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- 저자 : Han Tae‐ (검색결과 39 건)
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Park, Yang‐,Kyun,Son, Tae‐,geun,Kim, Hwiyoung,Lee, Jaegi,Sung, Wonmo,Kim, Il Han,Lee, Kunwoo,Bang, Young‐,bong,Ye, Sung‐,Joon John Wiley and Sons Inc. 2013 Journal of applied clinical medical physics Vol.14 No.5
<P>Phase‐based respiratory‐gated radiotherapy relies on the reproducibility of patient breathing during the treatment. To monitor the positional reproducibility of patient breathing against a 4D CT simulation, we developed a real‐time motion verification system (RMVS) using an optical tracking technology. The system in the treatment room was integrated with a real‐time position management system. To test the system, an anthropomorphic phantom that was mounted on a motion platform moved on a programmed breathing pattern and then underwent a 4D CT simulation with RPM. The phase‐resolved anterior surface lines were extracted from the 4D CT data to constitute 4D reference lines. In the treatment room, three infrared reflective markers were attached on the superior, middle, and inferior parts of the phantom along with the body midline and then RMVS could track those markers using an optical camera system. The real‐time phase information extracted from RPM was delivered to RMVS via in‐house network software. Thus, the real‐time anterior‐posterior positions of the markers were simultaneously compared with the 4D reference lines. The technical feasibility of RMVS was evaluated by repeating the above procedure under several scenarios such as ideal case (with identical motion parameters between simulation and treatment), cycle change, baseline shift, displacement change, and breathing type changes (abdominal or chest breathing). The system capability for operating under irregular breathing was also investigated using real patient data. The evaluation results showed that RMVS has a competence to detect phase‐matching errors between patient's motion during the treatment and 4D CT simulation. Thus, we concluded that RMVS could be used as an online quality assurance tool for phase‐based gating treatments.</P><P>PACS number: 87.55.Qr</P>
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Caveolin‐1 deficiency induces premature senescence with mitochondrial dysfunction
Yu, Dong‐,Min,Jung, Seung Hee,An, Hyoung‐,Tae,Lee, Sungsoo,Hong, Jin,Park, Jun Sub,Lee, Hyun,Lee, Hwayeon,Bahn, Myeong‐,Suk,Lee, Hyung Chul,Han, Na‐,Kyung,Ko, Jesang,Lee, Jae&# BLACKWELL PUBLISHING 2017 AGING CELL Vol.16 No.4
<P><B>Summary</B></P><P>Paradoxical observations have been made regarding the role of caveolin‐1 (Cav‐1) during cellular senescence. For example, caveolin‐1 deficiency prevents reactive oxygen species‐induced cellular senescence despite mitochondrial dysfunction, which leads to senescence. To resolve this paradox, we re‐addressed the role of caveolin‐1 in cellular senescence in human diploid fibroblasts, A549, HCT116, and Cav‐1<SUP><I>−/−</I></SUP> mouse embryonic fibroblasts. Cav‐1 deficiency (knockout or knockdown) induced cellular senescence via a p53‐p21‐dependent pathway, downregulating the expression level of the cardiolipin biosynthesis enzymes and then reducing the content of cardiolipin, a critical lipid for mitochondrial respiration. Our results showed that Cav‐1 deficiency decreased mitochondrial respiration, reduced the activity of oxidative phosphorylation complex I (CI), inactivated SIRT1, and decreased the NAD<SUP>+</SUP>/NADH ratio. From these results, we concluded that Cav‐1 deficiency induces premature senescence via mitochondrial dysfunction and silent information regulator 2 homologue 1 (SIRT1) inactivation.</P>
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Na, Tae‐,Young,Han, Young‐,Hyun,Ka, Na‐,Lee,Park, Han‐,Su,Kang, Yun Pyo,Kwon, Sung Won,Lee, Byung‐,Hoon,Lee, Mi‐,Ock John WileySons, Ltd 2015 The Journal of pathology Vol.235 No.5
