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      • KCI등재

        On Synergistic Effects of Hierarchical γ′ Precipitates and Discontinuous Plastic Flow in a Ni-based Single Crystal Superalloy with an [001] Orientation

        Yunling Du,Yanhong Yang,Shuai Guan,Xinguang Wang,Chuanyong Cui,Jinguo Li,Yizhou Zhou,Xiaofeng Sun 대한금속·재료학회 2024 METALS AND MATERIALS International Vol.30 No.1

        A discontinuous plastic flow is detected in a single-crystal superalloy with an [001] orientation during tensile tests over a wide temperature range. Results reveals that the synergistic impact of normal γ′ precipitates and nanoscale γ′ precipitates in γ matrix on the dislocations motion is the root of the serrated flow.

      • KCI등재

        Protective Effects of Aqueous Extract of Radix Isatidis on Lipopolysaccharide-Induced Sepsis in C57BL/6J Mice

        Deqing Ruan,Wenjing Liu,Yanhong Shi,Menghui Tan,Li Yang,Zhengtao Wang,Yue Zhou,Rui Wang 한국식품영양과학회 2020 Journal of medicinal food Vol.23 No.1

        Endotoxic shock exhibits a considerably high mortality risk. It is defined as a systemic inflammatory response syndrome caused by a microbial infection. Radix Isatidis has anti-inflammatory, antiviral, and antipyretic effects and is used worldwide. This study investigated the antiendotoxin sepsis effects of an aqueous R. Isatidis extract (RIE) and explored the possible pharmacological molecular mechanisms. Male C57BL/6J mice were intravenously injected with 15 mg/kg lipopolysaccharide (LPS) to induce endotoxic shock. The results demonstrated that the survival rate of mice pretreated with RIE increased, and LPS-induced liver and lung damage were reduced by inhibiting inflammation. For elucidating detailed molecular mechanisms, we focused on LPS-induced transcription factors: nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF3). Our results demonstrated that the protective effects of RIE were strongly dependent on IRF3-induced interferon-β, not on NF-κB-induced tumor necrosis factor-α and interleukin-1β. In addition, RIE suppressed the phosphorylation of IRF3, not NF-κB. In conclusion, this study revealed the antiendotoxic properties of RIE on LPS-induced sepsis and provided mechanistic evidence for the beneficial effects of RIE.

      • KCI등재

        Creep Properties of a Nickel-Based Single Crystal Superalloy with Low Density

        Yuling Du,Zihao Tan,Yanhong Yang,Xinguang Wang,Yizhou Zhou,Jingguo Li,Xiaofeng Sun 대한금속·재료학회 2021 METALS AND MATERIALS International Vol.27 No.12

        A novel nickel-based single crystal superalloy with low density had been designed and the creep deformation mechanismsof the experiment alloy under two conditions (1050 °C/200 MPa and 1100 °C/137 MPa) had been systematically discussed. The topological inversion had been observed after fracture under the above two conditions. The effects of temperature andstress on creep life of the experiment alloy had been found no significant difference under the two conditions. It was indicatedthat the small decrease in temperature exerted limited influence on the creep behaviors of single crystal superalloys in therange of high temperature.

      • KCI등재

        Ordered Reverse k Nearest Neighbor Search via On-demand Broadcast

        ( Li Li ),( Guohui Li ),( Quan Zhou ),( Yanhong Li ) 한국인터넷정보학회 2014 KSII Transactions on Internet and Information Syst Vol.8 No.11

        The Reverse k Nearest Neighbor (RkNN) query is valuable for finding objects influenced by a specific object and is widely used in both scientific and commercial systems. However, the influence level of each object is unknown, information that is critical for some applications (e.g. target marketing). In this paper, we propose a new query type, Ordered Reverse k Nearest Neighbor (ORkNN), and make efforts to adapt it in an on-demand scenario. An Order-k Voronoi diagram based approach is used to answer ORkNN queries. In particular, for different values of k, we pre-construct only one Voronoi diagram. Algorithms on both the server and the clients are presented. We also present experimental results that suggest our proposed algorithms may have practical applications.

