2002년 기부횟수 자료의 재분석: 수정 및 보완

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.

[PA-0007] Transcription factors regulated by LEAFY COTYLEDON 2 in triacylglycerol accumulation

Inyoung Kim(Inyoung Kim),Hyung Ju Do(Hyung Ju Do),Hyun Uk Kim(Hyun Uk Kim) 한국육종학회 2022 한국육종학회 공동학술발표집 Vol.2022 No.-

Unenhanced Breast MRI With Diffusion-Weighted Imaging for Breast Cancer Detection: Effects of Training on Performance and Agreement of Subspecialty Radiologists

Kim Yeon Soo,Lee Su Hyun,Kim Soo-Yeon,Kim Eun Sil,Park Ah Reum,Chang Jung Min,Park Vivian Youngjean,Yoon Jung Hyun,Kang Bong Joo,Yun Bo La,Kim Tae Hee,Ko Eun Sook,Chu A Jung,Kim Jin You,Youn Inyoung,C 대한영상의학회 2024 Korean Journal of Radiology Vol.25 No.1

Objective: To investigate whether reader training improves the performance and agreement of radiologists in interpreting unenhanced breast magnetic resonance imaging (MRI) scans using diffusion-weighted imaging (DWI). Materials and Methods: A study of 96 breasts (35 cancers, 24 benign, and 37 negative) in 48 asymptomatic women was performed between June 2019 and October 2020. High-resolution DWI with b-values of 0, 800, and 1200 sec/mm2 was performed using a 3.0-T system. Sixteen breast radiologists independently reviewed the DWI, apparent diffusion coefficient maps, and T1-weighted MRI scans and recorded the Breast Imaging Reporting and Data System (BI-RADS) category for each breast. After a 2-h training session and a 5-month washout period, they re-evaluated the BI-RADS categories. A BI-RADS category of 4 (lesions with at least two suspicious criteria) or 5 (more than two suspicious criteria) was considered positive. The per-breast diagnostic performance of each reader was compared between the first and second reviews. Inter-reader agreement was evaluated using a multi-rater κ analysis and intraclass correlation coefficient (ICC). Results: Before training, the mean sensitivity, specificity, and accuracy of the 16 readers were 70.7% (95% confidence interval [CI]: 59.4–79.9), 90.8% (95% CI: 85.6–94.2), and 83.5% (95% CI: 78.6–87.4), respectively. After training, significant improvements in specificity (95.2%; 95% CI: 90.8–97.5; P = 0.001) and accuracy (85.9%; 95% CI: 80.9–89.8; P = 0.01) were observed, but no difference in sensitivity (69.8%; 95% CI: 58.1–79.4; P = 0.58) was observed. Regarding inter-diffusionreader agreement, the κ values were 0.57 (95% CI: 0.52–0.63) before training and 0.68 (95% CI: 0.62–0.74) after training, with a difference of 0.11 (95% CI: 0.02–0.18; P = 0.01). The ICC was 0.73 (95% CI: 0.69–0.74) before training and 0.79 (95% CI: 0.76–0.80) after training (P = 0.002). Conclusion: Brief reader training improved the performance and agreement of interpretations by breast radiologists using unenhanced MRI with DWI.

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>

Rev-erbα Negatively Regulates Osteoclast and Osteoblast Differentiation through p38 MAPK Signaling Pathway

Kim, Kabsun,Kim, Jung Ha,Kim, Inyoung,Seong, Semun,Kim, Nacksung Korean Society for Molecular and Cellular Biology 2020 Molecules and cells Vol.43 No.1

The circadian clock regulates various physiological processes, including bone metabolism. The nuclear receptors Reverbs, comprising Rev-erbα and Rev-erbβ, play a key role as transcriptional regulators of the circadian clock. In this study, we demonstrate that Rev-erbs negatively regulate differentiation of osteoclasts and osteoblasts. The knockdown of Rev-erbα in osteoclast precursor cells enhanced receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation, as well as expression of nuclear factor of activated T cells 1 (NFATc1), osteoclast-associated receptor (OSCAR), and tartrate-resistant acid phosphatase (TRAP). The overexpression of Rev-erbα leads to attenuation of the NFATc1 expression via inhibition of recruitment of c-Fos to the NFATc1 promoter. The overexpression of Rev-erbα in osteoblast precursors attenuated the expression of osteoblast marker genes including Runx2, alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteocalcin (OC). Rev-erbα interfered with the recruitment of Runx2 to the promoter region of the target genes. Conversely, knockdown of Rev-erbα in the osteoblast precursors enhanced the osteoblast differentiation and function. In addition, Rev-erbα negatively regulated osteoclast and osteoblast differentiation by suppressing the p38 MAPK pathway. Furthermore, intraperitoneal administration of GSK4112, a Rev-erb agonist, protects RANKL-induced bone loss via inhibition of osteoclast differentiation in vivo. Taken together, our results demonstrate a molecular mechanism of Rev-erbs in the bone remodeling, and provide a molecular basis for a potential therapeutic target for treatment of bone disease characterized by excessive bone resorption.

