31 research outputs found

    <i>KIR2DS4</i> gene expression and natural killer (NK) cell function in subjects with chronic HIV-1 infection.

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    <p><b>A</b>. Flow cytometry gating strategy for NK cells. <b>B</b>. Staining of membrane-bound KIR2DS4 on cells derived from subjects with full-length <i>KIR2DS4</i> gene (g+), to facilitate the sorting of two populations positive (p+) or negative (p−) for the gene product. <b>C</b>. Staining of membrane-bound KIR2DS4 on cells derived from subjects with truncated KIR2DS4 gene only, i.e., negative for full-length <i>KIR2DS4</i> gene and gene product (g−/p−). <b>D</b>. Percentage of NK cells expressing KIR2DS4 before and after stimulation with HLA-deficient target cells (K562 and 221). <b>E</b>. Distribution of NK cell subsets among 43 subjects with and without the full-length <i>KIR2DS4</i> genotype. <b>F–H</b>. Representative results for staining cell surface CD107a (lysosomal-associated membrane protein 1) and intracellular IFN-γ or MIP-1β before (red) and after (blue) stimulation with K562 cells. In <b>D</b> and <b>E</b>, the horizontal bars connected by a vertical line correspond to the median and interquartile range.</p

    Linear correlation between HIV-1-related outcomes and KIR2DS4 expression in the absence of antiretroviral therapy.

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    <p>Results are based on data from 23 subjects with full-length <i>KIR2DS4</i> gene (samples drawn from a single visit). <b>A</b>. Correlation of KIR2DS4 expression with plasma HIV-1 viral load (VL) at the time of sampling. <b>B</b>. Correlation with CD4<sup>+</sup> T-cell (CD4) count (cells/µL) at the time of sampling. In each panel, solid and dotted lines correspond to the projected trend line and its 95% confidence intervals, respectively (by linear regression).</p

    Additional file 1 of Analysis of proteome and post-translational modifications of 2-hydroxyisobutyrylation reveals the glycolysis pathway in oral adenoid cystic carcinoma

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    Additional file 1: Supplementary text. Detailed research methods. Supplementary Fig. 1. PPI and cluster of hyper-modified DHMPs. Supplementary Fig. 2. PPI and cluster of hypo-modified DHMPs. Supplementary Table 1. Statistics of Mass Spectrometry Data. Supplementary Table 2. Clinical characteristics of OACC patients. Supplementary Table 3. Go enrichment analyses of differentially expressed proteins. Supplementary Table 4. KEGG pathway enrichment of differentially expressed proteins. Supplementary Table 5. Go enrichment analyses of differentially expressed and 2-hydroxyisobutyrylated modified proteins. Supplementary Table 6. KEGG pathway enrichment of differentially expressed and 2-hydroxyisobutyrylated modified proteins. Supplementary Table 7. Top 10 hub proteins in hyper-and hypo modified DHMPs based on degree. Supplementary Table 8. KEGG enrichment in up cluster 1–6. Supplementary Table 9. KEGG enrichment in down cluster 1–2. Supplementary Table 10. The Khib of glycolysis pathway enzyme

    Associations of full-length <i>KIR2DS4</i> gene with longitudinal viral load (VL) and CD4<sup>+</sup> T-cell (CD4) count in 207 youth with chronic (seroprevalent) HIV-1 infection.

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    <p><b>Notes</b>: The overall <i>r</i><sup>2</sup> = 0.039 and 0.033 in the multivariable models for VL and CD4 count, respectively. There is no clear interaction between full-length <i>KIR2DS4</i> (gene) and sex (<i>p</i> = 0.274).</p

    Characteristics of two study populations with longitudinal and cross-sectional data, respectively.

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    <p><b>Notes</b>: HIV-1 viral load (VL) in plasma (RNA copies/mL) and CD4<sup>+</sup> T-cell (CD4) count in peripheral blood (cells/µL) are the two outcomes (see text). The two subgroups with existing PBMC samples share similar features at study entry (<i>p</i>>0.45 in all comparisons).</p

    Assessment of polyfunctional profile of natural killer (NK) cells during chronic HIV-1 infection.

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    <p>Results are obtained after stimulation with K562 cells and subtraction of background staining. <b>A</b>. Functional properties of NK cells grouped by presence (+) and absence (−) of full-length <i>KIR2DS4</i> (g = gene) and membrane-bound KIR2DS4 receptor (p = product), as gauged by production of CD107a, IFN-γ and MIP-1β. <b>B</b>. Summary data for mono- and poly-functional NK cells. <b>C</b>. Distribution of polyfunctional NK cells. <b>D</b>. Distribution of NK cells NK cells producing MIP-1β alone. The g+/p+ and g+/p− cells are derived from individuals carrying full-length <i>KIR2DS4</i> gene, while the g−/p− NK cells are derived from individuals with truncated <i>KIR2DS4</i> gene only. In <b>C</b> and <b>D</b>, the horizontal bars connected by a vertical line correspond to the median and interquartile range.</p

    Effects of mechanical srain on ECM metabolism in human uterosacral ligament fibroblasts at the protein levels.

