Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-8-10
pubmed:abstractText
According to a current hypothesis, pulmonary emphysema results from damage to the elastic fiber network caused by an imbalance within the lower respiratory tract between elastase(s) and protease inhibitors. This hypothesis is based largely on studies of persons with genetic deficiency of serum alpha 1-proteinase inhibitor. We recently reported a spontaneously occurring emphysema in the pallid mouse with an inherited deficiency of serum alpha 1-proteinase inhibitor. This animal reproduces important features of the human condition. We describe here the changes in alveolar elastolytic burden and in the bronchoalveolar lavage (BAL) cell population, which precede and accompany the development of emphysema in pallid mice.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
40-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Pallid mice with genetic emphysema. Neutrophil elastase burden and elastin loss occur without alteration in the bronchoalveolar lavage cell population.
pubmed:affiliation
Institute of Pathological Anatomy, University of Siena, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't