      • KCI등재

        Allylpyrocatechol ameliorates sepsis-induced lung injury via SIRT1-mediated suppression of p65 and nucleocytoplasmic translocation of HMGB1

        Mu Yanfei,Mu Xiaosong,Yang Yan,Zhou Yanhong 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.4

        Background Sepsis is a deadly clinical condition. Allylpyrocatechol is bioactive flavonoid that has shown promising anti-inflammatory and antioxidant activity. The effects of allylpyrocatechol on sepsis-induced lung injury have not been fully established. Objective This study investigated the effects of allylpyrocatechol in a mouse model of sepsis-induced lung injury. Results RAW264.7 macrophages were used for in vitro studies. A mouse model of sepsis was established by cecal ligation and puncture (CLP). The PaO2/FiO2 ratio was measured in conjunction with lung tissue histology, and edema was determined by the wet:dry tissue ratio. ELISA was performed to analyze levels of IL-6, TNF-α, NOx, and HMGB1. Malondialdehyde (MDA) levels were measured to determine lipid peroxidation status. Protein expression was investigated via Western blotting analyses. Molecular docking studies were done to study the affinity of SIRT1 with Allylpyrocatechol. It was observed that Allylpyrocatechol inhibited the production of HMGB1 and suppressed pro-inflammatory responses in macrophages treated with bacterial lipopolysaccharide (LPS) in vitro, and in CLP sepsis mice in vivo. Moreover, it ameliorated the reduction of SIRT1 levels in both LPS-treated macrophages and CLP mice, alleviated sepsis-induced lung edema, reduced lipid peroxidation, improved lung tissue histology findings, reduced mortality, and improved the PaO2/FiO2 ratio in CLP mice. Allylpyrocatechol caused significant reductions in serum levels of IL-6, nitric oxide, TNF-α, and HMGB1, as well as nuclear translocation of inducible nitric oxide synthase, SIRT1, and HMGB1 in lungs of CLP mice. Molecular docking analysis suggested affinity of SIRT1 with Allylpyrocatechol. Conclusion The findings suggest that Allylpyrocatechol protects mice against lung injury via SIRT1-mediated suppression of HMGB1 nuclear translocation and p-p65 activation. Background Sepsis is a deadly clinical condition. Allylpyrocatechol is bioactive flavonoid that has shown promising anti-inflammatory and antioxidant activity. The effects of allylpyrocatechol on sepsis-induced lung injury have not been fully established. Objective This study investigated the effects of allylpyrocatechol in a mouse model of sepsis-induced lung injury. Results RAW264.7 macrophages were used for in vitro studies. A mouse model of sepsis was established by cecal ligation and puncture (CLP). The PaO2/FiO2 ratio was measured in conjunction with lung tissue histology, and edema was determined by the wet:dry tissue ratio. ELISA was performed to analyze levels of IL-6, TNF-α, NOx, and HMGB1. Malondialdehyde (MDA) levels were measured to determine lipid peroxidation status. Protein expression was investigated via Western blotting analyses. Molecular docking studies were done to study the affinity of SIRT1 with Allylpyrocatechol. It was observed that Allylpyrocatechol inhibited the production of HMGB1 and suppressed pro-inflammatory responses in macrophages treated with bacterial lipopolysaccharide (LPS) in vitro, and in CLP sepsis mice in vivo. Moreover, it ameliorated the reduction of SIRT1 levels in both LPS-treated macrophages and CLP mice, alleviated sepsis-induced lung edema, reduced lipid peroxidation, improved lung tissue histology findings, reduced mortality, and improved the PaO2/FiO2 ratio in CLP mice. Allylpyrocatechol caused significant reductions in serum levels of IL-6, nitric oxide, TNF-α, and HMGB1, as well as nuclear translocation of inducible nitric oxide synthase, SIRT1, and HMGB1 in lungs of CLP mice. Molecular docking analysis suggested affinity of SIRT1 with Allylpyrocatechol. Conclusion The findings suggest that Allylpyrocatechol protects mice against lung injury via SIRT1-mediated suppression of HMGB1 nuclear translocation and p-p65 activation.

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