PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10587794

Virtual bronchoscopy.

S L Aquino·D J Vining
View original source ↗Export metadata ↓

Abstract

The sophistication of three-dimensional (3-D) radiographic imaging from CT data has accelerated with the development and ongoing advances of helical CT. Virtual bronchoscopy (VB), the ability to create 3-D models of the airways and navigate through the tracheobronchial tree lumen in realtime simulated bronchoscopy, has gained popularity over the past 3 years. The ability of VB to image the airway and mediastinal structures simultaneously and in a 3-D format has helped revolutionize CT imaging. Unlike conventional bronchoscopy, VB can display the extent of narrowing caused by an airway lesion, the presence of patentcy beyond a stenosis, and the relationship between an airway lesion and the adjacent mediastinal structures.

Explore related subjects

BronchiBronchoscopyHumansImage Processing, Computer-AssistedLungLung NeoplasmsSensitivity and SpecificityTomography, X-Ray ComputedUser-Computer InterfaceJournal ArticleResearch Support, Non-U.S. Gov'tReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S L Aquino, D J Vining. 1999. Virtual bronchoscopy.. https://doi.org/10.1016/s0272-5231(05)70251-3

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Neutrophil elastase stimulates human airway epithelial cells to produce PGE2 through activation of p44/42 MAPK and upregulation of cyclooxygenase-2.

The responses of airway epithelium following exposure to neutrophil elastase (NE) were investigated. Human bronchial epithelial cells were explanted on insert surfaces of a modified air-liquid interface culture system to which NE was added to stimulate epithelial cells. PGE2 release significantly increased within 10 min of incubation with NE and peaked 3 h after NE (20 microg/ml) stimulation. This action required proteolytic activity as alpha1-antitrypsin blocked NE-induced PGE2 release. The production of PGE2 was also inhibited by indomethacin; a selective cyclooxygenase (COX)-2 inhibitor, celecoxib; and dexamethasone. Moreover, the mRNA expression for COX-2 relative to that for a housekeeping gene was approximately eightfold that of the unstimulated cells. Dexamethasone inhibited COX-2 gene transcription. We further observed that NE-induced PGE2 release involved activation of p44/42, but not p38, MAP kinases. Such p44/42 MAP kinases were rapidly phosphorylated, with the concentration of phosphorylated p44/42 MAP kinases peaking at 10 min after stimulation and declining in culture at 90 min. The specific p44/42 MAP kinase inhibitor UO126 completely blocked p44/42 phosphorylation and, subsequently, PGE2 production. The airway epithelium may play important bronchoprotective and immunomodulatory roles in chronic neutrophilic inflammation.

Bronchi↗