46 research outputs found

    MOESM4 of Tissue-specific expression of histone H3 variants diversified after species separation

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    Additional file 4: Predicted CDS of rat histone H3 variants, contains Table S3 for the rat H3 sequence prediction results as an Excel file, which is the same format as Table S2

    MOESM5 of Tissue-specific expression of histone H3 variants diversified after species separation

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    Additional file 5: Similarity of amino acid and DNA sequence, contains Table S4, which shows amino acid and DNA sequence similarities between mouse H3 variant proteins/genes in Excel file

    Concentrations of chemokines and cytokines in BALF from mice after influenza virus infection and subsequent induction of allergic airway responses.

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    <p>The concentrations of chemokines and cytokines in BALF from pH1N1/OVA, pH1N1/PBS, Mock/OVA, and Mock/PBS mice were measured on Day 2 and 3 post-infection (5 mice/group). (A) Concentrations of MCP-1/CCL2, MIP-1α/CCL3, and IP-10/CXCL10 in BALF. (B) Concentrations of cytokines, IL-4, IL-6, IL-12, TNF-α, GM-CSF, and VEGF, in BALF. (C) Concentrations of IFN-α, IFN-β, and IFN-γ in BALF. (D) Concentrations of IL-5 and IL-13 in BALF. Data are expressed as scatter plots with the mean. *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001, and ****<i>p</i><0.0001 (two-way ANOVA). The experiments were repeated twice independently.</p

    Influenza virus infection of OVA-challenged NC/Nga mice with pre-existing acute allergic airway inflammation.

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    <p>(A) Schematic showing OVA sensitization, OVA-induced allergic airway inflammation, and influenza virus infection. NC/Nga mice were sensitized twice (via the IP route) with OVA (Day -16 and Day -9) and then subsequently challenged IN with OVA on two consecutive days (Day -2 and Day -1). On the day following the final OVA challenge (Day 0), the mice were inoculated IN with a sublethal dose of influenza virus A/H1N1pdm09 (pH1N1). (B) Representative lung tissue sections from OVA/pH1N1, PBS/pH1N1, OVA/Mock, and PBS/Mock mice on Day 3 post-infection (3 mice/group). Hematoxylin and eosin (H&E) staining. Original magnification: ×10. (C) Weight loss was monitored after infection (10 mice/group). Error bars represent the mean ± SEM. Weight change data were combined from two independent experiments. (D) On Day 3 post-infection, virus titers in the BALF were measured in a plaque assay (5 mice/group). Data are expressed as scatter plots with the mean viral titer ± SD. (E) Total cell counts and the proportion of inflammatory cells in the BALF assessed on Day 0 and Day 3 post-infection (5 mice/group). Data are expressed as scatter plots with the mean ± SD. (F to I) Concentrations of chemokines and cytokines, and interferons in BALF from influenza virus-infected mice with pre-existing allergic airway inflammation. The concentrations of chemokines (F), proinflammatory cytokines (G), interferons (H), Th2 cytokines (I) in BALF from PBS/Mock, OVA/Mock, PBS/pH1N1 and OVA/pH1N1 mice were measured before (Day 0) and after (Day 3) infection (5 mice/group). Data are expressed as scatter plots with the mean ± SD. *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001, and ****<i>p</i><0.0001 (two-way ANOVA or Mann-Whitney U test). Br, Bronchiole. The experiments were repeated independently at least twice.</p

    EGCG, EGC and ECG induced apoptosis in MOLM-14 cells.

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    <p>MOLM-14 cells at a density of 1×10<sup>5</sup> cells/ml were treated with 60 µM EGCG, 100 µM EGC, 200 µM ECG or DMSO alone as control for 16 hours. Total cell lysates were subjected to western blot analysis with indicated antibodies (A) or staining with PE-Annexin V and analyzed by FACS Calibur. Collected data were analyzed by FlowJo software (B).</p

    Influenza virus infection and subsequent induction of acute allergic airway responses by OVA in OVA-sensitized NC/Nga mice.

