Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-3-22
pubmed:abstractText
Nonresolving inflammation is a major driver of disease. Perpetuation of inflammation is an inherent risk because inflammation can damage tissue and necrosis can provoke inflammation. Nonetheless, multiple mechanisms normally ensure resolution. Cells like macrophages switch phenotypes, secreted molecules like reactive oxygen intermediates switch impact from pro- to anti-inflammatory, and additional mediators of resolution arise, including proteins, lipids, and gasses. Aside from persistence of initiating stimuli, nonresolution may result from deficiencies in these mechanisms when an inflammatory response begins either excessively or subnormally. This greatly complicates the development of anti-inflammatory therapies. The problem calls for conceptual, organizational, and statistical innovations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1097-4172
pubmed:author
pubmed:copyrightInfo
2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
19
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
871-82
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Nonresolving inflammation.
pubmed:affiliation
Department of Microbiology and Immunology, Cornell University, New York, NY 10065, USA. cnathan@med.cornell.edu
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't