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Search Results: 1 - 10 of 120071 matches for " Renxi Wang "
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Analysis of the Break Size Influence on the Damage Accident of Single Heat Transfer Tube of Ship Nuclear Power Steam Generator  [PDF]
Meng Cai, Wei Wang, Junzhong Sun, Renxi Jin
World Journal of Engineering and Technology (WJET) , 2017, DOI: 10.4236/wjet.2017.54B003
In view of the problem that the breakage size is not enough to analyze the damage of the heat transfer tube of the ship nuclear power steam generator under the condition that the breakage loop cannot be isolated, this paper analyzes the damage safety analysis model based on the MELCOR program, Damage of heat transfer tubes at different break sizes (2 mm and 6 mm) to reactor power, primary loop pressure, regulator water level, core water level, vapor pressure, break flow, fuel element cladding breakage, etc. The influence of the breakage size on the damage effect of the heat transfer tube has improved the analysis and handling capacity of the damage of the heat transfer tube, and improved the reactor accident handling capacity under the condition of the damage of the heat transfer tube.
SjAPI, the First Functionally Characterized Ascaris-Type Protease Inhibitor from Animal Venoms
Zongyun Chen, Bin Wang, Jun Hu, Weishan Yang, Zhijian Cao, Renxi Zhuo, Wenxin Li, Yingliang Wu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0057529
Abstract: Background Serine protease inhibitors act as modulators of serine proteases, playing important roles in protecting animal toxin peptides from degradation. However, all known serine protease inhibitors discovered thus far from animal venom belong to the Kunitz-type subfamily, and whether there are other novel types of protease inhibitors in animal venom remains unclear. Principal Findings Here, by screening scorpion venom gland cDNA libraries, we identified the first Ascaris-type animal toxin family, which contains four members: Scorpiops jendeki Ascaris-type protease inhibitor (SjAPI), Scorpiops jendeki Ascaris-type protease inhibitor 2 (SjAPI-2), Chaerilus tricostatus Ascaris-type protease inhibitor (CtAPI), and Buthus martensii Ascaris-type protease inhibitor (BmAPI). The detailed characterization of Ascaris-type peptide SjAPI from the venom gland of scorpion Scorpiops jendeki was carried out. The mature peptide of SjAPI contains 64 residues and possesses a classical Ascaris-type cysteine framework reticulated by five disulfide bridges, different from all known protease inhibitors from venomous animals. Enzyme and inhibitor reaction kinetics experiments showed that recombinant SjAPI was a dual function peptide with α-chymotrypsin- and elastase-inhibiting properties. Recombinant SjAPI inhibited α-chymotrypsin with a Ki of 97.1 nM and elastase with a Ki of 3.7 μM, respectively. Bioinformatics analyses and chimera experiments indicated that SjAPI contained the unique short side chain functional residues “AAV” and might be a useful template to produce new serine protease inhibitors. Conclusions/Significance To our knowledge, SjAPI is the first functionally characterized animal toxin peptide with an Ascaris-type fold. The structural and functional diversity of animal toxins with protease-inhibiting properties suggested that bioactive peptides from animal venom glands might be a new source of protease inhibitors, which will accelerate the development of diagnostic and therapeutic agents for human diseases that target diverse proteases.