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    <p>(A) Three groups of hUSLFs (NT、MT、GT) were applied with mechanical strain of 0、5333μ, and then assayed by Western blot analyses. Quantitative analysis of (B) COL1A1, (C) COL3A1, (D) Elastin, (E) MMP-2, (F) MMP-9, (G) TIMP-2 and (H) TGF-β1 protein levels based on the bands of the Western blot. One-way analysis of variance was performed, followed by an unpaired t-test. n = 3, a, <i>P</i><0.05, vs. 0 μ, NT; b, <i>P</i><0.05, vs. 0 μ, MT; c, <i>P</i><0.05, vs. 5333 μ, NT; d, <i>P</i><0.05, vs. 5333 μ, MT. COL1A1, collagen, type 1, α1; COL3A1, collagen, type 3, α1; MMP-2, matrix metalloproteinase-2; MMP-9, matrix metalloproteinase-9; TIMP-2, tissue inhibitor of metalloproteinase-2; TGF-β1, transforming growth factor-β1.</p

    Microscopic images of ROS generation induced by mechanical stain using DCF-DA staining.

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    <p>(A) Three groups of hUSLFs (NT、MT、GT) were applied with mechanical strain of 0、5333μ, and then incubated with DCF-DA. The cells were observed under a fluorescent microscope (magnification, x200). (B) The intensity of DCF-mediated fluorescence was quantified using Image J software and reflected the levels of intracellular ROS. Values are expressed as the mean fluorescence intensity ± standard deviation of five fields of view per group. One-way analysis of variance was performed, followed by an unpaired t-test. n = 3, a, <i>P</i><0.05, vs. 0 μ, NT; b, <i>P</i><0.05, vs. 0 μ, MT; c, <i>P</i><0.05, vs. 5333 μ, NT; d, <i>P</i><0.05, vs. 5333 μ, MT. ROS, reactive oxygen species; DCF-DA, 2',7'-dichlorodihydrofluorescein diacetate.</p

    Microscopic images of 8-OHdG and 4-HNE production induced by mechanical strain using an immunofluorescent assay.

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    <p>(A) (8-OHdG) (B) (4-HNE) Three groups of hUSLFs (NT、MT、GT) were applied with mechanical strain of 0、5333μ, followed by incubation with 8-OHdG and 4-HNE antibodies, and then staining with DAPI. The cells were observed under a fluorescent microscope (magnification, x200). (C) (8-OHdG) (D) (4-HNE) Quantitative analysis based on fluorescence intensity, obtained using image-pro plus 6.0 software. Values are expressed as the mean fluorescence intensity ± standard deviation of five fields of view per group. One-way analysis of variance was performed, followed by an unpaired t-test. n = 3, a, <i>P</i><0.05, vs. 0 μ, NT; b, <i>P</i><0.05, vs. 0 μ, MT; c, <i>P</i><0.05, vs. 5333 μ, NT; d, <i>P</i><0.05, vs. 5333 μ, MT. 8-OHdG, 8-hydroxyguanosine; 4-HNE, 4-hydroxynonenal.</p

    Assessment of the mitochondrial membrane potential by JC-1 staining.

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    <p>Representative fluorescence photomicrographs of in-situ JC-1-stained cells in various treatment groups (magnification, x200). (A-C) Three groups of hUSLFs (NT、MT、GT) were applied with mechanical strain of 0、5333μ, and then stained with JC-1 fluorescent probe. Images on the left show red fluorescence, indicating a high mitochondrial membrane potential; the middle panel shows green fluorescence, indicative of a loss of mitochondrial membrane potential. The right-hand panel shows merged red and green fluorescence. (D) Red and green fluorescence intensity was quantified by Image J software. The ratio of red to green fluorescence intensity is indicative of the mitochondrial membrane potential. Values are expressed as the mean fluorescence intensity ± standard deviation of five fields of view per group. One-way analysis of variance was performed, followed by an unpaired t-test. n = 3, a, <i>P</i><0.05, vs. 0 μ, NT; b, <i>P</i><0.05, vs. 0 μ, MT; c, <i>P</i><0.05, vs. 5333 μ, NT; d, <i>P</i><0.05, vs. 5333 μ, MT.</p
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