41 research outputs found

    A 43-year-old female patient with mixed meningioma in the left CPA.

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    <p>The preoperative axial T2WI (a) shows the left IAC filled by a hypertintense mass. The left IAC is not dilated and its signal intensity is similar to that of the tumor (white arrow). The preoperative post-contrast axial image (b) demonstrates a heterogeneously enhanced mass with a maximal axial area of 506mm<sup>2</sup>. The left IAC is also slightly enhanced (white arrow). The postoperative axial T2WI (c) shows the absence of the preoperative mass in the left CPA but the IAC is still filled by abnormal signal intensity (white arrow). The postoperative post-contrast axial T1WI (d) reveals heterogeneously enhanced IAC (white arrow).</p

    A 55-year-old male patient with meningothelial meningioma in the right CPA.

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    <p>The preoperative axial T2WI (a) shows the right IAC filled and enlarged (white arrow) by a hypertintense mass. Peritumoral edema is seen as patchy high signal intensity in the right cerebellar hemisphere and vermis. The preoperative post-contrast axial image (b) shows a heterogeneously enhanced mass with a maximal axial area of 1104mm<sup>2</sup>. The right IAC is also enhanced (white arrow). The postoperative axial T2WI (c) reveals that the IAC is still filled by abnormal signal intensity (white arrow). The postoperative post-contrast axial T1WI (d) shows heterogeneous enhancement of the enlarged IAC (white arrow).</p

    A 60-year-old male patient with mixed meningioma in the left CPA.

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    <p>The preoperative axial T2WI (a) shows an isointense mass in the left CPA. Part of the tumor intrudes into the left IAC (black arrow). The preoperative post-contrast axial image (b) shows an enhanced mass with a maximal axial area of 135mm<sup>2</sup>. The intruding part of the tumor is also enhanced (black arrow). The postoperative axial T2WI (c) shows that the preoperative mass is no longer visible and that the left ICA is essentially uninvolved (black arrow). The postoperative post-contrast axial T1WI (d) shows no enhanced lesion in the CPA and inner opening of the IAC.</p

    Characteristics of the patients with and without IAC involvement by meningioma of the cerebellopontine angle.

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    <p>*Nonparametric test.</p><p>**Evaluation of postoperative residual tumor was performed in 52 of 71 patients with IAC involvement and 84 of 122 patients without IAC involvement.</p><p>Characteristics of the patients with and without IAC involvement by meningioma of the cerebellopontine angle.</p

    Characteristics of patients according to IAC involvement subtype.

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    <p><sup>a</sup>Nonparametric test.</p><p><sup>b</sup>Patients with intruding vs. filled and dilated IAC involvement.</p><p><sup>c</sup>The meningothelial subtype occurred significantly more frequently in patients with the filled IAC subtype than in patients with intruding IAC (χ<sup>2</sup> = 1.631, <i>P</i> = 0.442).</p><p>Characteristics of patients according to IAC involvement subtype.</p

    CsA prevents AAA development in the rat elastase and the mouse CaCl<sub>2</sub> models.

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    <p>A. Macroscopic pictures of representative rat AAAs 14 days after elastase perfusion. B. External diameter increase at 14 days as a percentage of AAA diameters just after elastase perfusion. C. Macroscopic pictures of mouse AAAs at 14 day. D. Mouse external and internal aortic diameter quantification. Open circles represent individual values from vehicle- and CsA-treated animals and closed circles represent means±SD. *P<.05, **P<0.01 <i>vs</i> vehicle.</p

    CsA induction of AAA stabilization is mediated by TGF-beta.

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    <p>A. Effect of the administration of a blocking antibody against active TGF-beta on the stabilizing effect of CsA on aortic diameter of expanding AAAs in rats. B and C. Impact of anti-TGF-beta blocking antibody on αSMA-positive cell density (A) and monocyte/macrophage infiltration (C) in rat AAAs treated with CsA. Open circles represent individual values and closed circles represent means±SD. **P<.01 <i>vs</i> isotype antibody.</p

    CsA preserves VSMC and elastin content and modulates TGF-beta1 and MMP-9 expression in mouse AAAs.

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    <p>A. Representative anti-αSMA immunostaining performed on AAA cross sections from vehicle- or CsA-treated rats, 14 days after elastase perfusion (red: αSMA staining; blue : nuclei). B, C. Representative anti-αSMA (B) or elastin fibers (C) staining (<i>right</i>) and computer-assisted quantification (<i>left</i>) performed on AAA cross sections from vehicle- or CsA-treated mice at 14 days. D. Representative anti-active TGF-beta1 staining <i>(right)</i> and computer-assisted quantification <i>(left)</i> performed on AAA cross sections from vehicle- and CsA-treated mice at 14 days. E. ELISA quantification of MMP-9 on AAA extracts from vehicle- and CsA-treated mice. Results are reported to the total protein level. Open circles represent individual values from vehicle- and CsA-treated mice and closed circles represent means±SD. *P<.05, **P<.01 <i>vs</i> vehicle. NI : neointima; ILT: intraluminal thrombus. Scale bars : 50 µm.</p
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