스마트 공유자전거 시스템 디자인

하영은(Youngeun Ha),강현진(Hyunjin Kang),신종호(Jongho Shin),안성희(Sunghee Ahn) 한국HCI학회 2020 한국HCI학회 학술대회 Vol.2020 No.2

세종시의 공유자전거 서비스 ‘어울링 ’은 친환경 교통수단 도입 방안으로 소개되어 현재까지 운영되고 있다. 매년 증가하는 수요에 따라 ‘어울링’ 서비스의 규모는 증가해왔지만 공유자전거 반납 대여와 자전거 재분에 대한 사용자 서비스 시스템은 개선 필요가 있다. 본 연구는 세종시의 스마트시티 발전 방향에 따라 시민들의 삶의 질 향상과 도시 지속가능성 향상[2]을 위한 시스템 개선 방안을 검토한다. 본 연구는 UX 방법론을기반으로 세종시 ‘어울링’ 공유자전거를 이용하여 출퇴근하는 유저(user)들의 이용 현황을 분석한 후 문제점을 파악하고 니즈를 충족시켜, 세종시 시민들에게 적합한 공유자전거 서비스 시스템을 디자인하는 것을 목적으로 한다. 문헌조사와 현장조사의 결과 공유자전거 이용 시 대여·반납 절차가 번거롭고, 정거장마다 수요와 공급의 균형이 이루어지지 않는다는 문제점을 도출하였다. 이처럼 기존 공유자전거 서비스의 유저사용성, 접근성과 관리 측면의 문제점을 해결하기 위한 어플리케이션 서비스, 잠금장치, 공유자전거 독(dock) 스테이션을 포함한 스마트 공유자전거 시스템 디자인을 제시하고자 한다. 또한, 세종시 ‘어울링’ 공유 자전거의 이용 현황과 관리 프로세스를 해결하기 위한 대책으로 무인 자율주행차를 이용한 재분배 방안을 제시한다.

Calnexin as a dual-role biomarker: antibody-based diagnosis and therapeutic targeting in lung cancer

( Soyeon Lim ),( Youngeun Ha ),( Boram Lee ),( Junho Shin ),( Taiyoun Rhim ) 생화학분자생물학회 2024 BMB Reports Vol.57 No.3

Lung cancer carries one of the highest mortality rates among all cancers. It is often diagnosed at more advanced stages with limited treatment options compared to other malignancies. This study focuses on calnexin as a potential biomarker for diagnosis and treatment of lung cancer. Calnexin, a molecular chaperone integral to N-linked glycoprotein synthesis, has shown some associations with cancer. However, targeted therapeutic or diagnostic methods using calnexin have been proposed. Through 1D-LCMSMS, we identified calnexin as a biomarker for lung cancer and substantiated its expression in human lung cancer cell membranes using Western blotting, flow cytometry, and immunocytochemistry. Anti-calnexin antibodies exhibited complement-dependent cytotoxicity to lung cancer cell lines, resulting in a notable reduction in tumor growth in a subcutaneous xenograft model. Additionally, we verified the feasibility of labeling tumors through in vivo imaging using antibodies against calnexin. Furthermore, exosomal detection of calnexin suggested the potential utility of liquid biopsy for diagnostic purposes. In conclusion, this study establishes calnexin as a promising target for antibody-based lung cancer diagnosis and therapy, unlocking novel avenues for early detection and treatment.

언어유희 번역 재고

최송하(Choi, Song-Ha),윤영은(Yoon, YoungEun) 한국영어학회 2016 영어학 Vol.16 No.2

Effects of Scutellariae Radix on gene expression in macrophage cell line using microarray.

JEON Sujin,LEE Ho Young,HA Hyekyung,CHANG Youngeun,JUNG Da-Young,CHOI Ji-Yoon,KIM Chungsook,KANG Sam sik,SON Kun-Ho 대한약학회 2006 大韓藥學會 總會 및 學術大會 Vol.2006 No.2

The Effects of Dentifrice Mixed with Potassium Nitrate, Cetylpyridinium Chloride and Zea Mays L. Extractin Preventing Dentin Hypersensitivity and Gum Diseases

Kyung-Sook Hwang,Sun-Kyoung Lee,Seong-Hoon Kim,Jeehyun Hwang,Ha-Jeong Kwon,Sangkyun Chae,Youngeun Sung,Chanho Kim,Johnhwan Lee,Young Duk Park 대한예방치과학회 2012 International Journal of Clinical Preventive Denti Vol.8 No.1

