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Kang, Lix2010,Jung,Kwon, Eunx2010,Soo,Lee, Kwang Min,Cho, Chanmi,Lee, Jaex2010,In,Ryu, Young Bae,Youm, Tae Hyun,Jeon, Jimin,Cho, Mi Ra,Jeong, Seonx2010,Yong,Lee, Sangx2010,Rae,Kim, Wook,Yang John Wiley and Sons Inc. 2018 British journal of pharmacology Vol.175 No.23
<P><B>Background and Purpose</B></P><P>3′‐Sialyllactose (3′‐SL) is a safe compound that is present in high levels in human milk. Although it has anti‐inflammatory properties and supports immune homeostasis, its effect on collagen‐induced arthritis (CIA) is unknown. In this study, we investigated the prophylactic and therapeutic effect of 3′‐SL on the progression of rheumatoid arthritis (RA) in <I>in vitro</I> and <I>in vivo</I> models.</P><P><B>Experimental Approach</B></P><P>The anti‐arthritic effect of 3′‐SL was analysed with fibroblast‐like synoviocytes <I>in vitro</I> and an <I>in vivo</I> mouse model of CIA. RT‐PCR, Western blotting and ELISA were performed to evaluate its effects <I>in vitro</I>. Histological analysis of ankle and knee joints of mice with CIA was performed using immunohistochemistry, as well as safranin‐O and haematoxylin staining.</P><P><B>Key Results</B></P><P>3′‐SL markedly alleviated the severity of CIA in the mice by reducing paw swelling, clinical scores, incidence rate, serum levels of inflammatory cytokines and autoantibody production. Moreover, 3′‐SL reduced synovitis and pannus formation and suppressed cartilage destruction by blocking secretion of chemokines, pro‐inflammatory cytokines, https://en.wikipedia.org/wiki/Matrix_metalloproteinases and osteoclastogenesis <I>via</I> NF‐κB signalling. Notably, phosphorylation of p65, which is a key protein in the NF‐κB signalling pathway, was totally blocked by 3′‐SL in the RA models.</P><P><B>Conclusions and Implications</B></P><P>3′‐SL ameliorated pathogenesis of CIA by suppressing catabolic factor expression, proliferation of inflammatory immune cells and osteoclastogenesis. These effects were mediated <I>via</I> blockade of the NF‐κB signalling pathway. Therefore, 3′‐SL exerted prophylactic and therapeutic effects and could be a novel therapeutic agent for the treatment of RA.</P>
Cho, Euix2010,Sic,Lee, Keunx2010,Soo,Son, Youngx2010,Ok,Jang, Yong‐,Suk,Lee, Seungx2010,Youp,Kwak, Sox2010,Yeong,Yang, Yeonx2010,Mi,Park, Seungx2010,Moon,Lee, Jeongx2010,Chae Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.111 No.5
<P><B>Abstract</B></P><P>Little is known about the effects of mechanical forces on osteoclastogenesis by bone marrow macrophages (BMMs) in the absence of mechanosensitive cells, including osteoblasts and fibroblasts. In this study, we examined the effects of mechanical force on osteoclastogenesis by applying centrifugal force to BMMs using a horizontal microplate rotor. Our findings, as measured by an in vitro model system, show that tumor necrosis factor (TNF)‐α is capable of inducing osteoclast differentiation from BMMs and bone resorption in the presence of macrophage‐colony stimulating factor (M‐CSF) and is further facilitated by receptor activator of nuclear factor‐kappaB (NF‐κB) ligand (RANKL). Application of force to BMMs accelerated TNF‐α‐induced osteoclastogenesis; this was inhibited either by anti‐TNF‐α or anti‐TNF‐α receptor but not by OPG. TNF‐α also increased c‐Fms expression at both mRNA and protein levels in BMMs. An anti‐c‐Fms antibody completely inhibited osteoclast differentiation and bone resorption induced by TNF‐α but partially blocked osteoclastogenesis stimulated in combination with RANKL. These results suggest that TNF‐α (in the presence of M‐CSF) is capable of inducing osteoclastogenesis from BMMs, and that osteoclastogenesis is significantly stimulated by force application through the activation of c‐Fms‐mediated signaling. Overall, the present study reveals the facilitating effect of mechanical force on osteoclastic differentiation from BMMs without the addition of mechanosensitive cells. J. Cell. Biochem. 111: 1260–1269, 2010. © 2010 Wiley‐Liss, Inc.</P>
