High levels of S100A8/A9 proteins aggravate ventilator-induced lung injury via TLR4 signaling. - Wikidata - awgldk - TriplyDB

High levels of S100A8/A9 proteins aggravate ventilator-induced lung injury via TLR4 signaling.

High levels of S100A8/A9 proteins aggravate ventilator-induced lung injury via TLR4 signaling.

http://www.wikidata.org/entity/Q34850574

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House Dust Mite Allergen Regulates Constitutive Apoptosis of Normal and Asthmatic Neutrophils via Toll-Like Receptor 4 S100A9 induced inflammatory responses are mediated by distinct damage associated molecular patterns (DAMP) receptors in vitro and in vivo.Myocardial Hypertrophic Preconditioning Attenuates Cardiomyocyte Hypertrophy and Slows Progression to Heart Failure Through Upregulation of S100A8/A9.Combining patient proteomics and in vitro cardiomyocyte phenotype testing to identify potential mediators of heart failure with preserved ejection fraction.S100A8/A9, a potent serum and molecular imaging biomarker for synovial inflammation and joint destruction in seronegative experimental arthritis.Deficiency of myeloid-related proteins 8 and 14 (Mrp8/Mrp14) does not block inflammaging but prevents steatosis.IL-1β expression in the distal lung epithelium disrupts lung morphogenesis and epithelial cell differentiation in fetal mice.The receptor for advanced glycation end products in ventilator-induced lung injury.Alarmin S100A8 Activates Alveolar Epithelial Cells in the Context of Acute Lung Injury in a TLR4-Dependent Manner.Imaging, myeloid precursor immortalization, and genome editing for defining mechanisms of leukocyte recruitment in vivo.Molecular Mechanisms of Ventilator-Induced Lung Injury.S100A8/A9 promotes parenchymal damage and renal fibrosis in obstructive nephropathy

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P2860

High levels of S100A8/A9 proteins aggravate ventilator-induced lung injury via TLR4 signaling.

http://www.wikidata.org/entity/Q34850574

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2013 nî lūn-bûn

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2013 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2013 թվականի հուլիսին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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type

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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prefLabel

High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

@ast

High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

@en

High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

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High levels of S100A8/A9 prote ...... ung injury via TLR4 signaling.

@en

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Alexander P J Vlaar

http://www.w3.org/2001/XMLSchema#string

Catharina W Wieland

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Elske van den Berg

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Geartsje Jongsma

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Hamid Aslami

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Johannes Roth

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Joris J T H Roelofs

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Maria T Kuipers

http://www.w3.org/2001/XMLSchema#string

Thomas Vogl

http://www.w3.org/2001/XMLSchema#string

P2860

Proinflammatory activities of S100: proteins S100A8, S100A9, and S100A8/A9 induce neutrophil chemotaxis and adhesion

Loss of S100A9 (MRP14) results in reduced interleukin-8-induced CD11b surface expression, a polarized microfilament system, and diminished responsiveness to chemoattractants in vitro

Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network

Mrp8 and Mrp14 are endogenous activators of Toll-like receptor 4, promoting lethal, endotoxin-induced shock

DAMPs, PAMPs and alarmins: all we need to know about danger

Proteomic and computational analysis of bronchoalveolar proteins during the course of the acute respiratory distress syndrome

Alarmins: awaiting a clinical response

Calcium-induced noncovalently linked tetramers of MRP8 and MRP14 detected by ultraviolet matrix-assisted laser desorption/ionization mass spectrometry.

Early changes in lung gene expression due to high tidal volume.

S100A8 chemotactic protein is abundantly increased, but only a minor contributor to LPS-induced, steroid resistant neutrophilic lung inflammation in vivo.

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10.1371/JOURNAL.PONE.0068694

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Tom van der Poll

Nicole P Juffermans

Marcus J Schultz

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2013-07-18T00:00:00Z

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250926221

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23874727

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Toll-like receptor

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3715539

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