• Title/Summary/Keyword: HSC

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Beyond the Molecular Facilitator, CD82: Roles in Metastasis Suppressor, Stem Cell Niche, Muscle Regeneration, and Angiogenesis (분자 촉진제를 넘어, CD82: 전이억제자, 줄기세포 니쉬, 근육 재생 및 혈관신생에서의 역할)

  • Lee, Hyun-Chae;Han, Jung-Hwa;Hur, Jin
    • Journal of Life Science
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    • v.31 no.9
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    • pp.856-861
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    • 2021
  • CD82/KAI1, identified as a metastasis suppressor, was initially known only as a molecular facilitator, but its various functions have recently been revealed. CD82 plays an important role in the stem-progenitor cell, angiogenesis, and muscle. We would like to introduce the recently reported functions and roles of CD82 in this review. CD82 is a member of the tetraspanin family, which consists of four transmembrane domains. The interaction between CD82 and cell adhesion molecules suppresses the metastasis of cancer. CD82 regulates the cell cycle of stem-progenitor cells in the stem cell niche. In the bone marrow, CD82 is expressed on long-term repopulating hematopoietic stem cells (LT-HSCs), which show multipotent differentiation potential. The interaction between CD82 and Duffy antigen receptor for chemokines (DARC) induces quiescence in LT-HSCs. CD82 also regulates Rac1 activity, resulting in the homing and engraftment of HSCs into the bone marrow niche. Besides, CD82 maintains the differentiation potential of muscle stem cells and prevents angiogenesis by inhibiting the expression of cytokines, such as IL-6 and VEGF and adhesion molecules in endothelial cells. CD82 is a key membrane protein that distinguishes the hierarchy of stem-progenitor cells, and is also important for amplification and verification of cellular resources. Further studies on the function of CD82 in various organs and cells are expected to advance cell biology and cell therapy.

Search for Faint Quasars at z~5 using Medium-band Observations

  • Shin, Suhyun;Im, Myungshin;Kim, Yongjung;Hyun, Minhee;Jeon, Yiseul;Ji, Tae-Geun;Byeon, Seoyeon;Park, Woojin;Ahn, Hojae;Taak, Yoon Chan;Kim, Sophia;lim, Gu;Hwang, Sungyong;Paek, Insu;Paek, Gregory;Kim, Minjin;Kim, Dohyeong;Kim, Jae-Woo;Yoon, Yongmin;Choi, Changsu;Hong, Jueun;Jun, Hyunsung David;Karouzos, Marios;Kim, Duho;Kim, Ji Hoon;Lee, Seong-Kook;Pak, Soojong;Park, Won-Kee
    • The Bulletin of The Korean Astronomical Society
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    • v.43 no.2
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    • pp.36.2-36.2
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    • 2018
  • Cosmic reionization era in the early universe was playing a leading part on making the present universe we know. However, we have not been able to reveal the main contributor to the cosmic reionization to date. Faint quasars have been mentioned as the alternative due to the uncertainty of the faint end slope of the quasars luminosity function. With the availability of the deep (~25mag) images from Subaru Hyper Suprime-Cam (HSC) Strategic Program survey, we have tried to find more quasar with low luminosity in the ELAIS-N1 field. Faint quasar candidates were selected from several multi-band color cut criteria based on the track of the simulated quasar at z ~ 5. The Infrared Medium-deep Survey (IMS) and The UKIRT Infrared Deep Sky Survey (UKIDSS) - Deep Extragalactic Survey (DXS) provide J band information which is used to cover the relatively long wavelength range of quasar spectra. To search the reliable candidates with possible Lyman break, medium-band observation was performed by the SED camera for QUasars in EArly uNiverse(SQUEAN) in the McDonald observatory and Seoul National University 4k Camera(SNUCAM) in the Maidanak observatory. Photometric redshifts of the observed candidates were estimated from chi-square minimization. Also, we predicted the importance of the faint quasar to the cosmic reionization from the expected number density of the faint quasar.

