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- 저자 : Yu D. J. (검색결과 860 건)
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Yu, K‐,H.,Hong, K‐,S.,Lee, B‐,C.,Oh, M‐,S.,Cho, Y‐,J.,Koo, J‐,S.,Park, J‐,M.,Bae, H‐,J.,Han, M‐,K.,Ju, Y‐,S.,Kang, D‐,W.,Appelros, P. Blackwell Publishing Ltd 2011 Acta neurologica Scandinavica Vol.123 No.5
<P>Yu K‐H, Hong K‐S, Lee B‐C, Oh M‐S, Cho Y‐J, Koo J‐S, Park J‐M, Bae H‐J, Han M‐K, Ju Y‐S, Kang D‐W, Appelros P, Norrving B, Terent A. Comparison of 90‐day case‐fatality after ischemic stroke between two different stroke outcome registries using propensity score matching analysis. Acta Neurol Scand: 2011: 123: 325–331. © 2010 John Wiley & Sons A/S.</P><P><B>Background – </B> It has not been clarified whether the disparity in ischemic stroke outcome between populations is caused by ethnic and geographic differences or by variations in case mix. Propensity score matching (PSM) analysis can overcome some analytical problems but is rarely used in stroke outcome research. This study was to compare the ischemic stroke case‐fatality between two PSM cohorts of Sweden and Korea.</P><P><B>Methods – </B> Prognostic variables related to baseline characteristics and stroke care were included in our PSM model. Then, we selected 7675 Swedish and 1220 Korean patients with ischemic stroke from each stroke registers and performed one‐to‐one matching based on propensity scores of each patient.</P><P><B>Results – </B> After PSM, all measured variables were well balanced in 1163 matched subjects, and the 90‐day case‐fatality was identical 6.2% (HR 0.997, 95%CI 0.905–1.099) in Sweden and Korea.</P><P><B>Conclusions – </B> No difference is found in the 90‐day case‐fatality in propensity score‐matched Swedish and Korean patients with ischemic stroke.</P>
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IL-32γ inhibits cancer cell growth through inactivation of NF-κB and STAT3 signals
Oh, J H,Cho, M-C,Kim, J-H,Lee, S Y,Kim, H J,Park, E S,Ban, J O,Kang, J-W,Lee, D-H,Shim, J-H,Han, S B,Moon, D C,Park, Y H,Yu, D-Y,Kim, J-M,Kim, S H,Yoon, D-Y,Hong, J T Nature Publishing Group 2011 Oncogene Vol.30 No.30
<P>Several studies have shown physiological functions of interleukin (IL)-32, a novel cytokine. However, the role of IL-32 in cancer development has not been reported. In this study, we showed that IL-32γ inhibited tumor growth in IL-32γ-overexpressing transgenic mice inoculated with melanoma as well as colon tumor growth in xenograft nude mice inoculated with IL-32γ-transfected colon cancer cells (SW620). The inhibitory effect of IL-32γ on tumor growth was associated with the inhibition of constitutive activated nuclear transcription factor-κB (NF-κB) and of signal transducer and activator of transcription 3 (STAT3). The expression of antiapoptotic, cell proliferation and tumor-promoting genes (<I>bcl-2</I>, <I>X-chromosome inhibitor of apoptosis protein</I> (<I>IAP</I>), <I>cellular IAP</I> and <I>cellular FADD-like IL-1β-converting enzyme-inhibitory protein</I>, <I>cyclin D</I>), cyclin-dependent kinase 4, cycolooxygenase-2 and inducible nitric oxide synthase was decreased, whereas the expression of apoptotic target genes (<I>caspase-3</I> and <I>-9</I>, <I>bax</I>) increased. In tumor, spleen and blood, the number of cytotoxic CD8<SUP>+</SUP> T cells and CD57<SUP>+</SUP> natural killer cells and the levels of IL-10 increased, but that of tumor necrosis factor-α (TNF-α), IL-1β and IL-6 decreased. We also found that forced overexpression of IL-32γ inhibited colon cancer cell (SW620 and HCT116) growth accompanied with the inhibition of activated NF-κB and STAT3 <I>in vitro</I>. In addition, when IL-32γ was knocked down by small interfering RNA (siRNA) or neutralized with an anti-IL-32γ antibody, IL-32γ-induced colon cancer cell growth inhibition, the IL-32γ-induced decrease of TNF-α, IL-1 and IL-6 production, and the increase of IL-10 production were abolished. However, siRNA of NF-κB and STAT3 augmented IL-32γ-induced colon cancer cell growth inhibition. These findings indicate significant pathophysiological roles of IL-32γ in cancer development.</P>
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J. S. Hwang,D. M. Jang,K. S. Kim,J. S. Lee,S. C. Yu 한국자기학회 2013 Journal of Magnetics Vol.18 No.1
The magnetocaloric effect and magnetization behavior have been analyzed in the double-perovskite La0.7Ba0.3Mn1-XFeXO₃ compound with the sintering temperature at 1273 K. Samples were fabricated by the conventional solid-state reaction method. X-ray diffraction measurement revealed that all the samples had a single phase in orthorhombic. Detailed investigations of the magnetic entropy behavior of the samples were discussed with the variation of TC. The magnetic entropy changes, ΔSM of approximately 0.36-1.14 J/㎏ K were obtained in the temperature range of 145-350 K for the La0.7Ba0.3Mn1-XFeXO₃ compound. The enhancement of the magnetic entropy change is believed to be due to changes in the microstructure, which changes the magnetic part of the entropy of a solid around the magnetic ordering temperature.