Glutamic Acid Decarboxylase-Derived Epitopes with Specific Domains Expand CD4+CD25+ Regulatory T Cells
Guojiang Chen, Gencheng Han, Jiannan Feng, Jianan Wang, Renxi Wang, Ruonan Xu, Beifen Shen, Jiahua Qian, Yan Li
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0007034
Abstract: Background CD4+CD25+ regulatory T cell (Treg)-based immunotherapy is considered a promising regimen for controlling the progression of autoimmune diabetes. In this study, we tested the hypothesis that the therapeutic effects of Tregs in response to the antigenic epitope stimulation depend on the structural properties of the epitopes used. Methodology/Principal Findings Splenic lymphocytes from nonobese diabetic (NOD) mice were stimulated with different glutamic acid decarboxylase (GAD)-derived epitopes for 7–10 days and the frequency and function of Tregs was analyzed. We found that, although all expanded Tregs showed suppressive functions in vitro, only p524 (GAD524–538)-expanded CD4+CD25+ T cells inhibited diabetes development in the co-transfer models, while p509 (GAD509–528)- or p530 (GAD530–543)-expanded CD4+CD25+ T cells had no such effects. Using computer-guided molecular modeling and docking methods, the differences in structural characteristics of these epitopes and the interaction mode (including binding energy and identified domains in the epitopes) between the above-mentioned epitopes and MHC class II I-Ag7 were analyzed. The theoretical results showed that the epitope p524, which induced protective Tregs, possessed negative surface-electrostatic potential and bound two chains of MHC class II I-Ag7, while the epitopes p509 and p530 which had no such ability exhibited positive surface-electrostatic potential and bound one chain of I-Ag7. Furthermore, p524 bound to I-Ag7 more stably than p509 and p530. Of importance, we hypothesized and subsequently confirmed experimentally that the epitope (GAD570–585, p570), which displayed similar characteristics to p524, was a protective epitope by showing that p570-expanded CD4+CD25+ T cells suppressed the onset of diabetes in NOD mice. Conclusions/Significance These data suggest that molecular modeling-based structural analysis of epitopes may be an instrumental tool for prediction of protective epitopes to expand functional Tregs.
Research progress of magnetic resonance imaging contrast agents
Guoping Yan,Renxi Zhuo
Chinese Science Bulletin , 2001, DOI: 10.1007/BF03184316
Abstract: Magnetic resonance imaging (MRI) is a clinical diagnostic modality, which has become popular in hospitals around the world. Approximately 30% of MRI exams include the use of contrast agents. The research progress of the paramagnetic resonance imaging contrast agents was described briefly. Three important approaches in the soluble paramagnetic resonance imaging contrast agents design including nonionic, tissue-specific and macromolecular contrast agents were investigated. In addition, the problems in the research and development in future were discussed.
Recent progress in polymer-based gene delivery vectors
Shiwen Huang,Renxi Zhuo
Chinese Science Bulletin , 2003, DOI: 10.1007/BF03184167
Abstract: The gene delivery system is one of the three components of a gene medicine, which is the bottle neck of current gene therapy. Nonviral vectors offer advantages over the viral system of safety, ease of manufacturing, etc. As important nonviral vectors, polymer gene delivery systems have gained increasing attention and have begun to show increasing promising. In this review, the fundamental and recent progress of polymer-based gene delivery vectors is reviewed.

FENG Jun,WANG Huafen,LI Shuangfeng,ZHUO Renxi,

高分子学报 , 2008,
Abstract: 研究了14元环的碳酸丁二酯二聚体在固定化脂肪酶Novozym-435催化下的开环聚合反应制备聚碳酸丁二酯.聚合在常压,75℃的甲苯溶液中进行,反应条件温和.详细探讨了反应条件诸如单体浓度,酶浓度对于聚合的影响.结果显示Novozym-435具有与异辛酸亚锡可比拟的高催化活性,同时可以回收重复使用.聚合动力学研究表明碳酸丁二酯的酶促甲苯溶液开环聚合和环状内酯的酶促甲苯溶液聚合有所不同,没有表现出活性聚合的特征.
