http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Cho, Hyun‐,Min,Kim, Pyungx2010,Hwan,Chang, Hyun‐,Kyung,Shen, Yix2010,ming,Bonsra, Kwaku,Kang, Byungx2010,Jae,Yum, Soox2010,Young,Kim, Joox2010,Hyun,Lee, Sox2010,Yeong,Choi, Min John Wiley and Sons Inc. 2017 Stem cells translational medicine Vol.6 No.3
<P><B>Abstract</B></P><P>Human umbilical cord blood‐derived mesenchymal stem cells (hUCB‐MSCs) exhibit potency for the regeneration of infarcted hearts. Vascular endothelial growth factor (VEGF) is capable of inducing angiogenesis and can boost stem cell‐based therapeutic effects. However, high levels of VEGF can cause abnormal blood vessel growth and hemangiomas. Thus, a controllable system to induce therapeutic levels of VEGF is required for cell therapy. We generated an inducible VEGF‐secreting stem cell (VEGF/hUCB‐MSC) that controls the expression of VEGF and tested the therapeutic efficacy in rat myocardial infarction (MI) model to apply functional stem cells to MI. To introduce the inducible VEGF gene cassette into a safe harbor site of the hUCB‐MSC chromosome, the transcription activator‐like effector nucleases system was used. After confirming the integration of the cassette into the locus, VEGF secretion in physiological concentration from VEGF/hUCB‐MSCs after doxycycline (Dox) induction was proved in conditioned media. VEGF secretion was detected in mice implanted with VEGF/hUCB‐MSCs grown via a cell sheet system. Vessel formation was induced in mice transplanted with Matrigel containing VEGF/hUCB‐MSCs treated with Dox. Moreover, seeding of the VEGF/hUCB‐MSCs onto the cardiac patch significantly improved the left ventricle ejection fraction and fractional shortening in a rat MI model upon VEGF induction. Induced VEGF/hUCB‐MSC patches significantly decreased the MI size and fibrosis and increased muscle thickness, suggesting improved survival of cardiomyocytes and protection from MI damage. These results suggest that our inducible VEGF‐secreting stem cell system is an effective therapeutic approach for the treatment of MI. S<SMALL>TEM</SMALL> C<SMALL>ELLS</SMALL> T<SMALL>RANSLATIONAL</SMALL> M<SMALL>EDICINE</SMALL><I>2017;6:1040–1051</I></P>
Jo, Nam Hyun,Kim, Jung Young,Elx2010,Gamal, Mohammed I.,Choi, Wonx2010,Kyoung,Park, Jinx2010,Hun,Kim, Eun Jung,Cho, Jungx2010,Hyuck,Ha, Hyun‐,Joon,Choi, Tae Hyun,Oh, Changx2010,Hyun John Wiley Sons, Ltd. 2011 Journal of labelled compounds & radiopharmaceutica Vol.54 No.2
<P><B>Abstract</B></P><P>Synthesis, radiolabelling, and <I>in vitro</I> evaluation of a new <SUP>125</SUP>I‐labelled iodouracil hexitol nucleoside analogue are reported. The target compound was successfully synthesized by an iodination–destannylation method and then purified by reverse phase HPLC. The radiochemical purity of the product was >99% with decay‐corrected yields of 48±3%. <I>In vitro</I> cellular uptake testing was carried out using MCA and MCA‐tk cell lines for comparison of compound 1 with [<SUP>18</SUP>F]FHBG. The newly synthesized compound 1 showed higher accumulation in herpex simplex virus type 1 thymidine kinase (HSV1‐tk) gene expression cell line (MCA‐tk cell line) than in the wild type MCA cell line compared with [<SUP>18</SUP>F]FHBG. The MCA‐tk to MCA cellular uptake ratio for compound 1 was higher than that of [<SUP>18</SUP>F]FHBG from 2 h after incubation. The radioiodine‐labelled compound 1 (I‐125, <I>t</I><SUB>1/2</SUB>=59.37 days) has a longer physical half‐life than F‐18‐(<I>t</I><SUB>1/2</SUB>=110 min) labelled FHBG. Radioiodine‐labelled compound 1 could be used for monitoring gene expression for a long time. The selectivity for MCA‐tk cell line makes compound 1 a promising imaging agent for HSV1‐tk expression. Copyright © 2010 John Wiley & Sons, Ltd.</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>
Cho, Youngx2010,ra,Lee, Ji Hyeon,Kim, Ji Hye,Lee, Sox2010,Yeon,Yoo, Suna,Jung, Minx2010,kyo,Kim, Su Jung,Yoo, Hyun Ju,Pack, Changx2010,Gi,Rho, Jin Kyung,Son, Jaekyoung John Wiley and Sons Inc. 2018 MOLECULAR ONCOLOGY Vol.12 No.7