Lee, Yoox2010,Yong,Lee, Jix2010,Hoon,Cho, Jux2010,Young,Kim, Nax2010,Rae,Nam, Daex2010,Hyun,Choi, Inx2010,Suk,Nam, Ki Tae,Joo, Youngx2010,Chang WILEY‐VCH Verlag 2013 Advanced functional materials Vol.23 No.32
<P><B>Abstract</B></P><P>It remains a fundamental challenge in the development of stretchable electronics to understand how mechanical strain changes the electrical properties of materials. Although the piezoresistive behavior of poly(3,4‐ethylene‐ dioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) has been observed, its intrinsic origin is not yet fully understood because there are many extrinsic contributing factors and an experimental platform with which to assess such behavior has not been established. Here, systematic analysis shows that the matching Poisson's ratio and elastic modulus between PEDOT:PSS films and their underlying substrates is important in decoupling the factors that affect the material's piezoresistivity, allowing for tunable resistivity. Based on such a fundamental understanding, the conductivity of PEDOT:PSS can be controlled to be invariant and decrease as a function of applied tensile stress. Furthermore, a linear response of the resistivity with respect to mechanical strains of up to 60%, which has never before been realized, is shown. The irreversible conductivity enhancement is primarily caused by the coalescence‐induced growth of conductive PEDOT‐rich cores.</P>
Pro‐apoptotic Noxa is involved in ablative focal irradiation‐induced lung injury
Kim, Jeex2010,Youn,An, Yong‐,Min,Choi, Won Hoon,Kim, Jinx2010,Mo,Cho, Samju,Yoo, Byung Rok,Kang, Jeong Wook,Lee, Yunx2010,Sil,Lee, Yoonx2010,Jin,Cho, Jaeho CAROL DAVILA UNIVERSITY PRESS 2017 JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Vol.21 No.4
<P><B>Abstract</B></P><P>Although lung injury including fibrosis is a well‐documented side effect of lung irradiation, the mechanisms underlying its pathology are poorly understood. X‐rays are known to cause apoptosis in the alveolar epithelial cells of irradiated lungs, which results in fibrosis due to the proliferation and differentiation of fibroblasts and the deposition of collagen. Apoptosis and BH3‐only pro‐apoptotic proteins have been implicated in the pathogenesis of pulmonary fibrosis. Recently, we have established a clinically analogous experimental model that reflects focal high‐dose irradiation of the ipsilateral lung. The goal of this study was to elucidate the mechanism underlying radiation‐induced lung injury based on this model. A radiation dose of 90 Gy was focally delivered to the left lung of C57BL/6 mice for 14 days. About 9 days after irradiation, the mice began to show increased levels of the pro‐apoptotic protein Noxa in the irradiated lung alongside increased apoptosis and fibrosis. Suppression of Noxa expression by small interfering RNA protected cells from radiation‐induced cell death and decreased expression of fibrogenic markers. Furthermore, we showed that reactive oxygen species participate in Noxa‐mediated, radiation‐induced cell death. Taken together, our results show that Noxa is involved in X‐ray‐induced lung injury.</P>