<P><B>Abstract</B></P><P>Chronic ethanol consumption causes hepatic steatosis and inflammation, which are associated with liver hypoxia. Monocyte chemoattractant protein‐1 (MCP‐1) is a hypoxia response factor that determines recruitment and activation of monocytes to the site of tissue injury. The level of MCP‐1 is elevated in the serum and liver of patients with alcoholic liver disease (ALD); however, the molecular details regarding the regulation of MCP‐1 expression are not yet understood completely. Here, we show the role of liver X receptor α (LXRα) in the regulation of MCP‐1 expression during the development of ethanol‐induced fatty liver injury, using an antagonist, 22‐S‐hydroxycholesterol (22‐S‐HC). First, administration of 22‐S‐HC attenuated the signs of liver injury with decreased levels of MCP‐1 and its receptor CCR2 in ethanol‐fed mice. Second, hypoxic conditions or treatment with the LXRα agonist GW3965 significantly induced the expression of MCP‐1, which was completely blocked by treatment with 22‐S‐HC or infection by shLXRα lentivirus in the primary hepatocytes. Third, over‐expression of LXRα or GW3965 treatment increased MCP‐1 promoter activity by increasing the binding of hypoxia‐inducible factor‐1α to the hypoxia response elements, together with LXRα. Finally, treatment with recombinant MCP‐1 increased the level of expression of LXRα and LXRα‐dependent lipid droplet accumulation in both hepatocytes and Kupffer cells. These data show that LXRα and its ligand‐induced up‐regulation of MCP‐1 and MCP‐1‐induced LXRα‐dependent lipogenesis play a key role in the autocrine and paracrine activation of MCP‐1 in the pathogenesis of alcoholic fatty liver disease, and that this activation may provide a promising new target for ALD therapy.Copyright © 2014 The Authors. <I>The Journal of Pathology</I> published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.</P>
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Han, Tae‐,Hee,Choi, Mi‐,Ri,Woo, Seong‐,Hoon,Min, Sung‐,Yong,Lee, Chang‐,Lyoul,Lee, Tae‐,Woo WILEY‐VCH Verlag 2012 ADVANCED MATERIALS Vol.24 No.11
<P><B>A highly efficient simplified organic light‐emitting diode (OLED)</B> with a molecularly controlled strategy to form near‐perfect interfacial layer on top of the anode is demonstrated. A self‐organized polymeric hole injection layer (HIL) is exploited increasing hole injection, electron blocking, and reducing exciton quenching near the electrode or conducting polymers; this HIL allows simplified OLED comprised a single small‐molecule fluorescent layer to exhibits a high current efficiency (∼20 cd/A).</P>
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Park, Ji‐,Hae,Jung, Ye‐,Jin,Antar ,Aziz ,Mohamed, Mohamed,Hoon ,Lee, Tae,Lee, Chang‐,Ho,Han, Daeseok,Song, Myung‐,Chong,Kim, Jiyoung,Baek, Nam‐,In WILEY‐VCH Verlag 2014 Helvetica chimica acta Vol.97 No.3
<P><B>Abstract</B></P><P>Two new bisabolane sesquiterpenoids, <B>1</B> and <B>2</B>, along with five known ones, 13‐hydroxyxanthorrhizol (<B>3</B>), 12,13‐epoxyxanthorrhizol (<B>4</B>), xanthorrhizol (<B>5</B>), <I>β</I>‐curcumene (<B>6</B>), and <I>β</I>‐bisabolol (<B>7</B>), were isolated from the rhizomes of <I>Curcuma xanthorrhiza</I> <SMALL>Roxb</SMALL><I>.</I> The chemical structures of the new compounds were determined to be (7<I>R</I>,10<I>R</I>)‐10,11‐dihydro‐10,11‐dihydroxyxanthorrhizol 3‐<I>O</I>‐<I>β</I>‐<SMALL>D</SMALL>‐glucopyranoside (<B>1</B>) and (−)‐curcuhydroquinone 2,5‐di‐<I>O</I>‐<I>β</I>‐<SMALL>D</SMALL>‐glucopyranoside (<B>2</B>) on the basis of 1D‐ and 2D‐NMR spectroscopic analyses and optical‐rotation characteristics. Compounds <B>2</B> and <B>3</B> decreased MMP‐1 expression in UVB‐treated human keratinocytes by <I>ca.</I> 8.9‐ and 7.6‐fold at the mRNA level, and by <I>ca.</I> 9.2‐ and 6.6‐fold at the protein level, respectively. The results indicate that the isolated compounds may have anti‐aging effects through inhibition of MMP‐1 expression in skin cells.</P>
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Cha, Yongjun,Kim, Hwang‐,Phill,Lim, Yoojoo,Han, Sae‐,Won,Song, Sang‐,Hyun,Kim, Tae‐,You John Wiley and Sons Inc. 2018 Molecular Oncology Vol.12 No.7
