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

A 39-year-old man with a history of repeated attacks of acute bronchitis and pneumonia since childhood was admitted complaining of cough, sputum, and a high fever. A diagnosis of Kartagener's syndrome was made because of the presence of mirror-image dextrocardia with complete situs inversus, bronchiectasis in right B6 and B10, and chronic sinusitis. Examination of the ciliary ultrastructure of the bronchial epithelium showed defective inner dynein arms and impaired nasal clearance was suggested by the saccharin particle method. Contrast venography of great veins revealed a McCotter type II bilateral superior vena cava and an absent inferior vena cava with (hemi-) azygos continuation. A search to find a similar case in the literature failed. Abnormal ciliary movement from the embryonic period was implicated as a causative factor in Kartagener's triad and the morphological abnormalities of the great veins.
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PMID:[A case of Kartagener's syndrome with bilateral superior vena cava and absent inferior vena cava]. 186 4

In a 70-year-old nonsmoking, asymptomatic man, chest radiography before a operation for early gastric cancer revealed a solitary nodular shadow in the right lower lobe. Laboratory studies for bacteria and mycobacteria were negative and histological diagnosis could not be obtained. Right lower lobectomy was performed because the mass could be malignant. Histologically the right B10 was almost completely obstructed by tuberculous granuloma and the distal bronchus were dilated containing inspissated mucus. The abnormal nodular shadow was considered the obstructive mucoid impaction secondary to tuberculous bronchitis. It is quite rare that solitary nodular shadow is found in such a case of endobronchial tuberculosis.
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PMID:[A case of endobronchial tuberculosis with peripheral mucoid impaction showing a solitary pulmonary nodular shadow]. 895 91

Chronic airway rejection is characterized by prolonged inflammation, epithelial damage, and eventual luminal obliterative bronchiolitis (OB). In cardiac allografts, the inducible nitric oxide synthase (iNOS) promotes acute rejection but paradoxically reduces neointimal formation, the hallmark of chronic rejection. The specific roles of NOS isoforms in modulating lymphocyte traffic and airway rejection are not known. Using a double lumen mouse tracheal transplant model, tracheal grafts from B10.A (allo) or C57BL/6J (iso) mice were transplanted into cyclosporine-treated wild-type (WT) iNOS(-/-) or endothelial NOS (eNOS)(-/-) recipients. OB was observed in WT tracheal allografts at 3 weeks (53 +/- 2% luminal occlusion vs. 17 +/- 1% for isografts, P < 0.05) with sites of obstructive lesion formation coinciding with areas of CD3(+) CD8(+) T cell-rich lymphocytic bronchitis. In contrast, allografts in iNOS(-/-) recipients exhibited reductions in local expression of proinflammatory chemokines and cytokines, graft T cell recruitment and apoptosis, and luminal obliteration (29 +/- 2%, P < 0.05 vs. WT allografts). Recipient eNOS deficiency, however, suppressed neither chemokine expression, lymphocyte infiltration, nor airway occlusion (54 +/- 2%). These data demonstrate that iNOS exacerbates luminal obliteration of airway allografts in contrast with the known suppression by iNOS of cardiac allograft vasculopathy. Because iNOS(-/-) airways transplanted into WT allograft hosts are not protected from rejection, these data suggest that iNOS expressed by graft-infiltrating leukocytes exerts the dominant influence on airway rejection.
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PMID:Recipient iNOS but not eNOS deficiency reduces luminal narrowing in tracheal allografts. 1243 23