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3篇 您的检索式:作者名="DONG JunTang"
    题名 作者 年代 出处 被引量
1Extraction of Informative Blocks from Web Pages Based on VIPS显示文摘Cunhe Li Juan Dong Juntang Chen 2010Journal of Computational Information System2010,,:1
2First-principles study on electronic structures and optical properties of the single-walled (n, 0) ZnO nanotubes显示文摘Using the first-principles calculations, we studied the geometric structures, electronic structures and optical properties of the single-walled (n, 0) ZnO nanotubes (NTs). The calculated results show that all the bind energies of the single-walled (n,0) ZnO NTs are of negative values, which indicate that the ZnO NTs can exist stably as single-walled NTs. While the calculated results of electronic structure indicate that the single-walled (n,0) ZnO NTs are a type of direct wide band-gap semiconductor materials, the whole valence bands are spread and drift to low-energy direction with the increase of the NT diameter. The defect energy levels caused by quantum size and surface effects emerge on the top of the valence bands. Furthermore, the calculated results of optical properties reveal that the dielectric peaks have a blue shift and the edge of absorption band corresponds to ultraviolet band with the decrease of the NT diameter. The single-walled (n, 0) ZnO NTs can be applied to ultraviolet semiconductor systems.DONG JunTang ZHANG FuChun ZHANG WeiHu ZHANG ZhiYong 2013Science China(Physics,Mechanics & Astronomy)2013,56,4:1
3MANF brakes TLR4 signaling by competitively binding S100A8 with S100A9 to regulate macrophage phenotypes in hepatic fibrosis显示文摘The mesencephalic astrocyte-derived neurotrophic factor(MANF)has been recently identified as a neurotrophic factor,but its role in hepatic fibrosis is unknown.Here,we found that MANF was upregulated in the fibrotic liver tissues of the patients with chronic liver diseases and of mice treated with CCl4.MANF deficiency in either hepatocytes or hepatic mono-macrophages,particularly in hepatic mono-macrophages,clearly exacerbated hepatic fibrosis.Myeloid-specific MANF knockout increased the population of hepatic Ly6C^(high)macrophages and promoted HSCs activation.Furthermore,MANF-sufficient macrophages(from WT mice)transfusion ameliorated CCl4-induced hepatic fibrosis in myeloid cells-specific MANF knockout(MKO)mice.Mechanistically,MANF interacted with S100A8 to competitively block S100A8/A9 heterodimer formation and inhibited S100A8/A9-mediated TLR4-NF-κB signal activation.Pharmacologically,systemic administration of recombinant human MANF significantly alleviated CCl_(4)-induced hepatic fibrosis in both WT and hepatocytes-specific MANF knockout(HKO)mice.This study reveals a mechanism by which MANF targets S100A8/A9-TLR4 as a“brake”on the upstream of NF-κB pathway,which exerts an impact on macrophage differentiation and shed light on hepatic fibrosis treatment.Chao Hou Dong Wang Mingxia Zhao Petek Ballar Xinru Zhang Qiong Mei Wei Wang Xiang Li Qiang Sheng Jun Liu Chuansheng Wei Yujun Shen Yi Yang Peng Wang Juntang Shao Sa Xu Fuyan Wang Yang Sun Yuxian Shen 2023Acta Pharmaceutica Sinica B2023,13,10:0
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