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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2005-2-7
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pubmed:abstractText |
We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n=290) and white (n=379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/HL-33728,
http://linkedlifedata.com/resource/pubmed/grant/HL-33733,
http://linkedlifedata.com/resource/pubmed/grant/HL-33740,
http://linkedlifedata.com/resource/pubmed/grant/HL-33748,
http://linkedlifedata.com/resource/pubmed/grant/HL-33749,
http://linkedlifedata.com/resource/pubmed/grant/HL-33750,
http://linkedlifedata.com/resource/pubmed/grant/HL-33752,
http://linkedlifedata.com/resource/pubmed/grant/HL-33758,
http://linkedlifedata.com/resource/pubmed/grant/HL-33760,
http://linkedlifedata.com/resource/pubmed/grant/HL-33765,
http://linkedlifedata.com/resource/pubmed/grant/HL-33770,
http://linkedlifedata.com/resource/pubmed/grant/HL-33772,
http://linkedlifedata.com/resource/pubmed/grant/HL-33778,
http://linkedlifedata.com/resource/pubmed/grant/HL-39913,
http://linkedlifedata.com/resource/pubmed/grant/HL-45693,
http://linkedlifedata.com/resource/pubmed/grant/HL-45694,
http://linkedlifedata.com/resource/pubmed/grant/HL-45715,
http://linkedlifedata.com/resource/pubmed/grant/HL-45718,
http://linkedlifedata.com/resource/pubmed/grant/HL-45719,
http://linkedlifedata.com/resource/pubmed/grant/HL-45720,
http://linkedlifedata.com/resource/pubmed/grant/HL33746
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0021-9150
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
178
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
241-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15694930-Adolescent,
pubmed-meshheading:15694930-Adult,
pubmed-meshheading:15694930-African Continental Ancestry Group,
pubmed-meshheading:15694930-Aorta,
pubmed-meshheading:15694930-Arteriosclerosis,
pubmed-meshheading:15694930-Autopsy,
pubmed-meshheading:15694930-Coronary Vessels,
pubmed-meshheading:15694930-DNA Mutational Analysis,
pubmed-meshheading:15694930-European Continental Ancestry Group,
pubmed-meshheading:15694930-Genotype,
pubmed-meshheading:15694930-Humans,
pubmed-meshheading:15694930-Male,
pubmed-meshheading:15694930-Peptidyl-Dipeptidase A,
pubmed-meshheading:15694930-Polymorphism, Genetic,
pubmed-meshheading:15694930-Prevalence,
pubmed-meshheading:15694930-Risk Factors
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pubmed:year |
2005
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pubmed:articleTitle |
ACE insert/delete polymorphism and atherosclerosis.
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pubmed:affiliation |
Louisiana State University Health Sciences Center, Department of Pathology, 1901 Perdido Street, New Orleans, LA 70112, USA. wschee@lsuhsc.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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