<P>Although regorafenib has demonstrated survival benefits in patients with metastatic colorectal and gastrointestinal stromal tumors, no proven biomarker has been identified for predicting sensitivity to regorafenib. Here, we investigated preclinical activity of regorafenib in gastric and colorectal cancer cells to identify genetic alterations associated with sensitivity to regorafenib. Mutation profiles and copy number assays of regorafenib target molecules indicated that amplification of fibroblast growth factor receptor 2 (FGFR2) was the only genetic alteration associated with <I>in vitro</I> sensitivity to regorafenib. Regorafenib effectively inhibited phosphorylation of FGFR2 and its downstream signaling molecules in a dose‐dependent manner and selectively in FGFR2‐amplified cells. Regorafenib induced G1 arrest (SNU‐16, KATO‐III) and apoptosis (NCI‐H716); however, no significant changes were seen in cell lines without FGFR2 amplification. In SNU‐16 mice xenografts, regorafenib significantly inhibited tumor growth, proliferation, and FGFR signaling compared to treatment with control vehicle. Regorafenib effectively abrogates activated FGFR2 signaling in FGFR2‐amplified gastric and colorectal cancer and, therefore, might be considered for integration into treatment in patients with FGFR2‐amplified gastric and colorectal cancers.</P>
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Tissue‐type‐specific transcriptome analysis identifies developing xylem‐specific promoters in poplar
Ko, Jae‐,Heung,Kim, Hyun‐,Tae,Hwang, Ildoo,Han, Kyung‐,Hwan Blackwell Publishing Ltd 2012 Plant biotechnology journal Vol.10 No.5
<P><B>Summary</B></P><P>Plant biotechnology offers a means to create novel phenotypes. However, commercial application of biotechnology in crop improvement programmes is severely hindered by the lack of utility promoters (or freedom to operate the existing ones) that can drive gene expression in a tissue‐specific or temporally controlled manner. Woody biomass is gaining popularity as a source of fermentable sugars for liquid fuel production. To improve the quantity and quality of woody biomass, developing xylem (DX)‐specific modification of the feedstock is highly desirable. To develop utility promoters that can drive transgene expression in a DX‐specific manner, we used the Affymetrix Poplar Genome Arrays to obtain tissue‐type‐specific transcriptomes from poplar stems. Subsequent bioinformatics analysis identified 37 transcripts that are specifically or strongly expressed in DX cells of poplar. After further confirmation of their DX‐specific expression using semi‐quantitative PCR, we selected four genes (<I>DX5</I>, <I>DX8</I>, <I>DX11</I> and <I>DX15</I>) for <I>in vivo</I> confirmation of their tissue‐specific expression in transgenic poplars. The promoter regions of the selected DX genes were isolated and fused to a β‐glucuronidase (GUS)‐reported gene in a binary vector. This construct was used to produce transgenic poplars <I>via Agrobacterium</I>‐mediated transformation. The GUS expression patterns of the resulting transgenic plants showed that these promoters were active in the xylem cells at early seedling growth and had strongest expression in the developing xylem cells at later growth stages of poplar. We conclude that these DX promoters can be used as a utility promoter for DX‐specific biomass engineering.</P>
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Jang, Eunyoung,Nam, Gnu,Woo, Hyein,Lee, Junseong,Han, Mi‐,Kyung,Kim, Sung‐,Jin,You, Tae‐,Soo Wiley-VCH 2015 European journal of inorganic chemistry Vol.2015 No.17