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Kim, H.Y.,Jeon, J.,Hollender, J.,Yu, S.,Kim, S.D. Elsevier Scientific Pub. Co 2014 Journal of hazardous materials Vol.279 No.-
The potential bioaccumulation and distribution of antibiotics in non-target organisms have been inadequately studied in spite of their widespread occurrence in aquatic systems. We investigated the ability of tetracycline to bioaccumulate through aqueous and dietary routes in an aquatic organism, the freshwater crustacean Daphnia magna. D. magna was exposed to algal food (Pseudokirchneriella subcapitata) contaminated with tetracycline for dietary uptake. Tetracycline was transferred to D. magna more through aqueous uptake than through dietary uptake. The uptake rate constant of tetracycline for D. magna was k<SUB>in,water</SUB>=0.33+/-0.045 via the aqueous route and k<SUB>in,food</SUB>=0.16+/-0.012 via the dietary route for 1.0mgL<SUP>-1</SUP> tetracycline. Bioconcentration factors of 4.40+/-0.91Lkg<SUP>-1</SUP> and 3.66+/-0.50Lkg<SUP>-1</SUP> for 0.1 and 1.0mgL<SUP>-1</SUP> tetracycline were found for D. magna. The biomagnification factor of 0.19+/-0.04 indicates that magnification of tetracycline through the food web will not occur. The change in the internal concentration of the target compound was also studied for multigenerational (F1-F4) exposure. The internal concentration in D. magna showed a decreasing trend with increasing generations except for the parent generation. The bioaccumulation tendency showed a biphasic change in multigenerational exposure.
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김단비,김민지,김해솔,김희정,박윤선,손유경,송예진,유예림,이다예,이서영,이지현,강숙정,김부연 이화여자대학교간호학회 2020 이화간호학회지 Vol.- No.54
Purpose: The purpose of this descriptive study was to examine hospital choice factors among elderly patients to understand their experience and use as data to move towards senior-friendly hospitals. Methods: The individual in-depth interviews were conducted from August 13th to 18th, 2019. The participants consisted of eight senior citizens aged 65 and above that suffered from chronic illnesses and had regular hospital visits. Results: This study found that when elderly patients choose the hospital, they considered ‘awareness such as brand name of the hospital', ‘quality of medical service',‘convenience', ‘healthcare team / hospital employee', ‘personal experience', ‘children’s recommendation’ and etc,. The significant point was that all these factors were related to personal experiences from specific hospitals. Conclusion: This study analyzed the hospital choice factors of the elderly patients with high hospital utilization rates and found that the results were mainly affected by the distinct characteristics of elderly patients. The implications of this study are that we proposed further research directions and means for the improvement of the hospital. We suggest hospitals to increase labor allocation for elderly patients with difficulties dealing with unmanned systems such as kiosk and strengthen the role of healthcare providers as instructors for higher satisfaction.
