Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-2-2
pubmed:abstractText
HYPOTHESIS/BACKGROUND: Endotoxin can induce morphologic changes to middle ear epithelium, which can disturb the mucociliary clearance system (MCS) and lead to otitis media with effusion (OME). The bactericidal/permeability-increasing (BPI) protein is a major component of neutrophil granules and binds with high affinity to endotoxin. In this study, the capacity to inhibit the effects of endotoxin by rBPI21, a recombinant amino-terminal analog derived from BPI, was investigated on cultured human middle ear epithelium using light microscopy and scanning- and transmission electron microscopy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0192-9763
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
625-30
pubmed:dateRevised
2011-1-11
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Inhibition of endotoxin effects on cultured human middle ear epithelium by bactericidal permeability-increasing protein.
pubmed:affiliation
Department of Otorhinolaryngology, Leiden University Medical Center, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't