Endothelial nitric oxide synthase gene polymorphism and ischemic heart disease
Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process un...
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| Veröffentlicht in: | The American heart journal 2004-11, Vol.148 (5), p.847-851 |
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| creator | Spence, Mark S. McGlinchey, Paul G. Patterson, Chris C. Allen, Adrian R. Murphy, Gillian Bayraktutan, Ulvi Fogarty, Damian G. Evans, Alun E. McKeown, Pascal P. |
| description | Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process underlying IHD. Endothelial NO is synthesized from the amino acid
l-arginine by the endothelial isoform of NO synthase (eNOS). Thus, polymorphisms of the
eNOS gene, by altering production of NO within the vascular endothelium, are potential risk factors for IHD. Several groups have investigated the role of the G894T polymorphism of the
eNOS gene in IHD by using case-control association studies; however, its role is unclear because of contradictory results from these studies. We applied family-based association tests to investigate the role of this polymorphism in IHD in a well-defined Irish population.
A total of 1023 individuals from 388 families (discordant sibships and parent-offspring trios) were recruited. Linkage disequilibrium between the polymorphism and IHD was tested for by using the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test.
Both the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test analyses found no statistically significant excess transmission of either allele to affected individuals (
P = .57 and
P = .38, respectively).
Using robust family-based association tests specifically designed for the study of complex diseases, we found no evidence that the G894T polymorphism of the
eNOS gene has a significant role in the development of IHD in our population. |
| doi_str_mv | 10.1016/j.ahj.2004.05.019 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67039405</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0002870304002789</els_id><sourcerecordid>67039405</sourcerecordid><originalsourceid>FETCH-LOGICAL-c409t-a32484e6155bb4a7b1279e93a6669ae770f4b0991ff19c55787c38f7ed8ca9923</originalsourceid><addsrcrecordid>eNp9kE2L1TAUhoMozp3RH-BGCqK71pM2n7iSYRyFQTe6Dml6alPa5Jr0ivffm8u9MODC1SHwnPe8eQh5RaGhQMX7ubHT3LQArAHeANVPyI6ClrWQjD0lOwBoayWhuyLXOc_lKVolnpMrynnbdVTsyNe7MMRtwsXbpQp-S95V8Y8fsMrHsE02Y_UTA1b7uBzXmPaTz2tlw1D57CZcCz2hTVs1-IwFfkGejXbJ-PIyb8iPT3ffbz_XD9_uv9x-fKgdA73VtmuZYihKj75nVva0lRp1Z4UQ2qKUMLIetKbjSLXjXCrpOjVKHJSzWrfdDXl3zt2n-OuAeTNrKYTLYgPGQzaifFoz4AV88w84x0MKpZuhHBgTSvFTHD1TLsWcE45mn_xq09FQMCfVZjZFtTmpNsBNUV12Xl-SD_2Kw-PGxW0B3l4Am51dxmSD8_mRE61Qkp6OfzhzWIT99phMdh6Dw8EndJsZov9Pjb8xlJqr</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1504468852</pqid></control><display><type>article</type><title>Endothelial nitric oxide synthase gene polymorphism and ischemic heart disease</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><source>ProQuest Central UK/Ireland</source><creator>Spence, Mark S. ; McGlinchey, Paul G. ; Patterson, Chris C. ; Allen, Adrian R. ; Murphy, Gillian ; Bayraktutan, Ulvi ; Fogarty, Damian G. ; Evans, Alun E. ; McKeown, Pascal P.</creator><creatorcontrib>Spence, Mark S. ; McGlinchey, Paul G. ; Patterson, Chris C. ; Allen, Adrian R. ; Murphy, Gillian ; Bayraktutan, Ulvi ; Fogarty, Damian G. ; Evans, Alun E. ; McKeown, Pascal P.</creatorcontrib><description>Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process underlying IHD. Endothelial NO is synthesized from the amino acid
l-arginine by the endothelial isoform of NO synthase (eNOS). Thus, polymorphisms of the
eNOS gene, by altering production of NO within the vascular endothelium, are potential risk factors for IHD. Several groups have investigated the role of the G894T polymorphism of the
eNOS gene in IHD by using case-control association studies; however, its role is unclear because of contradictory results from these studies. We applied family-based association tests to investigate the role of this polymorphism in IHD in a well-defined Irish population.
