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      • KCI등재

        Effects of ion irradiation on microstructure and properties of zirconium alloysdA review

        Chunguang Yan,Rongshan Wang,Yanli Wang,Xitao Wang,Guanghai Bai 한국원자력학회 2015 Nuclear Engineering and Technology Vol.47 No.3

        Zirconium alloys are widely used in nuclear reactors as structural materials. During the operation, they are exposed to fast neutrons. Ion irradiation is used to simulate the damage introduced by neutron irradiation. In this article, we briefly review the neutron irradiation damage of zirconium alloys, then summarize the effect of ion irradiation on microstructural evolution, mechanical and corrosion properties, and their relationships. The microstructure components consist of dislocation loops, second phase precipitates, and gas bubbles. The microstructure parameters are also included such as domain size and microstrain determined by X-ray diffraction and the S-parameter determined by positron annihilation. Understanding the relationships of microstructure and properties is necessary for developing new advanced materials with higher irradiation tolerance.

      • KCI등재

        Altered microRNA Expression Profiles of Extracellular Vesicles in Nasal Mucus From Patients With Allergic Rhinitis

        Geping Wu,Guanghai Yang,Ruxin Zhang,Guangyin Xu,Ling Zhang,Wu Wen,Jianbing Lu,Jianyong Liu,Yan Yu 대한천식알레르기학회 2015 Allergy, Asthma & Immunology Research Vol.7 No.5

        Purpose: Allergic rhinitis (AR) is an inflammatory disorder of the upper airway. Exosomes or extracellular vesicles are nanosized vesicles of endosomal origin released from inflammatory and epithelial cells that have been implicated in allergic diseases. In this study, we characterized the microRNA (miRNA) content of exosomes in AR. Methods: Extracellular vesicles were isolated from nasal mucus from healthy control subjects (n=10) and patients with severe AR (n=10). Vesicle RNA was analyzed by using a TaqMan microRNA assays Human Panel-Early Access kit (Applied Biosystems, Foster City, CA, USA) containing probes for 366 human miRNAs, and selected findings were validated with quantitative RT-PCR. Target prediction and pathway analysis for the differentially expressed miRNAs were performed using DIANA-mirPath. Results: Twenty-one vesicle miRNAs were up -regulated and 14 miRNAs were under-regulated significantly (P<0.05) in nasal mucus from AR patients when compared to healthy controls. Bioinformatic analysis by DIANA-mirPath demonstrated that 32 KEGG biological processes were significantly enriched (P<0.05, FDR corrected) among differentially expressed vesicle miRNA signatures. Among them, the B-cell receptor signaling pathway (P=3.709E-09), the natural killer cell-mediated cytotoxicity (P=8.466E-05), the T-cell receptor signaling pathway (P=0.00075), the RIG-I-like receptor signaling pathway (P=0.00127), the Wnt signaling pathway (P=0.00130), endocytosis (P=0.00440), and salivary secretion (P=0.04660) were the most prominent pathways enriched in quantiles with differential vesicle miRNA patterns. Furthermore, miR-30-5p, miR-199b-3p, miR-874, miR-28-3p, miR-203, and miR-875-5p, involved in B-cell receptor and salivary secretion signaling pathways, were selected for validation using independent samples from 44 AR patients and 20 healthy controls. MiR-30-5p and miR-199b-3p were significantly increased in extracellular vesicles from nasal mucus when compared to healthy controls, while miR-874 and miR-28-3p were significantly down-regulated. In addition, miRNA-203 was significantly increased in AR patients, while miRNA-875-5p was found to be significantly decreased in AR patients. Conclusions: This study demonstrated that vesicle miRNA may be a regulator for the development of AR.

      • A Novel Small Molecule Facilitates the Reprogramming of Human Somatic Cells into a Pluripotent State and Supports the Maintenance of an Undifferentiated State of Human Pluripotent Stem Cells

        Lee, Jungwoon,Xia, Yan,Son, Mi‐,Young,Jin, Guanghai,Seol, Binna,Kim, Min‐,Jeong,Son, Myung Jin,Do, Misol,Lee, Minho,Kim, Dongsup,Lee, Kyeong,Cho, Yee Sook WILEY‐VCH Verlag 2012 Angewandte Chemie Vol.124 No.50

        <P><B>Pluripotenz‐Booster</B>: RSC133, ein neues synthetisches Derivat von Indolacrylsäure/Indolpropionsäure, zeigt zweifache Aktivität, indem es Histondeacetylase und DNA‐Methyltransferase inhibiert. Außerdem verbessert es wirksam die Reprogrammierung von menschlichen somatischen Zellen in einen pluripotenten Zustand und unterstützt Wachstum und Erhaltung von humanen pluripotenten Stammzellen (hPSCs).</P>

      • SCISCIESCOPUS

        Synthesis and Structure–Activity Relationship of (<i>E</i>)-Phenoxyacrylic Amide Derivatives as Hypoxia-Inducible Factor (HIF) 1α Inhibitors

        Naik, Ravi,Won, Misun,Kim, Bo-Kyung,Xia, Yan,Choi, Hyun Kyung,Jin, Guanghai,Jung, Youngjin,Kim, Hwan Mook,Lee, Kyeong American Chemical Society 2012 Journal of medicinal chemistry Vol.55 No.23