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    <p>(A) Schematic representation of the protocol for OVA sensitization, influenza virus infection, and OVA-induced allergic airway responses. NC/Nga mice were sensitized twice by IP injection of OVA on Day -14 and Day -7 and then infected with a sublethal dose of influenza virus A/H1N1pdm09 (pH1N1) or Mock allantoic fluid (Day 0). On the 2 days following infection, the mice were challenged again with OVA or PBS via the IN route (Day +1 and Day +2). (B) Weight loss was monitored after infection (20 mice in the pH1N1 infection groups and 10 mice in the Mock groups). Error bars represent the mean ± SEM. Weight change data were combined from three (pH1N1 infection groups) or two (Mock groups) independent experiments. (C) On Day 3 post-infection, virus titers in the BALF were measured in a plaque assay (5 mice/group). Data are expressed as scatter plots with the mean viral titer ± SD. (D) Representative lung tissue sections from pH1N1/OVA, pH1N1/PBS, Mock/OVA, and Mock/PBS mice on Day 3 post-infection (3 mice/group). Sections were stained with hematoxylin and eosin (H&E). Original magnification: ×10 or ×40 (inset). (E) Total cell counts and the proportion of inflammatory cells in the BALF form pH1N1/PBS and pH1N1/OVA mice assessed on Day 2 and Day 3 post-infection (5 mice/group). Data are expressed as scatter plots with the mean ± SD. (F) Total cell counts and the proportion of inflammatory cells in the BALF form Mock/PBS and Mock/OVA mice assessed on Day 2 and Day 3 post-infection (5 mice/group). Data are expressed as scatter plots with the mean ± SD. *<i>p</i><0.05, **<i>p</i><0.01, ***<i>p</i><0.001, and ****<i>p</i><0.0001 (two-way ANOVA or Mann-Whitney U test). IP, intraperitoneal; IN, intranasal; BALF, bronchoalveolar lavage fluid; ns, not significant; Br, Bronchiole. The experiments were repeated independently at least twice.</p

    Isobolograms of simultaneous exposure to EGCG and PKC412 in MOLM-13, MOLM-14, MV4-11 and KOCL-48 cell lines.

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    <p>The isobolograms shown are representative of at least three independent experiments. Each point represents the mean value of at least three independent experiments. The combination of EGCG with PKC412 showed additive effect (MOLM-13 and MOLM-14) and antagonism effect (MV4-11 and KOCL-48).</p

    Treatment of influenza virus-infected/OVA-challenged NC/Nga mice with a neuraminidase inhibitor, zanamivir (ZAN).

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    <p>(A) Schematic showing OVA sensitization, influenza virus infection, OVA-induced allergic airway responses, and ZAN treatment. NC/Nga mice were sensitized twice (via the IP route) with OVA (Day -14 and Day -7) and then infected with a sublethal dose of influenza virus A/H1N1pdm09 (pH1N1) or Mock infected with allantoic fluid (Day 0). On the day following infection, mice were administered OVA or PBS with or without 800 μg of ZAN (via the IN route) for two consecutive days (Day +1 and Day +2). (B) On Day 3 post-infection, virus titers in the BALF were measured in a plaque assay (5 mice/group). Data are expressed as scatter plots with the mean viral titer ± SD. *<i>p</i><0.05 (one-way ANOVA). The experiments were repeated twice independently. (C) Concentration of MCP-1/CCL2 in the BALF measured on Day 3 post-infection (5 mice/group). Data are expressed as scatter plots with the mean ± SD. *<i>p</i><0.05 (two-way ANOVA). The experiments were repeated twice independently. (D) Representative sections of lung tissue obtained from pH1N1-infected/OVA-challenged or pH1N1-infected/PBS-challenged mice (treated or not with ZAN) on Day 3 post-infection and stained for influenza A virus NP antigen (IAV NP). The data are representative of 3 mice/group from two independent experiments. Original magnification: 20×. (E) Representative PAS-stained sections of lung tissue from pH1N1-infected/OVA-challenged mice (treated or not with ZAN) obtained on Day 21 post-infection. The Data are representative of 5 to 10 mice/group from two independent experiments. Original magnification: 20×. Br, Bronchiole. (F) Numbers of PAS positive epithelial cells in lung tissues from pH1N1-infected/OVA-challenged or pH1N1-infected/PBS-challenged mice (treated or not with ZAN) on Day 3 post-infection were obtained by visual estimation over the entire area of the section. The data are expressed as scatter plots with the mean ± SD of results for 5 to 10 mice/group from two independent experiments. **<i>p</i> <0.01, and ****<i>p</i><0.0001 (two-way ANOVA).</p

    Down-regulation of FLT3 expression and its downstream molecules in EGC-treated AML cells.

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    <p>MOLM-13, MOLM-14, MV4-11 and KOCL-48 cells at a density of 1×10<sup>5</sup> cells/ml were treated with indicated concentration of EGC or DMSO alone as control for 8 hours. Total cell lysates were subjected to western blot analysis with indicated antibodies.</p

    Down-regulation of FLT3 expression and its downstream molecules in EGCG-treated AML cells.

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    <p>MOLM-13, MOLM-14, MV4-11, KOCL-48 and THP-1 cells at a density of 1×10<sup>5</sup> cells/ml were treated with indicated concentration of EGCG or DMSO alone as control for 8 hours. Total cell lysates were subjected to western blot analysis with indicated antibodies.</p
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