On‐Nanowire Band‐Graded Si:Ge Photodetectors
Kim, Cheolx2010,Joo,Lee, Hyunx2010,Seung,Cho, Yong‐,Jun,Yang, Jeex2010,Eun,Lee, Ru Ri,Lee, Ja Kyung,Jo, Moonx2010,Ho WILEY‐VCH Verlag 2011 Advanced Materials Vol.23 No.8
<P><B>An on‐nanowire (on‐NW) band‐graded photodetector that pertains to the on‐nanowire composition gradation from pure Si to pure Ge</B>, Si<SUB>1–<I>x</I></SUB>Ge<SUB><I>x</I></SUB> (0 ≤ <I>x</I> ≤ 1), is reported. The spectral onset of interband photocarrier generation and photocurrent amplitude are on‐NW de‐multiflexed over the continuously varying energy band gap and surface trap state density in an individually addressable manner. </P>
Ko, Youngx2010,Ho,Kim, Jex2010,Hyung,Jin, Lix2010,Hua,Ko, Sukx2010,Min,Kwon, Bongx2010,Joon,Kim, Joosung,Kim, Taek,Cho, Yong‐,Hoon WILEY‐VCH Verlag 2011 ADVANCED MATERIALS Vol.23 No.45
<P>Electrically driven hybrid light‐emitting diodes (LEDs) consisting of quantum dots, wires, and wells based on the nanometer‐sized pyramid GaN structure are reported by Taek Kim, Yong‐Hoon Cho, and co‐workers on page 5364. The LEDs exhibit mixed emissions from InGaN quantum dots, wires, and wells formed at the tops, edges, and sidewalls of the pyramids, respectively. The hybrid LEDs containing low‐dimensional quantum structures provide a broad‐band, highly efficient visible lighting source. </P>
Amyloid β‐induced elevation of O‐GlcNAcylated c‐Fos promotes neuronal cell death
Choi, Heesun,Kim, Chaeyoung,Song, Hyundong,Cha, Moonx2010,Yong,Cho, Hyun Jin,Son, Sung Min,Kim, Haeng Jun,Mookx2010,Jung, Inhee BLACKWELL PUBLISHING 2019 Aging Cell Vol.18 No.1
<P><B>Abstract</B></P><P>Alzheimer's disease (AD) is an age‐related neurodegenerative disease characterized by progressive memory loss resulting from cumulative neuronal cell death. O‐linked β‐N‐acetyl glucosamine (O‐GlcNAc) modification of the proteins reflecting glucose metabolism is altered in the brains of patients with AD. However, the link between altered O‐GlcNAc modification and neuronal cell death in AD is poorly understood. Here, we examined the regulation of O‐GlcNAcylation of c‐Fos and the effects of O‐GlcNAcylated c‐Fos on neuronal cell death during AD pathogenesis. We found that amyloid beta (Aβ)‐induced O‐GlcNAcylation on serine‐56 and 57 of c‐Fos was resulted from decreased interaction between c‐Fos and O‐GlcNAcase and promoted neuronal cell death. O‐GlcNAcylated c‐Fos increased its stability and potentiated the transcriptional activity through higher interaction with c‐Jun, resulting in induction of Bim expression leading to neuronal cell death. Taken together, Aβ‐induced O‐GlcNAcylation of c‐Fos plays an important role in neuronal cell death during the pathogenesis of AD.</P>
Mechanism of alveolar bone loss in a collagen‐induced arthritis model in mice
Park, Jungx2010,Chul,Su, Chuanxin,Jung, Imx2010,Hee,Choi, Seongx2010,Ho,Cho, Kyoox2010,Sung,Kim, Chong‐,Kwan,Park, Yong‐,Beom,Lee, Soox2010,Kon,Kim, Changx2010,Sung Blackwell Publishing Ltd 2011 Journal of Clinical Periodontology Vol.38 No.2
