38 research outputs found

    Simultaneous Sampling of NO, NO_2, HONO and HNO_3 in the Atmosphere by a Filter-Pack Method

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    application/pdfAsian Journal pf Atmospheric Environment. 2022, 16 (2)journal articl

    Observation of B+→pp̅π+, B0→pp̅K0, and B+→pp̅K*+

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    journal articl

    A CHEBYSHEV SERIES METHOD FOR THE NUMERICAL SOLUTION OF FREDHOLM INTEGRAL EQUATIONS WITH ASSOCIATED EIGEN-VALUE PROBLEM.

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    application/pdfdepartmental bulletin pape

    Construction of photosynthetic system by using imidazolylporphyrinatozinc(II) Dimer

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    奈良先端科学技術大学院大学博士(工学)doctoral thesi

    名古屋大学稲武演習林における酸性雨モニタリングの観測データ

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    2006-12農林水産研究情報総合センターで作成したPDFファイルを使用している。departmental bulletin pape

    Effects of Osteopontin on MMP-1 Gene and Protein Expression in Two Human Lung Fibroblast Cell Lines

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    <div><p>(A) Representative Northern blot of 20 μg total cellular RNA per lane extracted from control cells and fibroblasts stimulated with 0.4 μg/ml and 1 μg/ml osteopontin. Both concentrations of osteopontin induced a down-regulation in the expression of MMP-1.</p> <p>(B) Osteopontin also reduced overexpression of MMP-1 in APMA-stimulated cells.</p> <p>(C) The expression level of MMP-1 by real-time PCR was determined as described in Materials and Methods and normalized to the level of 18S ribosomal RNA. In parallel experiments, osteopontin-stimulated cells were treated with anti-α<sub>v</sub>β<sub>3</sub> and anti-CD44. Bars represent mean ± SD (*<i>p</i> < 0.05).</p> <p>(D) Representative Western blot demonstrating a decrease of immunoreactive MMP-1 in conditioned media from fibroblasts stimulated with osteopontin. Fibroblasts treated with APMA and FGF-1 plus heparin used as positive controls strongly induced MMP-1 expression.</p> <p>C, control; FGF1, FGF-1 plus heparin; OPN, osteopontin; PMA, APMA-stimulated.</p></div

    Localization of Osteopontin in IPF Lungs

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    <p>Immunoreactive protein was revealed with AEC, and samples were counterstained with hematoxylin. Two representative IPF lung samples exhibited strong epithelial staining (original magnification, 40×) (A,B). Control lung showed no staining (C). Negative control section from IPF lung in which the primary antibody was replaced with nonimmune serum also showed no staining (40×) (D).</p

    DataSheet_1_Fibroblasts From Idiopathic Pulmonary Fibrosis Induce Apoptosis and Reduce the Migration Capacity of T Lymphocytes.docx

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    Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible lung disease of unknown etiology. Myofibroblasts are organized in peculiar subepithelial fibroblasts foci (FF), where they abnormally persist and exclude lymphocytes by unclear mechanisms. FF are the source of an excessive extracellular matrix, which results in progressive stiffening and destruction of the lung architecture. We hypothesized that the absence of T cells inside the FF could be related, at least partially, to an inefficient function of lymphocytes induced by IPF fibroblasts. Here, we evaluated the effect of a supernatant from IPF fibroblasts on T-cell apoptosis and migration capacity. Data showed that IPF fibroblasts secrete pro-apoptotic molecules (both from extrinsic and intrinsic pathways), generating a microenvironment that induces apoptosis of T cells at 3 h of culture, despite a weak anti-apoptotic profile exhibited by these T cells. At 24 h of culture, the supernatants from both IPF and control fibroblasts provoked T-cell death. However, at this time of culture, IPF fibroblasts caused a marked decrease in T-cell migration; in contrast, control lung fibroblasts induced an increase of T-cell migration. The reduction of T-cell migratory capacity provoked by IPF fibroblasts was associated with a negative regulation of RHOA and ROCK, two essential GTPases for migration, and was independent of the expression of chemokine receptors. In conclusion, our findings demonstrate that IPF fibroblasts/myofibroblasts induce apoptosis and affect T-cell migration, revealing a mechanism involved in the virtual absence of T lymphocytes inside the FF.</p
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