C5a Regulates IL-12+DC Migration to Induce Pathogenic Th1 and Th17 Cells in Sepsis
Ning Ma, Chen Xing, He Xiao, Yi Wang, Ke Wang, Chunmei Hou, Gencheng Han, Guojiang Chen, Bernadette Marrero, Yujuan Wang, Beifen Shen, Yan Li, Renxi Wang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0069779
Abstract: Objective It is well known that complement system C5a is excessively activated during the onset of sepsis. However, it is unclear whether C5a can regulate dentritic cells (DCs) to stimulate adaptive immune cells such as Th1 and Th17 in sepsis. Methods Sepsis was induced by cecal ligation and puncture (CLP). CLP-induced sepsis was treated with anti-C5a or IL-12. IL-12+DC, IFNγ+Th1, and IL-17+Th17 cells were analyzed by flow cytometry. IL-12 was measured by ELISA. Results Our studies here showed that C5a induced IL-12+DC cell migration from the peritoneal cavity to peripheral blood and lymph nodes. Furthermore, IL-12+DC cells induced the expansion of pathogenic IFNγ+Th1 and IL-17+Th17 cells in peripheral blood and lymph nodes. Moreover, IL-12, secreted by DC cells in the peritoneal cavity, is an important factor that prevents the development of sepsis. Conclusion Our data suggests that C5a regulates IL-12+DC cell migration to induce pathogenic Th1 and Th17 cells in sepsis.
Opposite Role of Tumor Necrosis Factor Receptors in Dextran Sulfate Sodium-Induced Colitis in Mice
Ke Wang, Gencheng Han, Yan Dou, Yi Wang, Guijun Liu, Renxi Wang, He Xiao, Xinying Li, Chunmei Hou, Beifen Shen, Renfeng Guo, Yan Li, Yanchun Shi, Guojiang Chen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0052924
Abstract: Tumor necrosis factor-α (TNF-α) is a key factor for the pathogenesis of inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, acute colitis was induced by dextran sulfate sodium (DSS) instillation in TNFR1 or 2?/? mice. TNFR1 ablation led to exacerbation of signs of colitis, including more weight loss, increased mortality, colon shortening and oedema, severe intestinal damage, and higher levels of myeloperoxidase compared to wild-type counterparts. While, TNFR2 deficiency had opposite effects. This discrepancy was reflected by alteration of proinflammatory cytokine and chemokine production in the colons. Importantly, TNFR1 ablation rendered enhanced apoptosis of colonic epithelial cells and TNFR2 deficiency conferred pro-apoptotic effects of lamina propria (LP)-immune cells, as shown by the decreased ratio of Bcl-2/Bax and enhanced nuclear factor (NF)-κB activity.
IL-17A Signaling in Colonic Epithelial Cells Inhibits Pro-Inflammatory Cytokine Production by Enhancing the Activity of ERK and PI3K
Xiaoqin Guo, Xingwei Jiang, Yan Xiao, Tingting Zhou, Yueling Guo, Renxi Wang, Zhi Zhao, He Xiao, Chunmei Hou, Lingyun Ma, Yanhua Lin, Xiaoling Lang, Jiannan Feng, Guojiang Chen, Beifen Shen, Gencheng Han, Yan Li
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0089714
Abstract: Our previous data suggested that IL-17A contributes to the inhibition of Th1 cell function in the gut. However, the underlying mechanisms remain unclear. Here we demonstrate that IL-17A signaling in colonic epithelial cells (CECs) increases TNF-α-induced PI3K-AKT and ERK phosphorylation and inhibits TNF-α induced expression of IL-12P35 and of a Th1 cell chemokine, CXCL11 at mRNA level. In a co-culture system using HT-29 cells and PBMCs, IL-17A inhibited TNF-?induced IL-12P35 expression by HT-29 cells and led to decreased expression of IFN-γ and T-bet by PBMCs. Finally, adoptive transfer of CECs from mice with Crohn's Disease (CD) led to an enhanced Th1 cell response and exacerbated colitis in CD mouse recipients. The pathogenic effect of CECs derived from CD mice was reversed by co-administration of recombinant IL-17A. Our data demonstrate a new IL-17A-mediated regulatory mechanism in CD. A better understanding of this pathway might shed new light on the pathogenesis of CD.
Current progress of polymeric gene vectors
Xuan Zeng,YunXia Sun,RenXi Zhuo,XianZheng Zhang
Science China Life Sciences , 2011, DOI: 10.1007/s11427-011-4245-z
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