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Modeling and dissection of longitudinal blood pressure and hypertension phenotypes in genetic epidemiological studies
We discuss analyses of the Genetic Analysis Workshop 13 data from the Framingham Heart Study and simulations based on this study. We summarize analyses that investigated measures of systolic blood pressure or hypertension as the main phenotype, with the main focus being the modeling of this complex...
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Published in: | Genetic epidemiology 2003, Vol.25 (S1), p.S72-S77 |
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container_title | Genetic epidemiology |
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creator | Bickeböller, H. Barrett, J.H. Jacobs, K.B. Rosenberger, A. |
description | We discuss analyses of the Genetic Analysis Workshop 13 data from the Framingham Heart Study and simulations based on this study. We summarize analyses that investigated measures of systolic blood pressure or hypertension as the main phenotype, with the main focus being the modeling of this complex longitudinal phenotype. The approaches include familial aggregation methods and one‐stage and two‐stage linkage methods. For one‐stage linkage methods, phenotype modeling is carried out jointly with the linkage analysis or incorporated in the analysis design. For two‐stage linkage methods, phenotypes are first modeled in order to develop summary measures that are then analyzed in a subsequent linkage analysis. Results depend on phenotype selection and on how analyses account for longitudinality, treatment effects, and heterodasticity. Genet Epidemiol 25 (Suppl. 1):S72–S77, 2003. © 2003 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/gepi.10287 |
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We summarize analyses that investigated measures of systolic blood pressure or hypertension as the main phenotype, with the main focus being the modeling of this complex longitudinal phenotype. The approaches include familial aggregation methods and one‐stage and two‐stage linkage methods. For one‐stage linkage methods, phenotype modeling is carried out jointly with the linkage analysis or incorporated in the analysis design. For two‐stage linkage methods, phenotypes are first modeled in order to develop summary measures that are then analyzed in a subsequent linkage analysis. Results depend on phenotype selection and on how analyses account for longitudinality, treatment effects, and heterodasticity. Genet Epidemiol 25 (Suppl. 1):S72–S77, 2003. © 2003 Wiley‐Liss, Inc.</description><identifier>ISSN: 0741-0395</identifier><identifier>EISSN: 1098-2272</identifier><identifier>DOI: 10.1002/gepi.10287</identifier><identifier>PMID: 14635172</identifier><identifier>CODEN: GENYEX</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - genetics ; Cardiology. Vascular system ; Cardiovascular Diseases - epidemiology ; Cardiovascular Diseases - genetics ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; familial aggregation ; Fundamental and applied biological sciences. Psychology ; Genetic Linkage ; Genetic Predisposition to Disease ; Humans ; Hypertension - epidemiology ; Hypertension - genetics ; Longitudinal Studies ; Medical sciences ; Models, Genetic ; Models, Statistical ; Molecular and cellular biology ; one-stage linkage designs ; Phenotype ; Systole ; two-stage linkage designs</subject><ispartof>Genetic epidemiology, 2003, Vol.25 (S1), p.S72-S77</ispartof><rights>2003 Wiley‐Liss, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright 2003 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4267-cea911ab06facf7a3ab51f7d01308496196fa64a44331193e72cb73ed37117ea3</citedby><cites>FETCH-LOGICAL-c4267-cea911ab06facf7a3ab51f7d01308496196fa64a44331193e72cb73ed37117ea3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,4024,4050,4051,23930,23931,25140,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15354113$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14635172$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bickeböller, H.</creatorcontrib><creatorcontrib>Barrett, J.H.</creatorcontrib><creatorcontrib>Jacobs, K.B.</creatorcontrib><creatorcontrib>Rosenberger, A.</creatorcontrib><title>Modeling and dissection of longitudinal blood pressure and hypertension phenotypes in genetic epidemiological studies</title><title>Genetic epidemiology</title><addtitle>Genet. Epidemiol</addtitle><description>We discuss analyses of the Genetic Analysis Workshop 13 data from the Framingham Heart Study and simulations based on this study. We summarize analyses that investigated measures of systolic blood pressure or hypertension as the main phenotype, with the main focus being the modeling of this complex longitudinal phenotype. The approaches include familial aggregation methods and one‐stage and two‐stage linkage methods. For one‐stage linkage methods, phenotype modeling is carried out jointly with the linkage analysis or incorporated in the analysis design. For two‐stage linkage methods, phenotypes are first modeled in order to develop summary measures that are then analyzed in a subsequent linkage analysis. Results depend on phenotype selection and on how analyses account for longitudinality, treatment effects, and heterodasticity. Genet Epidemiol 25 (Suppl. 