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HYPER SUPRIME-CAMERA SURVEY OF THE AKARI NEP WIDE FIELD

  • Goto, Tomotsugu;Toba, Yoshiki;Utsumi, Yousuke;Oi, Nagisa;Takagi, Toshinobu;Malkan, Matt;Ohayma, Youichi;Murata, Kazumi;Price, Paul;Karouzos, Marios;Matsuhara, Hideo;Nakagawa, Takao;Wada, Takehiko;Serjeant, Steve;Burgarella, Denis;Buat, Veronique;Takada, Masahiro;Miyazaki, Satoshi;Oguri, Masamune;Miyaji, Takamitsu;Oyabu, Shinki;White, Glenn;Takeuchi, Tsutomu;Inami, Hanae;Perason, Chris;Malek, Katarzyna;Marchetti, Lucia;Lee, HyungMoK;Im, Myung;Kim, Seong Jin;Koptelova, Ekaterina;Chao, Dani;Wu, Yi-Han;AKARI NEP Survey team;AKARIAll Sky Survey Team
    • Publications of The Korean Astronomical Society
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    • v.32 no.1
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    • pp.225-230
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    • 2017
  • The extragalactic background suggests half the energy generated by stars was reprocessed into the infrared (IR) by dust. At z~1.3, 90% of star formation is obscured by dust. To fully understand the cosmic star formation history, it is critical to investigate infrared emission. AKARI has made deep mid-IR observation using its continuous 9-band filters in the NEP field ($5.4deg^2$), using ~10% of the entire pointed observations available throughout its lifetime. However, there remain 11,000 AKARI infrared sources undetected with the previous CFHT/Megacam imaging (r ~25.9ABmag). Redshift and IR luminosity of these sources are unknown. These sources may contribute significantly to the cosmic star-formation rate density (CSFRD). For example, if they all lie at 1< z <2, the CSFRD will be twice as high at the epoch. We are carrying out deep imaging of the NEP field in 5 broad bands (g, r, i, z, and y) using Hyper Suprime-Camera (HSC), which has 1.5 deg field of view in diameter on Subaru 8m telescope. This will provide photometric redshift information, and thereby IR luminosity for the previously-undetected 11,000 faint AKARI IR sources. Combined with AKARI's mid-IR AGN/SF diagnosis, and accurate midIR luminosity measurement, this will allow a complete census of cosmic star-formation/AGN accretion history obscured by dust.

Inhibition of Graft Versus Host Disease Using CD4+CD25+ T Cells Induced with Interleukin-2 in Mismatched Allogeneic Murine Hematopoietic Stem Cell Transplantation (주조직적합항원이 불일치하는 마우스 동종 조혈모세포이식에서 IL-2로 유도된 CD4+CD25+ T세포를 이용한 이식편대숙주병의 억제)