A total of 1023 individuals from 388 families (discordant sibships and parent-offspring trios) were recruited. Linkage disequilibrium between the polymorphism and IHD was tested for by using the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test.
Both the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test analyses found no statistically significant excess transmission of either allele to affected individuals (
P = .57 and
P = .38, respectively).
Using robust family-based association tests specifically designed for the study of complex diseases, we found no evidence that the G894T polymorphism of the
eNOS gene has a significant role in the development of IHD in our population.</description><identifier>ISSN: 0002-8703</identifier><identifier>EISSN: 1097-6744</identifier><identifier>DOI: 10.1016/j.ahj.2004.05.019</identifier><identifier>PMID: 15523316</identifier><identifier>CODEN: AHJOA2</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Biological and medical sciences ; Cardiology. Vascular system ; Cardiovascular disease ; Female ; Genes ; Genotype ; Health risk assessment ; Heart attacks ; Humans ; Linkage Disequilibrium ; Male ; Medical sciences ; Myocardial Ischemia - enzymology ; Myocardial Ischemia - genetics ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase Type III ; Pedigree ; Polymorphism, Genetic ; Siblings ; Studies</subject><ispartof>The American heart journal, 2004-11, Vol.148 (5), p.847-851</ispartof><rights>2004 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Elsevier Limited Nov 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c409t-a32484e6155bb4a7b1279e93a6669ae770f4b0991ff19c55787c38f7ed8ca9923</citedby><cites>FETCH-LOGICAL-c409t-a32484e6155bb4a7b1279e93a6669ae770f4b0991ff19c55787c38f7ed8ca9923</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1504468852?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16268712$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15523316$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Spence, Mark S.</creatorcontrib><creatorcontrib>McGlinchey, Paul G.</creatorcontrib><creatorcontrib>Patterson, Chris C.</creatorcontrib><creatorcontrib>Allen, Adrian R.</creatorcontrib><creatorcontrib>Murphy, Gillian</creatorcontrib><creatorcontrib>Bayraktutan, Ulvi</creatorcontrib><creatorcontrib>Fogarty, Damian G.</creatorcontrib><creatorcontrib>Evans, Alun E.</creatorcontrib><creatorcontrib>McKeown, Pascal P.</creatorcontrib><title>Endothelial nitric oxide synthase gene polymorphism and ischemic heart disease</title><title>The American heart journal</title><addtitle>Am Heart J</addtitle><description>Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process underlying IHD. Endothelial NO is synthesized from the amino acid
l-arginine by the endothelial isoform of NO synthase (eNOS). Thus, polymorphisms of the
eNOS gene, by altering production of NO within the vascular endothelium, are potential risk factors for IHD. Several groups have investigated the role of the G894T polymorphism of the
eNOS gene in IHD by using case-control association studies; however, its role is unclear because of contradictory results from these studies. We applied family-based association tests to investigate the role of this polymorphism in IHD in a well-defined Irish population.
A total of 1023 individuals from 388 families (discordant sibships and parent-offspring trios) were recruited. Linkage disequilibrium between the polymorphism and IHD was tested for by using the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test.
Both the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test analyses found no statistically significant excess transmission of either allele to affected individuals (
P = .57 and
P = .38, respectively).