Objective: The purpose of this clinical study was to test the efficacy and safety of dentifrice which has effects of reducing dental hypersensitivity (sodium mono fluordie phosphate), anti bacterial and anti immflamatory effects. Methods: 91 Korean adult subjects have participated and scaling was given right before the initial oral examination to set the oral condition same amongst the subjects. After the run-in period over two weeks, subjects brushed only with distributed dentifrice for three month of time period. The final data sets from dentifrice B and dentifrice C were compared to the control group to compare the improvements using mixtures with sodium mono fluoride phosphate, cetylpyridium chloride, and Zea mays L. unsaponifiable extraction in different concentration. Results: Over three months period, both test group 1(B) and test group 2(C) each showed 34.98% and 27.95% improvements in reduction of dentin hypersensitivity. Both test group 1(B) and test group 2(B) showed 39.22% and 31.5% statistically significant improvements in plaque index (p<0.05). Test group 1(B) and test group 2(C) each showed 21.15% and 30.95% improvements in gingival index (p<0.05). Conclusion: The ingredients of sodium mono-fluoride phosphate to strengthen enamel, KNO3 to reduce dentin hypersensitivity, CPC and Zea Mays L. unsaponifiable extraction to prevent gingivitis were indeed effective in protecting sensitive gingiva. No side effects were found throughout the whole body including the oral cavity of the subjects.

GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver

Park, Sungjin,Kim, Sanghwa,Kim, Min Jung,Hong, Youngeun,Lee, Ah Young,Lee, Hyunji,Tran, Quangdon,Kim, Minhee,Cho, Hyeonjeong,Park, Jisoo,Kim, Kwang Pyo,Park, Jongsun,Cho, Myung-Haing Elsevier 2018 Biochemical and biophysical research communication Vol.495 No.1

<P><B>Abstract</B></P> <P>Autophagy is a biological recycling process via the self-digestion of organelles, proteins, and lipids for energy-consuming differentiation and homeostasis. The Golgi serves as a donor of the double-membraned phagophore for autophagosome assembly. In addition, recent studies have demonstrated that pulmonary and hepatic fibrosis is accompanied by autophagy. However, the relationships among Golgi function, autophagy, and fibrosis are unclear. Here, we show that the deletion of <I>GOLGA2</I>, encoding a cis-Golgi protein, induces autophagy with Golgi disruption. The induction of autophagy leads to fibrosis along with the reduction of subcellular lipid storage (lipid droplets and lamellar bodies) by autophagy in the lung and liver. <I>GOLGA2</I> knockout mice clearly demonstrated fibrosis features such as autophagy-activated cells, densely packed hepatocytes, increase of alveolar macrophages, and decrease of alveolar surfactant lipids (dipalmitoylphosphatidylcholine). Therefore, we confirmed the associations among Golgi function, fibrosis, and autophagy. Moreover, <I>GOLGA2</I> knockout mice may be a potentially valuable animal model for studying autophagy-induced fibrosis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GOLGA2/GM130 loss induces autophagy with Golgi disruption in liver cells and transgenic mice. </LI> <LI> GOLGA2/GM130 loss leads to degradation of lipid structures (LBs and LDs) by autophagy. </LI> <LI> GOLGA2/GM130 loss causes liver and lung fibrosis. </LI> </UL> </P>

S6 kinase 1 plays a key role in mitochondrial morphology and cellular energy flow

Tran, Quangdon,Jung, Jae-Hun,Park, Jisoo,Lee, Hyunji,Hong, Youngeun,Cho, Hyeonjeong,Kim, Minhee,Park, Sungjin,Kwon, So-Hee,Kim, Seon-Hwan,Thomas, George,Kim, Kwang Pyo,Cho, Myung-Haing,Park, Jongsun Elsevier 2018 Cellular signalling Vol.48 No.-

<P><B>Abstract</B></P> <P>Mitochondrial morphology, which is associated with changes in metabolism, cell cycle, cell development and cell death, is tightly regulated by the balance between fusion and fission. In this study, we found that S6 kinase 1 (S6K1) contributes to mitochondrial dynamics, homeostasis and function. Mouse embryo fibroblasts lacking S6K1 (S6K1-KO MEFs) exhibited more fragmented mitochondria and a higher level of Dynamin related protein 1 (Drp1) and active Drp1 (pS616) in both whole cell extracts and mitochondrial fraction. In addition, there was no evidence for autophagy and mitophagy induction in S6K1 depleted cells. Glycolysis and mitochondrial respiratory activity was higher in S6K1-KO MEFs, whereas OxPhos ATP production was not altered. However, inhibition of Drp1 by Mdivi1 (Drp1 inhibitor) resulted in higher OxPhos ATP production and lower mitochondrial membrane potential. Taken together the depletion of S6K1 increased Drp1-mediated fission, leading to the enhancement of glycolysis. The fission form of mitochondria resulted in lower yield for OxPhos ATP production as well as in higher mitochondrial membrane potential. Thus, these results have suggested a potential role of S6K1 in energy metabolism by modulating mitochondrial respiratory capacity and mitochondrial morphology.</P> <P><B>Highlights</B></P> <P> <UL> <LI> S6 kinase 1 contributes to mitochondrial dynamics, homeostasis and function. </LI> <LI> Glycolysis and mitochondrial respiratory activity was higher in S6K1-KO MEFs. </LI> <LI> The depletion of S6K1 increased Drp1-mediated fission. </LI> <LI> The fission form of mitochondria in S6K1-KO MEFs resulted in lower yield for OxPhos ATP production. </LI> </UL> </P>