<P>Matrine is a natural compound extracted from the herb <I>Sophora flavescens</I> Ait which is widely used in traditional Chinese medicine for treating various diseases. Recently, matrine was reported to have antitumor effects against a variety of cancers without any obvious side effects; however, the molecular mechanisms of its antiproliferative effects on cancer are unclear. Here, we report that matrine inhibits autophagy‐mediated energy metabolism, which is necessary for pancreatic cancer growth. We found that matrine significantly reduces pancreatic cancer growth <I>in vitro</I> and <I>in vivo</I> by insufficiently maintaining mitochondrial metabolic function and energy level. We also found that either pyruvate or α‐ketoglutarate supplementation markedly rescues pancreatic cancer cell growth following matrine treatment. Inhibition of mitochondrial energy production results from matrine‐mediated autophagy inhibition by impairing the function of lysosomal protease. Matrine‐mediated autophagy inhibition requires stat3 downregulation. Furthermore, we found that the antitumor effect of matrine on pancreatic cancer growth depends on the mutation of the KRAS oncogene. Together, our data suggest that matrine can suppress the growth of KRAS‐mutant pancreatic cancer by inhibiting autophagy‐mediated energy metabolism.</P>
On‐Nanowire Band‐Graded Si:Ge Photodetectors
Kim, Cheolx2010,Joo,Lee, Hyun‐,Seung,Cho, Yongx2010,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>
Cho, Sungx2010,Yun,Lee, Hyox2010,Jeong,Jeong, Soox2010,Jin,Lee, Hyox2010,Jung,Kim, Hyun‐,Seok,Chen, Chang Yan,Lee, Eunx2010,Ok,Kim, Sungx2010,Hoon Blackwell Publishing Ltd 2011 Journal of pineal research Vol.51 No.1
<P><B>Abstract: </B> Sphingosine kinase 1 (SPHK1) is a newly discovered modulator of hypoxia inducible factor 1α (HIF‐1α) with various biological activities such as cell growth, survival, invasion, angiogenesis, and carcinogenesis. Thus, in the present study, the biological mechanisms of melatonin were elucidated in association with SPHK1 pathway in PC‐3 prostate cancer cells under hypoxia. Melatonin inhibited the stability of HIF‐1α in a time‐ and concentration‐ dependent manners. Also, melatonin decreased SPHK1 activity in PC‐3 cells during hypoxia. Furthermore, melatonin suppressed AKT/glycogen synthase kinase‐3β (GSK‐3β) signaling pathway, which stabilizes HIF‐1α via inhibition of von Hippel‐Lindau tumor suppressor protein. Consistently, siRNA‐SPHK1 and sphingosine kinase inhibitor (SKI) effectively blocked the expression of HIF‐1α, phospho‐AKT and vascular endothelial growth factor (VEGF) production in PC‐3 cells under hypoxia, suggesting the role of SPHK1 in melatonin‐inhibited HIF‐1α accumulation. Moreover, reactive oxygen species (ROS) scavenger N‐acteylcysteine enhanced melatonin‐inhibited HIF‐1α expression and SPHK1 activity. Overall, our findings suggest that melatonin suppresses HIF‐1α accumulation via inhibition of SPHK1 pathway and ROS generation in PC‐3 cells under hypoxia.</P>
Kim, Sox2010,Yeon,Lee, Jinx2010,Gu,Cho, Woox2010,Sung,Cho, Kyongx2010,Hyun,Sakong, Jun,Kim, Jaex2010,Ryong,Chin, Byungx2010,Rho,Baek, Sukx2010,Hwan Nature Publishing Group 2010 Immunology and Cell Biology Vol.88 No.2
<P>This study examined the hypothesis that the control of NADPH oxidase‐2 (Nox2)‐mediated reactive oxygen species (ROS) regulates the expression of matrix metalloproteinases (MMPs) and the migration of macrophages. Lipopolysaccharide (LPS) stimulation of Raw264.7 cells and mice peritoneal macrophages increased the expression of MMP‐9, 10, 12 and 13 mRNA, and also increased Raw264.7 cell migration. Treatment with an antioxidant (<I>N</I>‐acetyl cysteine) or Nox inhibitors strongly inhibited the expression of MMPs by LPS and inhibited cell migration. LPS caused ROS production in macrophages and increased the mRNA expression of Nox isoforms Nox1 and Nox2 by 20‐fold and two‐fold, respectively. While Nox1 small interfering RNA (siRNA) did not inhibit LPS‐mediated expression of MMPs, Nox2 siRNA inhibited the expressions of MMP‐9, 10 and 12. Neither Nox1 nor Nox2 siRNA influenced the LPS‐mediated expression of MMP‐13. In addition, NAC or apocynin attenuated LPS‐induced ROS production and MMP‐9 expression. MMP‐9 expression and cell migration were controlled by ERK1/2–ROS signaling. Collectively, these results suggest that LPS stimulates ROS production via ERK and induce various types of MMPs expression and cell migration.</P>