<P>Park J‐C, Su C, Jung I‐H, Choi S‐H, Cho K‐S, Kim C‐K, Park Y‐B, Lee S‐K, Kim C‐S: Mechanism of alveolar bone loss in a collagen‐induced arthritis model in mice. J Clin Periodontol 2011; 38: 122–130. doi: 10.1111/j.1600‐051X.2010.01645.x</P><P><B>Abstract</B></P><P><B>Objective: </B> The aim of this study was to understand the cellular/molecular mechanisms of periodontal breakdown in a collagen‐induced arthritis (CIA) model in mice to enhance the understanding of rheumatoid arthritis (RA)‐associated alveolar bone loss in humans.</P><P><B>Materials and Methods: </B> All analyses were performed on paired samples from CIA and control group mice. Mandibles were retrieved for micro‐computed tomography (micro‐CT), histomorphometric analysis, and isolation of alveolar bone cells (ABCs). In vitro osteoclastogenic/osteogenic/adipogenic potentials of ABCs were evaluated and the mRNA expression of downstream effector genes was assessed. Bone formation of ABCs was assessed using an ectopic transplantation model.</P><P><B>Results: </B> Histomorphometric and micro‐CT data showed that alveolar bone loss was significantly increased in the CIA group (<I>p</I><0.05). Osteoclastogenesis was significantly increased in the CIA group in vivo (<I>p</I><0.05), with upregulated mRNA expressions of osteoclastogenesis‐associated genes. Osteoblasts appeared to undergo increased apoptosis, and the bone‐forming activity of ABCs concomitantly decreased with in vitro osteogenic differentiation and in vivo ectopic transplantation (<I>p</I><0.05). Also, adipogenesis‐associated mRNA expression was highly expressed in the CIA group, resulting in significantly enhanced adipocyte differentiation in vitro (<I>p</I><0.05).</P><P><B>Conclusions: </B> These data demonstrate that increased osteoclastic activity, decreased bone‐forming activity and enhanced adipogenesis promote alveolar bone loss in a CIA model in mice, and they suggest that these mechanisms could account for the same outcome in human RA.</P>
Cho, Heex2010,Nam,Lee, Jinx2010,Woo,Lee, Yong‐,Hwan John Wiley Sons, Ltd. 2011 International Journal of Communication Systems Vol.24 No.5
<P><B>Abstract</B></P><P>This paper considers cooperative power allocation with the use of partial channel state information (CSI) in a multi‐user dual‐hop relay system with multiple antennas. The end‐to‐end capacity can be improved by dynamically allocating the transmit power of the base station and relay according to co‐channel interference caused by the adjacent relays. The proposed scheme allocates the transmit power in association with the eigenvalues and angle difference between the eigenvectors of transmit correlation matrices of the desired and interference channel. It is shown by means of upper‐bound analysis that the end‐to‐end capacity of the proposed scheme can be maximized in highly correlated channel environments when the principal eigenvectors of transmit correlation matrices of the desired and interference channel are orthogonal to each other. It is also shown that the proposed scheme is robust to the channel estimation error. Finally, the performance of the proposed scheme is verified by the computer simulation. Copyright © 2010 John Wiley & Sons, Ltd.</P>
Aqueous‐Solution Route to Zinc Telluride Films for Application to CO<sub>2</sub> Reduction
Jang, Jix2010,Wook,Cho, Seungho,Magesh, Ganesan,Jang, Youn Jeong,Kim, Jae Young,Kim, Won Yong,Seo, Jeong Kon,Kim, Sungjee,Lee, Kunx2010,Hong,Lee, Jae Sung WILEY‐VCH Verlag 2014 Angewandte Chemie Vol.126 No.23
<P><B>Abstract</B></P><P>As a photocathode for CO<SUB>2</SUB> reduction, zinc‐blende zinc telluride (ZnTe) was directly formed on a Zn/ZnO nanowire substrate by a simple dissolution–recrystallization mechanism without any surfactant. With the most negative conduction‐band edge among p‐type semiconductors, this new photocatalyst showed efficient and stable CO formation in photoelectrochemical CO<SUB>2</SUB> reduction at −0.2–−0.7 V versus RHE without a sacrificial reagent.</P>