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김병수,이주형,김인영,박수범,박태규,Kim, Byung Soo,Lee, Juhyung,Kim, Inyoung,Park, Su-Bum,Park, Tae-Kyu 한국통계학회 2014 응용통계연구 Vol.27 No.5
Kim 등 (2006)과 Kim 등 (2009)은 2002년에 (사)볼런티어 21에서 조사한 설문자료에 기초하여 우리나라 개인의 기부횟수에 영향을 주는 유의적 설명변수를 보고한 바 있다. 본고에서는 Kim 등 (2006)과 Kim 등 (2009)의 계산오류를 발견하여 이를 수정하고, 아울러 Kim 등 (2009)이 적용한 0이 팽창된 포아송 모형에 로지스틱 회귀모형을 추가하였다. 동 로지스틱 모형으로 기부행위(0, 1)에 영향을 주는 설명변수를 식별하고, 아울러 기부횟수가 작은 군(群)과 큰 군(群)을 판별하여 주는 설명변수를 식별하고자 한다. Kim et al. (2006) and Kim et al. (2009) reported a set of explanatory variables affecting donation frequency when they analyzed nationwide survey data on donations collected in 2002 by Volunteer 21, a nonprofit organization in Korea. The primary purpose of this paper is to correct computational errors found in Kim et al. (2006) and Kim et al. (2009), to rectify major results in the Tables and Figures and to supplement Kim et al. (2009) by providing new results. We add two logistic regressions to the ZIP and a mixture of two Poisson regressions of Kim et al. (2009). Through these two logistic regressions we could detect a set of explanatory variables affecting donation activity (0 or 1) and another set of explanatory variables, in which the volunteer (0, 1) variable is common, discriminating the infrequent donor group from the frequent donor group.
Kim, Kihwan,Kim, Juran,Gang, Myeng Gil,Kim, Se-Ho,Song, Soomin,Cho, Yunae,Shin, Donghyeop,Eo, Young-Joo,Jeong, Inyoung,Ahn, Seung Kyu,Cho, Ara,Kim, Jayeong,Yoon, Seokhyun,Choi, Pyuck-Pa,Jo, William,Ki Elsevier 2019 Solar energy materials and solar cells Vol.195 No.-
<P><B>Abstract</B></P> <P>In this work, copper indium gallium selenide (Cu(In,Ga)Se<SUB>2</SUB>; CIGS) absorbers were grown on polyimide (PI)/molybdenum substrates by a three-stage co-evaporation process at various temperatures, film formation was systemically studied using various advanced characterization methods such as transmission electron microscopy, micro-Raman spectroscopy, Kelvin probe force microscopy, and atom probe tomography. The CIGS films on PI were found to exhibit considerable physical and electrical variations with respect to the process temperature of three-stage co-evaporation. In particular, when the process temperature reached 400 °C, the CIGS absorber on PI began to exhibit controlled microstructure and intergrain properties. By adjusting the microstructure and intergrain properties of the absorber films by means of the process temperature of three-stage co-evaporation, flexible CIGS solar cells on PI with an efficiency of 16.7% (with anti-refection coating) were achieved.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CIGS absorber films were grown on flexible polyimide/molybdenum substrates. </LI> <LI> Low-temperature three-stage process (≤440 °C) with extrinsic Na addition was used to CIGS growth. </LI> <LI> CIGS film evolution was systemically observed using advanced material characterization techniques. </LI> <LI> Highly efficient CIGS cells on flexible polyimide substrates were realized while maintaining process manufacturability. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Tusc2/Fus1 regulates osteoclast differentiation through NF- κB and NFATc1
( Inyoung Kim ),( Jung Ha Kim ),( Kabsun Kim ),( Semun Seong ),( Nacksung Kim ) 생화학분자생물학회(구 한국생화학분자생물학회) 2017 BMB Reports Vol.50 No.9
Tumor suppressor candidate 2 (Tusc2, also known as Fus1) regulates calcium signaling, and Ca<sup>2+</sup>-dependent nuclear factor of activated T-cells (NFAT) and nuclear factor kappa B (NF-кB) pathways, which play roles in osteoclast differentiation. However, the role of Tusc2 in osteoclasts remains unknown. Here, we report that Tusc2 positively regulates the differentiation of osteoclasts. Overexpression of Tusc2 in osteoclast precursor cells enhanced receptor activator of nuclear factor кB ligand (RANKL)-induced osteoclast differentiation. In contrast, small interfering RNA-mediated knockdown of Tusc2 strongly inhibited osteoclast differentiation. In addition, Tusc2 induced the activation of RANKL-mediated NF-кB and calcium/calmodulin-dependent kinase IV (CaMKIV)/cAMP-response element (CRE)-binding protein CREB signaling cascades. Taken together, these results suggest that Tusc2 acts as a positive regulator of RANKL-mediated osteoclast differentiation. [BMB Reports 2017; 50(9): 454-459]
Endoplasmic Reticulum–Bound Transcription Factor CREBH Stimulates RANKL-Induced Osteoclastogenesis
Kim, Jung Ha,Kim, Kabsun,Kim, Inyoung,Seong, Semun,Nam, Kwang-Il,Kim, Kyung Keun,Kim, Nacksung American Association of Immunologists 2018 Journal of Immunology Vol. No.
