17 research outputs found

    HuR expression in non-cancer and cancer cells.

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    <p>IRS of nuclear HuR differed between cancer and non-cancer cells and between invasive and non-invasive cancer cells (A). Cytoplasmic HuR expression and the IRS of cytoplasmic HuR was higher in cancer than in non-cancer cells, and higher in invasive as compared to non-invasive cases (B).</p

    Anti-cancer mechanisms of GTP.

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    <p>Schematic illustration of the role of GTP intake in the modulation of malignant characteristics in bladder cancer. GTP intake suppresses the expression of COX-2 and HO-1 directly and that of HO-1 and VEGF-A indirectly via regulation of cytoplasmic HuR expression. Downregulation of COX-2 and HO-1 or HO-1 and VEGF-A leads to inhibition of cancer cell proliferation and angiogenesis, respectively, thereby suppressing tumor growth.</p

    HuR expression and GTP intake.

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    <p>IRS of cytoplasmic HuR increased from 14 to 24 weeks in the BBN but not the BBN + GTP group (A). Similar trends were also observed for MVD (B), proliferation index (C), and COX-2 (D), VEGF-A (E), and HO-1 (F) expression. On the other hand, tumor volume increased in both groups during this period (G).</p

    Representative examples of HuR immunoreactivity.

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    <p>HuR expression was observed in nuclei of both non-cancer (A) and cancer cells (B). In contrast, cytoplasmic HuR-positive non-cancer cells (arrows) were relatively rare (A). Although cytoplasmic expression of HuR was detected in bladder cancer cells (B and C), the percentage of cytoplasmic HuR-positive cancer cells in cases with muscle invasion (C) was higher than that in cases without muscle invasion (B).</p

    Additional file 1: Table S1. of The St. George’s Respiratory Questionnaire as a prognostic factor in IPF

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    Spearman’s correlation coefficients between SGRQ and baseline physiological measures. Table S2. The relationship between SGRQ and comorbidities. Table S3. SGRQ domain as predictors for mortality. (DOCX 29 kb

    Spiral Array construction.

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    <p>A representative block was selected from each case, and two continuous straight regions of interest (X and Y axes) were selected and marked by reviewing hematoxylin and eosin-stained slides. Two 120.0-μm-thick sections were sliced from each block and aligned with the X and Y axes. The two sections were rolled together into a cylindrical form and cut along the line reflecting the X and Y axes. Spiral Array cores were embedded vertically into a recipient block. Four-μm-thick sections were prepared from the Spiral Array blocks for further histopathological evaluation.</p
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