Subchronic endotoxin inhalation causes persistent airway disease.
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TNF polymorphisms modify endotoxin exposure-associated longitudinal lung function declineEndotoxin and gender modify lung function recovery after occupational organic dust exposure: a 30-year studyChronic endotoxin exposure produces airflow obstruction and lung dendritic cell expansionDispersal state of multiwalled carbon nanotubes elicits profibrogenic cellular responses that correlate with fibrogenesis biomarkers and fibrosis in the murine lungMultiple exposures to swine barn air induce lung inflammation and airway hyper-responsiveness.Imaging phenotype of occupational endotoxin-related lung function declineIntegrating murine gene expression studies to understand obstructive lung disease due to chronic inhaled endotoxinBacterial lipopolysaccharide enhances PDGF signaling and pulmonary fibrosis in rats exposed to carbon nanotubesChronic LPS inhalation causes emphysema-like changes in mouse lung that are associated with apoptosisCellular and molecular mechanisms in environmental and occupational inhalation toxicologyCigarette smoke and lipopolysaccharide induce a proliferative airway smooth muscle phenotypeInnate immune activation by inhaled lipopolysaccharide, independent of oxidative stress, exacerbates silica-induced pulmonary fibrosis in mice.The pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells.ATP binding cassette transporter G1 deletion induces IL-17-dependent dysregulation of pulmonary adaptive immunity.The IL-1 type 1 receptor is required for the development of LPS-induced airways diseaseRole of signal transducer and activator of transcription 1 in murine allergen-induced airway remodeling and exacerbation by carbon nanotubes.Using mouse genomics to understand idiopathic interstitial fibrosis.Increased susceptibility of Cftr-/- mice to LPS-induced lung remodeling.Controversy surrounding the increased expression of TGF beta 1 in asthma.Role of cyclooxygenase-2 in exacerbation of allergen-induced airway remodeling by multiwalled carbon nanotubes.Innate immunity and asthmaPersistence of LPS-induced lung inflammation in surfactant protein-C-deficient miceNickel nanoparticles cause exaggerated lung and airway remodeling in mice lacking the T-box transcription factor, TBX21 (T-bet)Signal transduction pathways linking the activation of alveolar macrophages with the recruitment of neutrophils to lungs in chronic obstructive pulmonary disease.A mechanistic review of silica-induced inhalation toxicity.Lipopolysaccharide induced connective tissue growth factor gene expression in human bronchial epithelial cells.Toll-like receptor 4 antagonist (E5564) prevents the chronic airway response to inhaled lipopolysaccharide.The role of Toll-like receptor 4 in environmental airway injury in mice.Fractional ventilation mapping using inert fluorinated gas MRI in rat models of inflammation and fibrosis.CD14 is an essential mediator of LPS-induced airway disease.Effects of Fengbaisan on the expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in lung tissue of rats with chronic obstructive pulmonary disease.The presence of LPS in OVA inhalations affects airway inflammation and AHR but not remodeling in a rodent model of asthma.
P2860
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P2860
Subchronic endotoxin inhalation causes persistent airway disease.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh
2003年學術文章
@zh-hant
name
Subchronic endotoxin inhalation causes persistent airway disease.
@en
Subchronic endotoxin inhalation causes persistent airway disease.
@nl
type
label
Subchronic endotoxin inhalation causes persistent airway disease.
@en
Subchronic endotoxin inhalation causes persistent airway disease.
@nl
prefLabel
Subchronic endotoxin inhalation causes persistent airway disease.
@en
Subchronic endotoxin inhalation causes persistent airway disease.
@nl
P2093
P2860
P1476
Subchronic endotoxin inhalation causes persistent airway disease.
@en
P2093
Haykal-Coates N
Schwartz DA
P2860
P304
P356
10.1152/AJPLUNG.00001.2003
P577
2003-06-06T00:00:00Z