Diesel exhaust particles activate human bronchial epithelial cells to express inflammatory mediators in the airways: a review. - Wikidata - awgldk - TriplyDB

Diesel exhaust particles activate human bronchial epithelial cells to express inflammatory mediators in the airways: a review.

Diesel exhaust particles activate human bronchial epithelial cells to express inflammatory mediators in the airways: a review.

http://www.wikidata.org/entity/Q33967941

about

Short-term diesel exhaust inhalation in a controlled human crossover study is associated with changes in DNA methylation of circulating mononuclear cells in asthmatics Role of oxidative stress on diesel-enhanced influenza infection in mice Recent advances in particulate matter and nanoparticle toxicology: a review of the in vivo and in vitro studies Cellular and molecular mechanisms in environmental and occupational inhalation toxicology Inflammation-related effects of diesel engine exhaust particles: studies on lung cells in vitro Identification of Potential Novel Biomarkers and Signaling Pathways Related to Otitis Media Induced by Diesel Exhaust Particles Using Transcriptomic Analysis in an In Vivo System Glutathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells.Analysis of interferon-beta mRNA stability control after poly(I:C) stimulation using RNA metabolic labeling by ethynyluridine.Antioxidant enzyme induction: a new protective approach against the adverse effects of diesel exhaust particles.Possible mechanisms for induction of oxidative stress and suppression of systemic nitric oxide production caused by exposure to environmental chemicals.Causation by Diesel Exhaust Particles of Endothelial Dysfunctions in Cytotoxicity, Pro-inflammation, Permeability, and Apoptosis Induced by ROS Generation.Biodiesel exhaust-induced cytotoxicity and proinflammatory mediator production in human airway epithelial cells.Tight junctions in pulmonary epithelia during lung inflammation.Aberrant CpG island methylation of the p16(INK4a) and estrogen receptor genes in rat lung tumors induced by particulate carcinogens.Air pollution particles produce airway wall remodeling in rat tracheal explants.Induction of lung epithelial cell transformation and fibroblast activation by Yunnan tin mine dust and their interaction.Diesel exhaust particulate matter induces multinucleate cells and zinc transporter-dependent apoptosis in human airway cells.Ozone enhances diesel exhaust particles (DEP)-induced interleukin-8 (IL-8) gene expression in human airway epithelial cells through activation of nuclear factors- kappaB (NF-kappaB) and IL-6 (NF-IL6).Cellular response of mucociliary differentiated primary bronchial epithelial cells to diesel exhaust.Diesel exhaust enhances influenza virus infections in respiratory epithelial cells.Diesel particulate material binds and concentrates a proinflammatory cytokine that causes neutrophil migration.Nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase and glutathione S-transferase M1 polymorphisms and childhood asthma.

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P2860

Diesel exhaust particles activate human bronchial epithelial cells to express inflammatory mediators in the airways: a review.

http://www.wikidata.org/entity/Q33967941

description

2000 nî lūn-bûn

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2000 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2000 թվականի հունիսին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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Diesel exhaust particles activ ...... tors in the airways: a review.

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P2860

An association between air pollution and mortality in six U.S. cities

Particulate air pollution as a predictor of mortality in a prospective study of U.S. adults

Nuclear factor-kappaB: a pivotal transcription factor in chronic inflammatory diseases

Acute inflammatory responses in the airways and peripheral blood after short-term exposure to diesel exhaust in healthy human volunteers

Dithiocarbamates as potent inhibitors of nuclear factor kappa B activation in intact cells.

Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2B) in vitro.

Copper-dependent inflammation and nuclear factor-kappaB activation by particulate air pollution.

Air pollution particles induce IL-6 gene expression in human airway epithelial cells via NF-kappaB activation.

Enhancement of allergic inflammation by the interaction between diesel exhaust particles and the immune system.

Diesel exhaust particles stimulate human airway epithelial cells to produce cytokines relevant to airway inflammation in vitro.

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