<P><B>Abstract</B></P><P>Five rare‐earth metal containing quaternary phosphides in the <I>RE</I>Li<I><SUB>x</SUB></I>Cu<SUB>2–<I>y</I></SUB>P<SUB>2</SUB> (<I>RE</I> = La, Pr, Nd, Gd, Er; 0.82 ≤ <I>x</I> ≤ 1; 1.19 ≤ <I>y</I> ≤ 1.54) series were synthesized by using high‐temperature synthetic methods, and they were characterized by single‐crystal X‐ray diffraction. The title compounds crystallize in the trigonal space group <I>P</I><TEX>$\bar {3}$</TEX><I>m</I>1 (<I>Z</I> = 1, Pearson code <I>hP</I>6) with four crystallographically independent atomic positions. The overall crystal structure can be described as a “Li‐filled” CaAl<SUB>2</SUB>Si<SUB>2</SUB>‐type structure, in which a partially occupied Li site is embedded within the “double‐deck” layers formed by two anionic components. Tight‐binding linear muffin‐tin orbital calculations including density of states, crystal orbital Hamilton population, and electron localization function analyses provided rationales for the overall electronic structure and chemical bonding of the title phase. PrLi<SUB>0.98(5)</SUB>Cu<SUB>1.54(1)</SUB>P<SUB>2</SUB> indicated an antiferromagnetic interaction of Pr at a relatively low temperature with a paramagnetic Curie temperature of –6.8 K and a thermal conductivity of 3.2 W mK<SUP>–1</SUP> at 323 K.</P>
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Jang, Eunyoung,Nam, Gnu,Woo, Hyein,Lee, Junseong,Han, Mi‐,Kyung,Kim, Sung‐,Jin,You, Tae‐,Soo Wiley-VCH 2015 European journal of inorganic chemistry Vol.2015 No.17
<P><B>The cover picture shows</B> schematically how the spilled pieces of Li metal are serendipitously inserted into the space within the double‐deck anionic layers and eventually form the Li‐filled double‐deck layered structure of the <I>RE</I>Li<SUB><I>x</I></SUB>Cu<SUB>2–<I>y</I></SUB>P<SUB><I>y</I></SUB> (<I>RE</I> = La, Pr, Nd, Gd, Er; 0.82 ≤ <I>x</I> ≤ 1; 1.19 ≤ <I>y</I> ≤ 1.54) series. Single‐crystal X‐ray diffraction data demonstrates partial occupation of Li and Cu sites. The compounds were thoroughly investigated by temperature‐dependent <SUP>7</SUP>Li NMR spectroscopy, thermal conductivity, as well as magnetization studies. Theoretical studies based on DOS, COHP, and ELF were also carried out. Details are discussed in the article by T.‐S. You et al. on p. 2786 ff. For more on the story behind the cover research, see the Cover Profile. </P>
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Han, Tae‐,Un,Cho, Soo‐,Kyung,Kim, Taehyeung,Joo, Young Bin,Bae, Sang‐,Cheol,Kang, Changwon Wiley Subscription Services, Inc., A Wiley Company 2013 Vol.65 No.3
<P><B>Abstract</B></P><P><B>Objective</B></P><P>To investigate whether a human X chromosome locus of IRAK1 and MECP2 is associated with susceptibility to rheumatoid arthritis (RA), an autoimmune disease that predominantly affects women.</P><P><B>Methods</B></P><P>A total of 2,334 unrelated Korean participants (including 1,318 patients with RA) were genotyped for 5 tag single‐nucleotide polymorphisms (SNPs) and 3 additional SNPs in an Xq28 region harboring MECP2 and IRAK1. Twenty‐nine additional neighboring SNPs were imputed using the Korean HapMap Project data. All 37 SNPs were statistically tested for association with RA susceptibility, and 2 SNPs associated with RA were examined for their functional effects.</P><P><B>Results</B></P><P>RA susceptibility was associated with multiple SNPs in a 79‐kb linkage disequilibrium block harboring both MECP2 and IRAK1. The most significant association was for MECP2 SNP rs1734792 (<I>P</I> = 0.00089), but 2 nonsynonymous IRAK1 SNPs, rs1059702 (<I>P</I> = 0.0034) and rs1059703 (<I>P</I> = 0.0042), which were in strong linkage disequilibrium with the MECP2 SNP (D′ = 0.87 and 0.91, respectively) affected IRAK1 protein activity. The major haplotype of the 2 nonsynonymous SNPs was associated with a 1.7‐fold increase in RA susceptibility versus the minor haplotype (<I>P</I> = 0.0082), and with increased IRAK1 activity, which was demonstrated by a 1.7‐fold increase in the intracellular activity of transcription factor NF‐κB.</P><P><B>Conclusion</B></P><P>Our findings indicate that RA susceptibility is associated with multiple SNPs in MECP2 and IRAK1, but high linkage disequilibrium between them does not allow for further localization. Therefore, both genes remain candidates. Nevertheless, the major haplotype of the 2 nonsynonymous IRAK1 SNPs encoding for pPhe196Ser and pSer532Leu confers enhanced IRAK1 activity and, consequently, enhanced susceptibility to RA, as compared to the minor haplotype.</P>
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