        <P>A series of (<I>E</I>)-phenoxyacrylic amide derivatives were synthesized and evaluated as hypoxia inducible factor (HIF) 1α inhibitors. The present structure–activity relationship study on this series identified the morpholinoethyl containing ester <B>4p</B> as a potent inhibitor of HIF-1α under hypoxic conditions (IC<SUB>50</SUB> = 0.12 μM in a cell-based HRE reporter assay) in HCT116 cells. The representative compound <B>4p</B> suppressed hypoxia-induced HIF-1α accumulation and targeted gene expression in a dose-dependent manner. The effect of HIF-1α inhibition by <B>4p</B> was further demonstrated by its inhibitory activity on in vitro tube formation and migration of cells, which may be valuable for development of novel therapeutics for cancer and tumor angiogenesis.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jmcmar/2012/jmcmar.2012.55.issue-23/jm301419d/production/images/medium/jm-2012-01419d_0016.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/jm301419d'>ACS Electronic Supporting Info</A></P>

      • KCI등재

        Effect of FTY-720 on Pulmonary Fibrosis in Mice via the TGF-β1 Signaling Pathway and Autophagy

        Jin Yuying,Liu Weidong,Gao Ge,Song Yilan,Liu Hanye,Li Liangchang,Zhou Jiaxu,Yan Guanghai,Cui Hong 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.4

        We investigated whether FTY-720 might have an effect on bleomycin-induced pulmonary fibrosis through inhibiting TGF-β1 pathway, and up-regulating autophagy. The pulmonary fibrosis was induced by bleomycin. FTY-720 (1 mg/kg) drug was intraperitoneally injected into mice. Histological changes and inflammatory factors were observed, and EMT and autophagy protein markers were studied by immunohistochemistry and immunofluorescence. The effects of bleomycin on MLE-12 cells were detected by MTT assay and flow cytometry, and the related molecular mechanisms were studied by Western Blot. FTY-720 considerably attenuated bleomycin-induced disorganization of alveolar tissue, extracellular collagen deposition, and α-SMA and E-cadherin levels in mice. The levels of IL-1β, TNF-α, and IL-6 cytokines were attenuated in bronchoalveolar lavage fluid, as well as protein content and leukocyte count. COL1A1 and MMP9 protein expressions in lung tissue were significantly reduced. Additionally, FTY- 720 treatment effectively inhibited the expressions of key proteins in TGF-β1/TAK1/P38MAPK pathway and regulated autophagy proteins. Similar results were additionally found in cellular assays with mouse alveolar epithelial cells. Our study provides proof for a new mechanism for FTY-720 to suppress pulmonary fibrosis. FTY-720 is also a target for treating pulmonary fibrosis.

      • KCI등재

        Effects of G-Rh2 on mast cell-mediated anaphylaxis via AKT-Nrf2/NF-κB and MAPK-Nrf2/NF-κB pathways

        Chang Xu,Liangchang Li,Chongyang Wang,Jingzhi Jiang,Li Li,Lianhua Zhu,Shan Jin,Zhehu Jin,Jung Joon Lee,Guanhao Li,Guanghai Yan 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4

        Background: The effect of ginsenoside Rh2 (G-Rh2) on mast cell-mediated anaphylaxis remains unclear. Herein, we investigated the effects of G-Rh2 on OVA-induced asthmatic mice and on mast cell-mediatedanaphylaxis. Methods: Asthma model was established for evaluating airway changes and ear allergy. RPMCs and RBL-2H3 were used for in vitro experiments. Calcium uptake, histamine release and degranulation weredetected. ELISA and Western blot measured cytokine and protein levels, respectively. Results: G-Rh2 inhibited OVA-induced airway remodeling, the production of TNF-a, IL-4, IL-8, IL-1b andthe degranulation of mast cells of asthmatic mice. G-Rh2 inhibited the activation of Syk and Lyn in lungtissue of OVA-induced asthmatic mice. G-Rh2 inhibited serum IgE production in OVA induced asthmaticmice. Furthermore, G-Rh2 reduced the ear allergy in IgE-sensitized mice. G-Rh2 decreased the earthickness. In vitro experiments G-Rh2 significantly reduced calcium uptake and inhibited histaminerelease and degranulation in RPMCs. In addition, G-Rh2 reduced the production of IL-1b, TNF-a, IL-8, andIL-4 in IgE-sensitized RBL-2H3 cells. Interestingly, G-Rh2 was involved in the FcεRI pathway activation ofmast cells and the transduction of the Lyn/Syk signaling pathway. G-Rh2 inhibited PI3K activity in adose-dependent manner. By blocking the antigen-induced phosphorylation of Lyn, Syk, LAT, PLCg2, PI3KERK1/2 and Raf-1 expression, G-Rh2 inhibited the NF-kB, AKT-Nrf2, and p38MAPK-Nrf2 pathways. However, G-Rh2 up-regulated Keap-1 expression. Meanwhile, G-Rh2 reduced the levels of p-AKT,p38MAPK and Nrf2 in RBL-2H3 sensitized IgE cells and inhibited NF-kB signaling pathway activation byactivating the AKT-Nrf2 and p38MAPK-Nrf2 pathways. Conclusion: G-Rh2 inhibits mast cell-induced allergic inflammation, which might be mediated by theAKT-Nrf2/NF-kB and p38MAPK-Nrf2/NF-kB signaling pathways

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