Search Results - "Endoh, Yasumi"

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    TLR9 ligands induce S100A8 in macrophages via a STAT3-dependent pathway which requires IL-10 and PGE2 by Hsu, Kenneth, Chung, Yuen Ming, Endoh, Yasumi, Geczy, Carolyn L

    Published in PloS one (06-08-2014)
    “…S100A8 and S100A9 are highly-expressed calcium-binding proteins in neutrophils and monocytes, and in subsets of macrophages in inflammatory lesions…”
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    Journal Article
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    S100A8 modulates mast cell function and suppresses eosinophil migration in acute asthma by Zhao, Jing, Endoh, Ikuko, Hsu, Kenneth, Tedla, Nicodemus, Endoh, Yasumi, Geczy, Carolyn L

    Published in Antioxidants & redox signaling (01-05-2011)
    “…S100A8 is implicated in the pathogenesis of inflammatory diseases. S100A8 is upregulated in macrophages by Toll-like receptors (TLR)-3, 4, and 9 agonists in an…”
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    Journal Article
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    IL-10-Dependent S100A8 Gene Induction in Monocytes/Macrophages by Double-Stranded RNA by Endoh, Yasumi, Chung, Yuen Ming, Clark, Ian A, Geczy, Carolyn L, Hsu, Kenneth

    Published in The Journal of immunology (1950) (15-02-2009)
    “…The S100 calcium-binding proteins S100A8 and S100A9 are elevated systemically in patients with viral infections. The S100A8-S100A9 complex facilitated viral…”
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    LILRA2 selectively modulates LPS-mediated cytokine production and inhibits phagocytosis by monocytes by Lu, Hao K, Mitchell, Ainslie, Endoh, Yasumi, Hampartzoumian, Taline, Huynh, Owen, Borges, Luis, Geczy, Carolyn, Bryant, Katherine, Tedla, Nicodemus

    Published in PloS one (30-03-2012)
    “…The activating immunoglobulin-like receptor, subfamily A, member 2 (LILRA2) is primarily expressed on the surface of cells of the innate immunity including…”
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    Regulation of S100A8 by Glucocorticoids by Hsu, Kenneth, Passey, Robert J, Endoh, Yasumi, Rahimi, Farid, Youssef, Peter, Yen, Tina, Geczy, Carolyn L

    Published in The Journal of immunology (1950) (15-02-2005)
    “…S100A8 (A8) has roles in inflammation, differentiation and development and is associated with oxidative defense. Murine A8 (mA8) is up-regulated in…”
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    Correction: LILRA2 Selectively Modulates LPS-Mediated Cytokine Production and Inhibits Phagocytosis by Monocytes by Lu, Hao K., Mitchell, Ainslie, Endoh, Yasumi, Hampartzoumian, Taline, Huynh, Owen, Borges, Luis, Geczy, Carolyn, Bryant, Katherine, Tedla, Nicodemus

    Published in PloS one (07-08-2012)
    “…Inflammation and Infection Research Centre, School of Medical Sciences, Department of Pathology, University of New South Wales, Australia Citation: Lu HK,…”
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    Inflammation and Atrial Fibrillation by Endoh, Yasumi, MD PhD, Endoh, Ikuko, MD PhD, Geczy, Carolyn, PhD, Nakagomi, Akihiro, MD PhD, Kusama, Yoshiki, MD PhD, Atarashi, Hirotsugu, MD PhD

    Published in Journal of Arrhythmia (01-01-2011)
    “…Abstract Atrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice. Accumulating evidence indicates a link between…”
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    TLR9 Ligands Induce S100A8 in Macrophages via a STAT3-Dependent Pathway which Requires IL-10 and PGE.sub.2 by Hsu, Kenneth, Chung, Yuen Ming, Endoh, Yasumi, Geczy, Carolyn L

    Published in PloS one (06-08-2014)
    “…S100A8 and S100A9 are highly-expressed calcium-binding proteins in neutrophils and monocytes, and in subsets of macrophages in inflammatory lesions…”
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    Journal Article
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    Clinical Significance of Wide QRS Complexes at the Termination of Paroxysmal Supraventricular Tachycardias by Endoh, Yasumi, Atarashi, Hirotsugu, Hayakawa, Hirokazu, Nagasawa, Kouichi, Kishida, Hiroshi, Takano, Teruo

    Published in Journal of Nippon Medical School (2002)
    “…Background: A wide QRS complex is not a rare electrocardiographic phenomenon at the termination of paroxysmal supraventricular tachycardia (PSVT), but no…”
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    83: S100A8 is induced in macrophages by oxidants and modulates redox responses in inflammation by Hsu, Kenneth, Hiroshima, Yuka, Endoh, Yasumi, Thomas, Shane R., Geczy, Carolyn L.

    Published in Cytokine (Philadelphia, Pa.) (01-11-2014)
    “…S100A8 expression is modulated by stressors that promote reactive oxygen species (ROS) generation. Its induction in macrophages activated by TLR-4, −7, and −9…”
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