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- 저자 : Jinhui Ren (검색결과 2 건)
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Jinhui Ren,Zhenghong Tian,Jingwu Bu 한국콘크리트학회 2018 International Journal of Concrete Structures and M Vol.12 No.6
A user-defined bonded-particle model (UBM) which is based on the modified parallel bond was established in this paper to investigate the tensile and compressive failure mechanism of concrete on the three-dimensional (3D) level. The contact constitutive relation and the failure criterion of the UBM can be added to the commercial discrete element software PFC<SUP>3D</SUP> by compiling them as a dynamic link library file and loading it into PFC<SUP>3D</SUP> whenever needed. In addition, the aggregate particles can be generated according to the volume fraction and the shape of each aggregate is irregular. Then, by comparing the results of numerical simulation with the results of laboratory tests, it is found that this bonded-particle model can simulate the tensile and compressive failure process of concrete well to a certain extent. Specifically, the two have basically similar failure patterns and stress–strain responses no matter under tension or compression loading condition. All results indicate that this UBM is a promising tool in understanding and predicting the tensile and compressive failure process of concrete.
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TRIM24-Mediated Acetylation of STAT6 Suppresses Th2-Induced Allergic Rhinitis
Yue Liyan,Jia Qiaojing,Dong Jinhui,Wang Jianxing,Ren Xiumin,Xu Ou 대한천식알레르기학회 2023 Allergy, Asthma & Immunology Research Vol.15 No.5
Purpose: Allergic rhinitis (AR) is a T helper type 2 (Th2)-mediated inflammatory disease. The E3 ligase tripartite motif-containing 24 (TRIM24) regulates the recruitment of acetyltransferase CREB-binding protein (CBP) to signal transducer and activator of transcription 6 (STAT6). CBP mediates the acetylation of STAT6 and decreases its activity. To date, the precise role of TRIM24 in AR has not been fully interpreted. Herein, our study aimed to explore the functions of TRIM24 in AR. Methods: The expression of TRIM24 in peripheral blood mononuclear cells (PBMCs) and CD4+ T cells from patients with AR was measured. TRIM24-conditional knockout mice with TRIM24 deficiency in CD4+ T cells were generated. Wide-type (WT) AR mice and TRIM24-conditional knockout AR mice were established. Then, AR symptoms and interleukin (IL)-4 levels were compared. Further, the proliferation, activation and polarization of CD4+ T cells from WT mice and TRIM24 knockout mice after stimulation were determined. The effects of TRIM24 deficiency on STAT6 activities were also evaluated. Results: Downregulated TRIM24 expression was detected in PBMCs and CD4+ T cells from patients with AR. TRIM24 conditional knockout mice had more sever AR symptoms with elevated IL-4 production. TRIM24-knockout CD4+ T cells had similar proliferation and activation when compared to WT CD4+ T cells, while they had enhanced Th2 polarization. TRIM24-knockout CD4+ T cells had decreased acetylation of STAT6 and enhanced STAT6 activities after IL-4 stimulation. The regulation of STAT6 activities by TRIM24 depended on TRIM24 N terminal RIGN domain and Lys383 acetylation site of STAT6. Conclusions: TRIM24 suppresses Th2-mediated AR by regulating the acetylation of STAT6.
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