Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149514 (bronchitis)
 6,902 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 21-year-old man suffered from cough, dyspnoea and hemoptysis following accidental aspiration of petroleum. Chest x-ray and computerized tomography one day after the aspiration showed infiltrates in the lower fields. Fiberbronchoscopy revealed severe bronchitis without any signs of necrosis. Flunisolide inhalation (200 micrograms/d) and intravenous application of prednisolone (50 mg/d) and clindamycine (600 mg/d) improved pulmonary function within a few days. The infiltrates resolved over the following two weeks. This favourable result clearly shows that conservative treatment has a role in petroleum aspiration.
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PMID:[Aspiration of petroleum by a "fire-eater"]. 764 61

To investigate abnormalities of airway epithelial ion transport underlying chronic inflammatory airway diseases, we performed electrophysiological, histological, and molecular biological experiments using rabbits exposed to SO2 as a model of bronchitis. By comparison with control, the SO2-exposed trachea exhibited decreased short circuit current (Isc) and conductance associated with increased potential difference. In normal trachea, apical ATP induced a transient Isc activation followed by a suppression, whereas the bronchitis model exhibited a prolonged activation without suppression. This pathological ATP response was abolished by diphenylamine 2-carboxylate or Cl--free bath solution. A significant increase in net Cl- flux toward the lumen was observed after ATP in our bronchitis model. Isoproterenol or adenosine evoked a sustained Isc increase in SO2-exposed, but not in normal, tracheas. The Northern blot analysis showed a strong expression of cystic fibrosis transmembrane conductance regulator (CFTR) mRNA in SO2-exposed epithelium. The immunohistochemical study revealed a positive label of CFTR on cells located luminally only in SO2-exposed rabbits. We concluded that the prolonged ATP response in our bronchitis model was of a superimposed normal and adenosine-activated current. The latter current was also activated by isoproterenol and appeared as a signature current for the bronchitis model airway. This was likely mediated by CFTR expressed in the course of chronic inflammation.
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PMID:Signature current of SO2-induced bronchitis in rabbit. 912 9