8 research outputs found

    Qualitative and quantitative analyses of two b values protocols for lesion conspicuity of prostate cancer in the DW-MR image and ADC map.

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    <p>Data are given as mean±standard deviation. (LCS - lesion conspicuity score, TNR - tumor-normal signal intensity ratio).</p><p><sup>*</sup>Significant differences between b = 0 and 1000 s/mm<sup>2</sup> and b = 0 and 2000 s/mm.</p

    A 77-year-old male with prostate cancer (PSA level of 7.45 ng/mL, Gleason score of 4+3) in the middle right region in the peripheral zone.

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    <p>Cancer lesion is shown as a homogeneous hypointense lesion with mass effect on T2-weighted imaging (arrow) (A) and focal early enhancement on dynamic contrast-enhanced MR imaging (arrow) (B). The lesion with a focal hyperintensity is depicted clearly in the DW image with b values of 0 and 2000 s/mm<sup>2</sup> (arrow) (D), as compared with the DW image with b values of 0 and 1000 s/mm<sup>2</sup> (arrow) (C). However, the lesion conspicuity with a focal hypointensity in the ADC map with b values of 0 and 2000 s/mm<sup>2</sup> (arrow) (F) was equivalent to that of ADC map with b values of 0 and 1000 s/mm<sup>2</sup> (arrow) (E).</p

    Sequence parameters for prostate MR protocol

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    <p>DW-MRI was acquired with motion-probing gradient (MPG) pulses applied sequentially along 3 orthogonal orientations with two kinds of b value sets (0 and 1000 s/mm<sup>2</sup> or 0 and 2000 s/mm<sup>2</sup>). (TR - repetition time, TE - echo time, ETL - echo train length, FSE - fast spin-echo, DW-MRI - diffusion weighted MR imaging, DCE-MRI - dynamic contrast-enhanced MR imaging, GRE - gradient-echo, NA - not applicable).</p

    Scatterplots showing the relationship between ADC values in prostate cancer and tumor Gleason scores.

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    <p>(A) b values of 0 and 1000 s/mm<sup>2</sup>. (B) b values of 0 and 2000 s/mm<sup>2</sup>. ADC values in b values of 0 and 1000 s/mm<sup>2</sup> and b values of 0 and 2000 s/mm<sup>2</sup> each negatively correlated with tumor Gleason score (ρ = –0.602, <i>p</i><0.001; ρ = –0.645, <i>p</i><0.001, respectively).</p

    LPA<sub>1/3</sub> inhibition of human MSCs reduced actin polymerization and increased cell-cycle quiescence.

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    <p><b>A, B.</b> Phenotypic characteristics of human MSCs treated with Ki16425 or vehicle alone for 48 h after plating. Shown are phase-contrast images (panel <b>A</b>) and fluorescent images in which filamentous actin (F-actin) was visualized with green phalloidin-FITC staining and nuclei were stained with red propidium iodide (panel <b>B</b>). Scale bars, 200 µm. <b>C.</b> Western blotting analysis to evaluate the phosphorylation and activation status of focal adhesion kinase (FAK). <b>D.</b> Cell-cycle analysis. Human MSCs treated with Ki16425 or vehicle alone for 72 h were fixed and then stained for DNA and RNA with 7-AAD and pyronin Y, respectively. Their cell-cycle status was assessed based on their DNA and RNA content by flow cytometry. A representative of three experiments is shown on the left side, and the bar graph summarizes the results of the G<sub>0</sub> proportion on the right side. The data are presented as the means ± standard error (<i>n</i> = 3). <b>E.</b> Western blotting analysis of signaling molecules associated with the Akt pathway. For panels <b>C</b> and <b>E</b>, human MSCs were cultured in the presence or absence of Ki16425 for the indicated times prior to cell lysis.</p

    Decreased self-renewal capacity associated with senescence was prevented in human MSCs following treatment with Ki16425, an LPA<sub>1</sub>/LPA<sub>3</sub> antagonist.

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    <p><b>A.</b> Growth kinetics during serial passage. Human MSCs at passage 2 (8.1 population doublings) were serially passaged every 9 days in the presence or absence of Ki16425. Cumulative population doublings are presented as the means of duplicates. <b>B.</b> Western blotting analysis of total and phosphorylated cPLA2 in human MSCs at passage 2. <b>C.</b> Real-time PCR analysis of LPA receptor gene expression in human MSCs at passage 2. Levels of mRNA were quantified relative to the mean of LPA<sub>1</sub> samples. <b>D.</b> CFU-F assay. Human MSCs at passage 2 were cultured in the presence or absence of Ki16425 for two additional passages (27 days). CFU-F colonies initiated from the treated cells (passage 5, 100 cells) were counted after 15 days of normal culture. On the right side are shown representative CFU-F colonies stained with crystal violet. <b>E.</b> SA-β-Gal assay. The total SA-β-Gal activities of Ki16425- and vehicle-treated human MSCs were quantified in the wells of six-well plates as the luminescent intensity (relative luminescence units, RLU). On the right side are shown representative human MSCs stained for SA-β-Gal. Scale bars in inset boxes, 200 µm. <b>F.</b> Telomere measurement. Telomere lengths were determined in Ki16425- and vehicle-treated human MSCs by real-time PCR and quantified relative to the mean of vehicle controls. <b>G.</b> Western blotting analysis of cell-cycle components. Human MSCs at passage 2 were cultured in the presence or absence of Ki16425 for the indicated days prior to cell lysis. Fold-change represents decrease in band intensity of Ki16425 treatment for 18 days compared with a control treatment for the same period of time. For panels <b>C</b>, <b>D</b>, <b>E</b>, and <b>F</b>, the data are presented as the means ± standard error (<i>n</i> = 3).</p
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