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Lee, J.J.,Yu, J.Y.,Zhang, W.Y.,Kim, T.J.,Lim, Y.,Kwon, J.S.,Kim, D.W.,Myung, C.S.,Yun, Y.P. North-Holland ; Elsevier Science Ltd 2011 european journal of pharmacology Vol.650 No.1
We have previously reported that fenofibrate displayed a potent antithrombotic effect by the inhibition of platelet aggregation. The present study was designed to investigate the effects of fenofibrate on the neointimal hyperplasia and its possible molecular mechanism. Neointimal hyperplasia was measured in balloon-inflated-induced vascular injury model of male Sprague-Dawley rats and cell proliferation was measured in primary cultured rat aortic vascular smooth muscle cells (VSMCs). Fenofibrate-treated group showed a significant reduction in neointimal formation (0.07+/-0.04mm<SUP>2</SUP>) from the control (0.13+/-0.04mm<SUP>2</SUP>). Fenofibrate significantly inhibited platelet-derived growth factor (PDGF)-BB-induced cell counting and [<SUP>3</SUP>H]-thymidine incorporation into DNA. Fenofibrate suppressed the PDGF-BB-inducible progression through G<SUB>0</SUB>/G<SUB>1</SUB> to S phase of cell cycle. Moreover, fenofibrate inhibited not only phosphorylation of retinoblastoma (Rb) protein and expression of cyclin D/E, CDK 2/4 and proliferating cell nuclear antigen (PCNA) proteins but also mitogen-activated protein kinase (MAPK) signaling pathways such as ERK ½, p38 and JNK phosphorylation. In conclusion, the present study demonstrates that fenofibrate significantly inhibits neointimal formation via G<SUB>0</SUB>/G<SUB>1</SUB> arrest of PDGF-BB-induced cell proliferation in association with the inhibition of MAPK, which resulted in the downregulation of expressions of cyclin D/E, CDK 2/4 and PCNA proteins, suggesting that fenofibrate may be useful for individuals with a high risk of thrombotic or cardiovascular diseases.
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Vitamin D-binding protein interacts with Aβ and suppresses Aβ-mediated pathology
Moon, M,Song, H,Hong, H J,Nam, D W,Cha, M-Y,Oh, M S,Yu, J,Ryu, H,Mook-Jung, I Macmillan Publishers Limited 2013 CELL DEATH AND DIFFERENTIATION Vol.20 No.4
The level of vitamin D-binding protein (DBP) is increased in the cerebrospinal fluid of patients with Alzheimer’s disease (AD), suggesting a relationship with its pathogenesis. In this study, we investigated whether and how DBP is related to AD using several different approaches. A pull-down assay and a surface plasmon resonance binding assay indicated direct interactions between purified DBP and amyloid beta (Aβ), which was confirmed in the brain of AD patients and transgenic AD model mice by immunoprecipitation assay and immunohistochemical double-staining method. Moreover, atomic force microscopic examination revealed that DBP reduced Aβ aggregation in vitro. DBP also prevented Aβ-mediated death in cultured mouse hippocampal HT22 cell line. Finally, DBP decreased Aβ-induced synaptic loss in the hippocampus and rescued memory deficits in mice after injection of Aβ into the lateral ventricle. These results provide converging evidence that DBP attenuates the harmful effects of Aβ by a direct interaction, and suggest that DBP is a promising therapeutic agent for the treatment of AD.
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Shen, H.,Wang, J.,Jiang, D.,Xu, P.,Zhu, X.,Zhang, Y.,Yu, X.,Won, M. H.,Su, P. Q.,Yan, B. C. Springer Science + Business Media 2017 Cellular and molecular neurobiology Vol.37 No.5
<P>Some anticonvulsant drugs are associated with cognitive ability in patients; Topiramate (TPM) is well known as an effective anticonvulsant agent applied in clinical settings. However, the effect of TPM on the cognitive function is rarely studied. In this study, we aimed to observe the effects of TPM on cell proliferation and neuronal differentiation in the dentate gyrus (DG) of the d-galactose-induced aging mice by Ki-67 and doublecortin (DCX) immunohistochemistry. The study is divided into four groups including control, d-galactose-treated group, 25 and 50 mg/kg TPM-treated plus d-galactose-treated groups. We found, 50 mg/kg (not 25 mg/kg) TPM treatment significantly increased the numbers of Ki-67(+) cells and DCX immunoreactivity, and improved neuroblast injury induced by d-galactose treatment. In addition, we also found that decreased immunoreactivities and protein levels of antioxidants including superoxide dismutase and catalase induced by d-galactose treatment were significantly recovered by 50 mg/kg TPM treatment in the mice hippocampal DG (P < 0.05). In conclusion, our present results indicate that TPM can ameliorate neuroblast damage and promote cell proliferation and neuroblast differentiation in the hippocampal DG via increasing SODs and catalase levels in the d-galactose mice.</P>
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