1):S72–S77, 2003. © 2003 Wiley‐Liss, Inc.</description><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - genetics</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular Diseases - epidemiology</subject><subject>Cardiovascular Diseases - genetics</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>familial aggregation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Linkage</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Hypertension - epidemiology</subject><subject>Hypertension - genetics</subject><subject>Longitudinal Studies</subject><subject>Medical sciences</subject><subject>Models, Genetic</subject><subject>Models, Statistical</subject><subject>Molecular and cellular biology</subject><subject>one-stage linkage designs</subject><subject>Phenotype</subject><subject>Systole</subject><subject>two-stage linkage designs</subject><issn>0741-0395</issn><issn>1098-2272</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqF0UGP1CAUB3BiNO64evEDmF70sEmVB7SUozuu4yar7kHjkVD62kU7UKGNO99eZmd0b3qCwI__I-8R8hzoa6CUvRlwcnnHGvmArICqpmRMsodkRaWAknJVnZAnKX2nFECo6jE5AVHzCiRbkeVj6HB0fiiM74rOpYR2dsEXoS_G4Ac3L53zZizaMYSumCKmtES80ze7CeOMPu39dIM-zPkkFc4XA3qcnS3yzzrcujCGwdmckvZxmJ6SR70ZEz47rqfk6_uLL-sP5dXnzeX67VVpBatladEoANPSuje2l4abtoJedhQ4bYSqQeWLWhghOAdQHCWzreTYcQkg0fBT8uqQO8Xwc8E0661LFsfReAxL0hK4olCJ_0JQjDWMNxmeHaCNIaWIvZ6i25q400D1fhp6Pw19N42MXxxTl3aL3T09tj-Dl0dgUm5PH423Lt27ilcCgGcHB_fLjbj7R0m9ubi-_FO8PLxxacbbv29M_KFryWWlv33a6PN362tV03NN-W9NLrLk</recordid><startdate>2003</startdate><enddate>2003</enddate><creator>Bickeböller, H.</creator><creator>Barrett, J.H.</creator><creator>Jacobs, K.B.</creator><creator>Rosenberger, A.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>2003</creationdate><title>Modeling and dissection of longitudinal blood pressure and hypertension phenotypes in genetic epidemiological studies</title><author>Bickeböller, H. ; Barrett, J.H. ; Jacobs, K.B. ; Rosenberger, A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4267-cea911ab06facf7a3ab51f7d01308496196fa64a44331193e72cb73ed37117ea3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - genetics</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular Diseases - epidemiology</topic><topic>Cardiovascular Diseases - genetics</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>familial aggregation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Linkage</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Hypertension - epidemiology</topic><topic>Hypertension - genetics</topic><topic>Longitudinal Studies</topic><topic>Medical sciences</topic><topic>Models, Genetic</topic><topic>Models, Statistical</topic><topic>Molecular and cellular biology</topic><topic>one-stage linkage designs</topic><topic>Phenotype</topic><topic>Systole</topic><topic>two-stage linkage designs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bickeböller, H.</creatorcontrib><creatorcontrib>Barrett, J.H.</creatorcontrib><creatorcontrib>Jacobs, K.B.</creatorcontrib><creatorcontrib>Rosenberger, A.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Genetic epidemiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bickeböller, H.</au><au>Barrett, J.H.</au><au>Jacobs, K.B.</au><au>Rosenberger, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modeling and dissection of longitudinal blood pressure and hypertension phenotypes in genetic epidemiological studies</atitle><jtitle>Genetic epidemiology</jtitle><addtitle>Genet. 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subjects | Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure - genetics Cardiology. Vascular system Cardiovascular Diseases - epidemiology Cardiovascular Diseases - genetics Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Clinical manifestations. Epidemiology. Investigative techniques. Etiology familial aggregation Fundamental and applied biological sciences. Psychology Genetic Linkage Genetic Predisposition to Disease Humans Hypertension - epidemiology Hypertension - genetics Longitudinal Studies Medical sciences Models, Genetic Models, Statistical Molecular and cellular biology one-stage linkage designs Phenotype Systole two-stage linkage designs |
title | Modeling and dissection of longitudinal blood pressure and hypertension phenotypes in genetic epidemiological studies |
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