  • Hyun, Jae Ho;Jeong, Dae Chul;Chung, Nak Gyun;Park, Soo Jeong;Min, Woo Sung;Kim, Tai Gyu;Choi, Byung Ock;Kim, Won Il;Han, Chi Wha;Kim, Hack Ki
    • IMMUNE NETWORK
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    • v.3 no.4
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    • pp.287-294
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    • 2003
  • Background: In kidney transplantation, donor specific transfusion may induce tolerance as a result of some immune regulatory cells against the graft. In organ transplantation, the immune state arises from a relationship between the immunocompromised graft and the immunocompetent host. However, a reverse immunological situation exists between the graft and the host in hematopoietic stem cell transplantation (HSCT). In addition, early IL-2 injections after an allogeneic murine HSCT have been shown to prevent lethal graft versus host disease (GVHD) due to CD4+ cells. We investigated the induction of the regulatory CD4+CD25+ cells after a transfusion of irradiated recipient cells with IL-2 into a donor. Methods: The splenocytes (SP) were obtained from 6 week-old BALB/c mice ($H-2^d$) and irradiated as a single cell suspension. The donor mice (C3H/He, $H-2^k$) received $5{\times}10^6$ irradiated SP, and 5,000 IU IL-2 injected intraperitoneally on the day prior to HSCT. The CD4+CD25+ cell populations in SP treated C3H/He were analyzed. In order to determine the in vivo effect of CD4+CD25+ cells, the lethally irradiated BALB/c were transplanted with $1{\times}10^7$ donor BM and $5{\times}10^6$ CD4+CD25+ cells. The other recipient mice received either $1{\times}10^7$ donor BM with $5{\times}10^6$ CD4+ CD25- cells or the untreated SP. The survival and GVHD was assessed daily by a clinical scoring system. Results: In the MLR assay, BALB/c SP was used as a stimulator with C3H/He SP, as a responder, with or without treatment. The inhibition of proliferation was $30.0{\pm}13%$ compared to the control. In addition, the MLR with either the CD4+CD25+ or CD4+CD25- cells, which were isolated by MidiMacs, from the C3H/He SP treated with the recipient SP and IL-2 was evaluated. The donor SP treated with the recipient cells and IL-2 contained more CD4+CD25+ cells ($5.4{\pm}1.5%$) than the untreated mice SP ($1.4{\pm}0.3%$)(P<0.01). There was a profound inhibition in the CD4+CD25+ cells ($61.1{\pm}6.1%$), but a marked proliferation in the CD4+CD25- cells ($129.8{\pm}65.2%$). Mice in the CD4+CD25+ group showed low GVHD scores and a slow progression from the post-HSCT day 4 to day 9, but those in the control and CD4+CD25- groups had a high score and rapid progression (P<0.001). The probability of survival was 83.3% in the CD4+CD25+ group until post-HSC day 35 and all mice in the control and CD4+CD25- groups died on post-HSCT day 8 or 9 (P=0.0105). Conclusion: Donor graft engineering with irradiated recipient SP and IL-2 (recipient specific transfusion) can induce abundant regulatory CD4+CD25+ cells to prevent GVHD.

Potential Role of Hedgehog Signaling in Radiation-induced Liver Fibrosis (방사선에 의한 간섬유증에서 헤지호그의 잠재적 역할)

  • Wang, Sihyung;Jung, Youngmi
    • Journal of Life Science
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    • v.23 no.5
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    • pp.710-720
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    • 2013
  • Radiotherapy is commonly used in treating many kinds of cancers which cannot be cured by other therapeutic strategies. However, radiotherapy also induces the damages on the normal tissues. Radiation-induced fibrosis is frequently observed in the patients undergoing radiotherapy, and becomes a major obstacle in the treatment of intrahepatic cancer. Hedgehog (Hh) that is an essential in the liver formation during embryogenesis is not detected in the healthy liver, but activated and modulates the repair process in damaged livers in adult. The expression of Hh increases with the degree of liver damage, regulating the proliferation of hepatic progenitors and hepatic stellate cells (HSC). In addition, Hh induces epithelial-to-mesencymal transition (EMT) and activation of myofibroblasts. In the irradiated livers, up-regulated expression of Hh signaling was associated with proliferation of progenitors, EMT induction, and increased fibrosis. Female-specific expression of Hh leaded to the expansion of progenitors and the accumulation of collagen in the irradiated livers of female mice, indicating that gender disparity in Hh expression may be related with radiation-susceptibility in female. Hence, Hh signaling becomes a novel object of studies for fibrogenesis induced by radiation. However, the absence of the established experimental animal models showing the similar physiopathology with human liver diseases and fibrosis-favorable microenvironment hamper the studies for the radiation-induced fibrosis, providing a few descriptive results. Therefore, further research on the association of Hh with radiation-induced fibrosis can identify the cell and tissue-specific effects of Hh and provides the basic knowledge for underlying mechanisms, contributing to developing therapies for preventing the radiation-induced fibrosis.