9 research outputs found

    Additional file 2: of Loss of ZG16 is associated with molecular and clinicopathological phenotypes of colorectal cancer

    No full text
    Additional ZG16 expression profiles, protein similarity and subcellular localization. (DOCX 794 kb

    Additional file 1: of Loss of ZG16 is associated with molecular and clinicopathological phenotypes of colorectal cancer

    No full text
    Table S1. Immunohistochemistry analysis of ZG-6 expression in different human tissues. (DOCX 13 kb

    Visualization 1: Q-switched fiber laser based on an acousto-optic modulator with injection seeding technique

    No full text
    The video of injection-locked process Originally published in Applied Optics on 10 June 2016 (ao-55-17-4584

    Additional file 1: of AEG-1 is involved in hypoxia-induced autophagy and decreases chemosensitivity in T-cell lymphoma

    No full text
    Hut-78 and Jurkat cells were incubated under normoxia, hypoxia or starvation environment for 48 h before detection. a Western blot assays and quantitative analysis of AEG-1, Beclin-1, and LC3-II in Jurkat cells under normoxia, hypoxia or starvation environment. b Quantitative analysis of LC3-II/LC3-I ratio in Jurkat cells under normoxia, hypoxia or starvation environment. The expression of AEG-1 (p < 0.05), LC3-II (p < 0.05), Beclin-1 (p < 0.05) and LC3-II/LC3-I ratio (p<0.05) was much higher in hypoxia or starvation environment than normoxia in Jurkat cells. c Western blot assays and quantitative analysis of AEG-1, Beclin-1, and LC3-II in Hut-78 cells under normoxia, hypoxia or starvation environment. d Quantitative analysis of LC3-II/LC3-I ratio in Hut-78 cells under normoxia, hypoxia or starvation environment. The expression of AEG-1 (p < 0.05), LC3-II (p < 0.05), Beclin-1 (p < 0.05) and LC3-II/LC3-I ratio (p<0.05) was much higher in hypoxia or starvation environment than normoxia in Hut-78 cells. NO: normoxia, NO: hypoxia. *p < 0.05, NO vs. LO or starvation. (TIF 574 kb

    Data_Sheet_1_Immune cell early activation, apoptotic kinetic, and T-cell functional impairment in domestic pigs after ASFV CADC_HN09 strain infection.docx

    No full text
    African swine fever (ASF) caused by the African swine fever virus (ASFV) is a fatal and highly contagious disease of domestic pigs characterized by rapid disease progression and death within 2 weeks. How the immune cells respond to acute ASFV infection and contribute to the immunopathogenesis of ASFV has not been completely understood. In this study, we examined the activation, apoptosis, and functional changes of distinct immune cells in domestic pigs following acute infection with the ASFV CADC_HN09 strain using multicolor flow cytometry. We found that ASFV infection induced broad apoptosis of DCs, monocytes, neutrophils, and lymphocytes in the peripheral blood of pigs over time. The expression of MHC class II molecule (SLA-DR/DQ) on monocytes and conventional DCs as well as CD21 expression on B cells were downregulated after ASFV infection, implying a potential impairment of antigen presentation and humoral response. Further examination of CD69 and ex vivo expression of IFN-γ on immune cells showed that T cells were transiently activated and expressed IFN-γ as early as 5 days post-infection. However, the capability of T cells to produce cytokines was significantly impaired in the infected pigs when stimulated with mitogen. These results suggest that the adaptive cellular immunity to ASFV might be initiated but later overridden by ASFV-induced immunosuppression. Our study clarified the cell types that were affected by ASFV infection and contributed to lymphopenia, improving our understanding of the immunopathogenesis of ASFV.</p
    corecore