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, Hyun‐,Ji,Kang, Jeongx2010,Han,Kim, Teoan,Park, Kwangx2010,Kyun,Kim, Cheorlx2010,Ho,Lee, Inx2010,Seon,Min, Kwanx2010,Sik,Magae, Junji,Nakajima, Hiroo,Bae, Youngx2010,Seuk,Chang, Wiley Subscription Services, Inc., A Wiley Company 2009 Journal of cellular biochemistry Vol.107 No.2
<P><B>Abstract</B></P><P>Fibrosis in glomerulosclerosis causes progressive loss of renal function. Transforming growth factor (TGF)‐β, one of the major profibrotic cytokines, induces the synthesis of plasminogen activator inhibitor (PAI)‐1, a factor that plays a crucial role in the development of fibrosis. Here, we found that an isoprenoid antibiotic, ascofuranone, suppresses expression of profibrotic factors including matrix proteins and PAI‐1 induced by TGF‐β in renal fibroblasts. Ascofuranone selectively inhibits phosphorylation of epidermal growth factor receptor (EGFR), and downstream kinases such as Raf‐1, MEK‐1/2, and ERK‐1/2. PAI‐1 transcription also is suppressed by treatment with kinase inhibitors for MEK‐1/2 or EGFR, and with small interfering RNA for EGFR. Ascofuranone inhibits cellular metalloproteinase activity, and an inhibitor of metalloproteinases suppresses EGFR phosphorylation and PAI‐1 transcription. These results suggest that ascofuranone suppresses expression of profibrotic factors through the inhibition of an EGFR‐dependent signal transduction pathway activated by metalloproteinases. J. Cell. Biochem. 107: 335–344, 2009. © 2009 Wiley‐Liss, Inc.</P>
Chang, Seox2010,Yoon,Cho, Jae Min,Kim, Dongx2010,Bin,Jang, Hyun‐,Jong,Ko, Seung Hyun,Jo, Yangx2010,Hyeok,Kim, Myungx2010,Jun Wiley Subscription Services, Inc., A Wiley Company 2012 Journal of cellular biochemistry Vol.113 No.5
<P><B>Abstract</B></P><P>Early growth response‐1 (EGR‐1), one of immediate early response genes, is involved in diverse cellular response. We recently reported that quercetin increased catalytic subunit of γ‐glutamylcysteine ligase (GCLC) via the interaction of EGR‐1 to GCLC promoter in INS‐1 beta‐cells. Therefore, this study investigated molecular mechanisms of quercetin‐induced EGR‐1 expression in INS‐1 cells. Quercetin significantly induced EGR‐1 protein and its mRNA expressions. This induction of EGR‐1 was completely blocked by pretreatment with a PKA inhibitor, H89 and partially blocked by a p38 inhibitor, SB203580. Additionally, the siRNA‐mediated inhibition of PKAα and p38 resulted in significant reduction of quercetin‐induced EGR‐1 promoter activity. Also, quercetin‐induced EGR‐1 protein expression was significantly decreased in the cells transfected with PKAα siRNA. Study using truncated EGR‐1 promoter constructs showed that serum response element (SRE) sites, not cAMP response element site, were essential for EGR‐1 transcription. However, electrophoretic mobility shift assay showed that quercetin did not affect the band intensity of DNA‐protein complex on SRE site of EGR‐1 promoter. Also, immune‐shift assay using serum response factor (SRF) and phospho‐SRF antibodies showed no difference between control and quercetin‐treated groups. Collectively, quercetin‐induced EGR‐1 expression is largely dependent on PKA and partly on p38 MAPK pathway, and SRE sites of EGR‐1 promoter are involved in quercetin‐induced EGR‐1 transcriptional activity. J. Cell. Biochem. 113: 1559–1568, 2012. © 2011 Wiley Periodicals, Inc.</P>