<P>Endoplasmic reticulum (ER) stress is triggered by various metabolic factors, such as cholesterol and proinflammatory cytokines. Recent studies have revealed that ER stress is closely related to skeletal disorders, such as osteoporosis. However, the precise mechanism by which ER stress regulates osteoclast differentiation has not been elucidated. In this study, we identified an ER-bound transcription factor, cAMP response element-binding protein H (CREBH), as a downstream effector of ER stress during RANKL-induced osteoclast differentiation. RANKL induced mild ER stress and the simultaneous accumulation of active nuclear CREBH (CREBH-N) in the nucleus during osteoclastogenesis. Overexpression of CREBH-N in osteoclast precursors enhanced RANKL-induced osteoclast formation through NFATc1 upregulation. Inhibiting ER stress using a specific inhibitor attenuated the expression of osteoclast-related genes and CREBH activation. In addition, inhibition of reactive oxygen species using <I>N</I>-acetylcysteine attenuated ER stress, expression of osteoclast-specific marker genes, and RANKL-induced CREBH activation. Furthermore, inhibition of ER stress and CREBH signaling pathways using an ER stress–specific inhibitor or CREBH small interfering RNAs prevented RANKL-induced bone destruction in vivo. Taken together, our results suggest that reactive oxygen species/ER stress signaling-dependent CREBH activation plays an important role in RANKL-induced osteoclastogenesis. Therefore, inactivation of ER stress and CREBH signaling pathways may represent a new treatment strategy for osteoporosis.</P>
Effect of centrifugation on tryptic protein digestion
Kim, Soohwan,Kim, Yeoseon,Lee, Dabin,Kim, Inyoung,Paek, Jihyun,Shin, Dongwon,Kim, Jeongkwon The Korean Society of Analytical Science 2017 분석과학 Vol.30 No.2
This study investigated the effect of centrifugation on tryptic digestion. This was done by applying different centrifugation speeds (6,000, 8,000, 10,000, 20,000, and $30,000{\times}g$) over various durations (0, 10, 20, 30, 40, 50, and 60 min) to digest two model proteins - cytochrome c and myoglobin. The intact proteins and resulting peptides were identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Centrifugation greatly improved the tryptic digestion efficiency of cytochrome c, where either an increase in centrifugation speed or in digestion duration significantly improved the digestion of cytochrome c. However, centrifugation did not noticeably improve the digestion of myoglobin; 16 h of centrifuge-assisted tryptic digestion at $30,000{\times}g$ barely removed the myoglobin protein peak. Similar results were also obtained when using conventional tryptic digestion with gentle mixing. When acetonitrile (ACN) was added to make 10% ACN buffer solutions, the myoglobin protein peak disappeared after 6 h of digestion using both centrifuge-assisted and conventional tryptic digestions.
Kim, Kabsun,Kim, Jung Ha,Kim, Inyoung,Seong, Semun,Kim, Nacksung Elsevier 2018 Bone Vol.113 No.-
<P><B>Abstract</B></P> <P>The tripartite motif protein 38 (TRIM38), a member of the TRIM family, is involved in various cellular processes such as cell proliferation, differentiation, apoptosis, and antiviral defense. However, the role of TRIM38 in osteoclast and osteoblast differentiation is not yet known. In this study, we report the involvement of TRIM38 in osteoclast and osteoblast differentiation. Overexpression of TRIM38, in osteoclast precursor cells, attenuated receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclast formation, RANKL-triggered NF-κB activation, and expression of osteoclast marker genes, such as NFATc1, osteoclast-associated receptor (OSCAR), and tartrate-resistant acid phosphatase (TRAP); and down-regulation of TRIM38 expression showed the opposite effects. Ectopic expression of TRIM38 in osteoblast precursors induced increased osteoblast differentiation and function. Elevated expression of alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteocalcin was also observed due to blockade of NF-κB activation. Conversely, knockdown of TRIM38 showed the opposite effects. TRIM38 also induced degradation of lysosome-dependent transforming growth factor beta-activated kinase 1 and MAP3K7-binding protein 2 (TAB2), further blocking NF-κB activation. Taken together, our data suggest that TRIM38 plays a critical role in bone remodeling as a negative regulator of NF-κB in both osteoclast and osteoblast differentiation.</P> <P><B>Highlights</B></P> <P> <UL> <LI> TRIM38 expression was regulated during osteoclast and osteoblast differentiation. </LI> <LI> TRIM38 negatively regulates osteoclast differentiation and activity. </LI> <LI> TRIM38 positively regulates osteoblast differentiation and function. </LI> <LI> TRIM38 regulates NF-kB activation through TAB2 degradation in osteoclasts and osteoblasts. </LI> </UL> </P>
MicroRNA-26a Regulates RANKL-Induced Osteoclast Formation
Kim, Kabsun,Kim, Jung Ha,Kim, Inyoung,Lee, Jongwon,Seong, Semun,Park, Yong-Wook,Kim, Nacksung Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.1
Osteoclasts are unique cells responsible for the resorption of bone matrix. MicroRNAs (miRNAs) are involved in the regulation of a wide range of physiological processes. Here, we examined the role of miR-26a in RANKL-induced osteoclastogenesis. The expression of miR-26a was upregulated by RANKL at the late stage of osteoclastogenesis. Ectopic expression of an miR-26a mimic in osteoclast precursor cells attenuated osteoclast formation, actin-ring formation, and bone resorption by suppressing the expression of connective tissue growth factor/CCN family 2 (CTGF/CCN2), which can promote osteoclast formation via upregulation of dendritic cell-specific transmembrane protein (DC-STAMP). On the other hand, overexpression of miR-26a inhibitor enhanced RANKL-induced osteoclast formation and function as well as CTGF expression. In addition, the inhibitory effect of miR-26a on osteoclast formation and function was prevented by treatment with recombinant CTGF. Collectively, our results suggest that miR-26a modulates osteoclast formation and function through the regulation of CTGF.