Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-5-16
pubmed:abstractText
Atherothrombotic disease arises secondary to a complex gene-environment interaction. In the initial stages, the condition is clinically silent but with more advanced disease, an occlusive thrombus is formed resulting in the classical clinical manifestations. Both environmental factors and genetic variations in elements of the clotting cascade influence thrombosis risk by inducing quantitative and qualitative changes in the mature protein, which may affect the final structure of the clot and determine its resistance to lysis. Understanding the fine details of gene-environment interactions in relation to thrombus formation will help to shed more light on disease pathogenesis. Consequently, this will allow the development of more efficacious treatment strategies and will also help to identify subjects at risk, thereby enabling the introduction of early preventative measures.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9150
pubmed:author
pubmed:issnType
Print
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
240-59
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Coagulation and atherothrombotic disease.
pubmed:affiliation
Academic Unit of Molecular Vascular Medicine, Leeds Institute of Genetics Health and Therapeutics, Faculty of Medicine and Health, The LIGHT Laboratories, Clarendon Way, University of Leeds, Leeds LS2 9JT, UK. r.ajjan@leeds.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't