caspase-3, caspase-7, and caspase-9, as well as poly (ADP-ribose) polymerase (PARP) were increased in MG-63 and U2OS cells, following treatment with I3C. Furthermore, protein expression levels of FOXO3, Bax, and Bim extra-large form were increased while those of Akt, JNK, p38, phosphorylated ERK, and Bcl-xL were decreased by I3C treatment in MG-63 and U2OS cells. Thus, the study indicates that I3C may induce apoptosis in human osteosarcoma MG-63 and U2OS cells via the activation of apoptotic signaling pathways by FOXO3.</P>