Role of CrkII Signaling in RANKL-Induced Osteoclast Differentiation and Function

Kim, Jung Ha,Kim, Kabsun,Kim, Inyoung,Seong, Semun,Nam, Kwang-Il,Lee, Seoung Hoon,Kim, Kyung Keun,Kim, Nacksung The American Association of Immunologists, Inc. 2016 JOURNAL OF IMMUNOLOGY Vol.196 No.3

<P>Rac1, a member of small GTPases, is a key regulator of osteoclast differentiation and function. The Crk family adaptor proteins, consisting of Src homology (SH) 2 and SH3 protein-binding domains, regulate cell proliferation, migration, and invasion through Rac1 activation. In this study, we examined the role of CrkII in osteoclast differentiation and function. Retroviral overexpression of CrkII in osteoclast precursors enhanced osteoclast differentiation and resorptive function through Rac1 activation. The knockdown of CrkII in osteoclast precursors using small interfering RNA inhibited osteoclast differentiation and its resorption activity. Unlike wild-type CrkII, overexpression of the three SH domains in mutant forms of CrkII did not enhance either osteoclast differentiation or function. Phosphorylation of p130 Crk-associated substrate (p130Cas) by osteoclastogenic cytokines in preosteoclasts increased the interaction between p130Cas and CrkII, which is known to be involved in Rac1 activation. Furthermore, transgenic mice over expressing CrkII under control of a tartrate-resistant acid phosphatase promoter exhibited a low bone mass phenotype, associated with increased resorptive function of osteoclasts in vivo. Taken together, our data suggest that the p130Cas/CrkII/Rac1 signaling pathway plays an important role in osteoclast differentiation and function, both in vitro and in vivo.</P>

TRIM38 regulates NF-κB activation through TAB2 degradation in osteoclast and osteoblast differentiation

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>

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 Ca²⁺-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]

A simple and robust route toward flexible CIGS photovoltaic devices on polymer substrates: Atomic level microstructural analysis and local opto-electronic investigation

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>

BCAP promotes osteoclast differentiation through regulation of the p38-dependent CREB signaling pathway

Kim, Jung Ha,Kim, Kabsun,Kim, Inyoung,Seong, Semun,Lee, Keun-Bae,Kim, Nacksung Elsevier 2018 Bone Vol.107 No.-

<P><B>Abstract</B></P> <P>Many studies have determined that PI3K-Akt signaling pathways play important roles in osteoclast differentiation and function. In the present study, we investigated the roles of B-cell adaptor for PI3K (BCAP), which is a PI3K binding molecule, in osteoclasts. Overexpression of BCAP in osteoclast precursor cells enhanced osteoclast differentiation induced by tumor necrosis factor alpha (TNF-α) as well as receptor activator of nuclear factor-κB ligand (RANKL). Conversely, osteoclast differentiation mediated by both cytokines was attenuated when BCAP expression was downregulated using small interfering RNA. Notably, BCAP induced Akt activation only upon stimulation by RANKL, but not by TNF-α. However, BCAP activated p38-dependent cAMP response element-binding protein (CREB) phosphorylation induced by both RANKL and TNF-α. Collectively, we showed that BCAP plays an important role in osteoclast differentiation by regulating the p38-dependent CREB signaling pathway, and that BCAP might be a new therapeutic target for bone diseases.</P> <P><B>Highlights</B></P> <P> <UL> <LI> BCAP positively regulates both RANKL- and TNF-α-induced osteoclast differentiation. </LI> <LI> BCAP increases the phosphorylation of Akt by RANKL, but not TNF-α. </LI> <LI> BCAP enhances both RANKL- and TNF-α-induced CREB activation. </LI> <LI> BCAP promotes osteoclast differentiation by regulating p38-dependent CREB signaling pathway rather than PI3K-Akt signaling pathway. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>