*PDAY Population and Atherosclerosis Phenotype*: From 1987 to 1994 PDAY centers collected standardized autopsy specimens and selected risk factor data from black and white males and females, age 15-34 yrs, who died within 72 hours after injury. Using an unlinked anonymous coding system, the specimens and data were submitted to central pathology laboratories for detailed histopathologic analyses. The right coronary artery and left half of the aorta were stained with Sudan IV and the percent of intimal surface involved with raised atherosclerotic lesions in the distal and thoracic aorta and right coronary artery was independently estimated by three pathologists. This produced a pathologically specific and quantitatively precise description of atherosclerosis extent that was strongly correlated with blood lipids and other conventional risk factors in the PDAY cohort*. For the current project the percent surface involvement in the distal and thoracic aorta and right coronary artery was summed and then adjusted for age^2, race and gender to produce a total raised lesion score which was the primary phenotype for our genetic association analyses.
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*PDAY Population and Atherosclerosis Phenotype*: From 1987 to 1994 PDAY centers collected standardized autopsy specimens and selected risk factor data from black and white males and females, age 15-34 yrs, who died within 72 hours after injury. Using an unlinked anonymous coding system, the specimens and data were submitted to central pathology laboratories for detailed histopathologic analyses. The right coronary artery and left half of the aorta were stained with Sudan IV and the percent of intimal surface involved with raised atherosclerotic lesions in the distal and thoracic aorta and right coronary artery was independently estimated by three pathologists. This produced a pathologically specific and quantitatively precise description of atherosclerosis extent that was strongly correlated with blood lipids and other conventional risk factors in the PDAY cohort*. For the current project the percent surface involvement in the distal and thoracic aorta and right coronary artery was summed and then adjusted for age^2, race and gender to produce a total raised lesion score which was the primary phenotype for our genetic association analyses.
boolean
C0200345 (UMLS CUI [1,1])
C0332142 (UMLS CUI [1,2])
C0442818 (UMLS CUI [1,3])
C0221198 (UMLS CUI [1,4])
C0205042 (UMLS CUI [1,5])
C0003483 (UMLS CUI [1,6])
Cases were defined as the PDAY subjects at >90th% for total raised lesion score.
Item
Cases were defined as the PDAY subjects at >90th% for total raised lesion score.
boolean
C1706256 (UMLS CUI [1,1])
C0442818 (UMLS CUI [1,2])
C0221198 (UMLS CUI [1,3])
C0449820 (UMLS CUI [1,4])
Controls were selected from among PDAY subjects with a total raised lesion score = 0 after matching to cases (2:1) on age, race and gender.
Item
Controls were selected from among PDAY subjects with a total raised lesion score = 0 after matching to cases (2:1) on age, race and gender.
boolean
C0009932 (UMLS CUI [1,1])
C0442818 (UMLS CUI [1,2])
C0221198 (UMLS CUI [1,3])
C0449820 (UMLS CUI [1,4])
In Phase I of the SEA Study quantitative genotyping was used to estimate allele frequency for >2.4 million SNPs in each of eight pools of DNA (3 case and 5 control pools). Pools were balanced for age, gender and genetic ancestry based on analysis of 311 ancestry informative markers typed on every sample before pool formation. Phase II and III of the SEA study involved individual level genotyping of promising SNPs in the PDAY subjects and subsequent replication in the MESA cohort. Phase II and III data are not included in the dbGap data set.
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In Phase I of the SEA Study quantitative genotyping was used to estimate allele frequency for >2.4 million SNPs in each of eight pools of DNA (3 case and 5 control pools). Pools were balanced for age, gender and genetic ancestry based on analysis of 311 ancestry informative markers typed on every sample before pool formation. Phase II and III of the SEA study involved individual level genotyping of promising SNPs in the PDAY subjects and subsequent replication in the MESA cohort. Phase II and III data are not included in the dbGap data set.
boolean
C0392762 (UMLS CUI [1,1])
C1509144 (UMLS CUI [1,2])
C1285573 (UMLS CUI [1,3])
C1285573 (UMLS CUI [2,1])
C0237401 (UMLS CUI [2,2])
*A more detailed description of the measurement of raised lesions in the PDAY cohort can be found in: Strong JP, Malcom GT, McMahan CA et al. Prevalence and extent of atherosclerosis in adolescents and young adults. Implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth study. JAMA 1999;281:727-35; PMID: 10052443.
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*A more detailed description of the measurement of raised lesions in the PDAY cohort can be found in: Strong JP, Malcom GT, McMahan CA et al. Prevalence and extent of atherosclerosis in adolescents and young adults. Implications for prevention from the Pathobiological Determinants of Atherosclerosis in Youth study. JAMA 1999;281:727-35; PMID: 10052443.
boolean
C1546922 (UMLS CUI [1,1])