Using robust family-based association tests specifically designed for the study of complex diseases, we found no evidence that the G894T polymorphism of the
eNOS gene has a significant role in the development of IHD in our population.</description><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Female</subject><subject>Genes</subject><subject>Genotype</subject><subject>Health risk assessment</subject><subject>Heart attacks</subject><subject>Humans</subject><subject>Linkage Disequilibrium</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Ischemia - enzymology</subject><subject>Myocardial Ischemia - genetics</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Pedigree</subject><subject>Polymorphism, Genetic</subject><subject>Siblings</subject><subject>Studies</subject><issn>0002-8703</issn><issn>1097-6744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kE2L1TAUhoMozp3RH-BGCqK71pM2n7iSYRyFQTe6Dml6alPa5Jr0ivffm8u9MODC1SHwnPe8eQh5RaGhQMX7ubHT3LQArAHeANVPyI6ClrWQjD0lOwBoayWhuyLXOc_lKVolnpMrynnbdVTsyNe7MMRtwsXbpQp-S95V8Y8fsMrHsE02Y_UTA1b7uBzXmPaTz2tlw1D57CZcCz2hTVs1-IwFfkGejXbJ-PIyb8iPT3ffbz_XD9_uv9x-fKgdA73VtmuZYihKj75nVva0lRp1Z4UQ2qKUMLIetKbjSLXjXCrpOjVKHJSzWrfdDXl3zt2n-OuAeTNrKYTLYgPGQzaifFoz4AV88w84x0MKpZuhHBgTSvFTHD1TLsWcE45mn_xq09FQMCfVZjZFtTmpNsBNUV12Xl-SD_2Kw-PGxW0B3l4Am51dxmSD8_mRE61Qkp6OfzhzWIT99phMdh6Dw8EndJsZov9Pjb8xlJqr</recordid><startdate>20041101</startdate><enddate>20041101</enddate><creator>Spence, Mark S.</creator><creator>McGlinchey, Paul G.</creator><creator>Patterson, Chris C.</creator><creator>Allen, Adrian R.</creator><creator>Murphy, Gillian</creator><creator>Bayraktutan, Ulvi</creator><creator>Fogarty, Damian G.</creator><creator>Evans, Alun E.</creator><creator>McKeown, Pascal P.</creator><general>Mosby, Inc</general><general>Elsevier</general><general>Elsevier Limited</general><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>3V.</scope><scope>7QO</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20041101</creationdate><title>Endothelial nitric oxide synthase gene polymorphism and ischemic heart disease</title><author>Spence, Mark S. ; McGlinchey, Paul G. ; Patterson, Chris C. ; Allen, Adrian R. ; Murphy, Gillian ; Bayraktutan, Ulvi ; Fogarty, Damian G. ; Evans, Alun E. ; McKeown, Pascal P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-a32484e6155bb4a7b1279e93a6669ae770f4b0991ff19c55787c38f7ed8ca9923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Female</topic><topic>Genes</topic><topic>Genotype</topic><topic>Health risk assessment</topic><topic>Heart attacks</topic><topic>Humans</topic><topic>Linkage Disequilibrium</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Ischemia - enzymology</topic><topic>Myocardial Ischemia - genetics</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Pedigree</topic><topic>Polymorphism, Genetic</topic><topic>Siblings</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Spence, Mark S.</creatorcontrib><creatorcontrib>McGlinchey, Paul G.</creatorcontrib><creatorcontrib>Patterson, Chris C.</creatorcontrib><creatorcontrib>Allen, Adrian R.</creatorcontrib><creatorcontrib>Murphy, Gillian</creatorcontrib><creatorcontrib>Bayraktutan, Ulvi</creatorcontrib><creatorcontrib>Fogarty, Damian G.</creatorcontrib><creatorcontrib>Evans, Alun E.</creatorcontrib><creatorcontrib>McKeown, Pascal P.</creatorcontrib><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>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Healthcare Administration Database (Alumni)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The American heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Spence, Mark S.</au><au>McGlinchey, Paul G.</au><au>Patterson, Chris C.</au><au>Allen, Adrian R.</au><au>Murphy, Gillian</au><au>Bayraktutan, Ulvi</au><au>Fogarty, Damian G.</au><au>Evans, Alun E.</au><au>McKeown, Pascal P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endothelial nitric oxide synthase gene polymorphism and ischemic heart disease</atitle><jtitle>The American heart journal</jtitle><addtitle>Am Heart J</addtitle><date>2004-11-01</date><risdate>2004</risdate><volume>148</volume><issue>5</issue><spage>847</spage><epage>851</epage><pages>847-851</pages><issn>0002-8703</issn><eissn>1097-6744</eissn><coden>AHJOA2</coden><abstract>Ischemic heart disease (IHD), the leading cause of death worldwide, is a multifactorial disease arising from the complex interplay of genetic and environmental factors. There is considerable evidence that nitric oxide (NO) plays an important role in protecting against atherosclerosis, the process underlying IHD. Endothelial NO is synthesized from the amino acid
l-arginine by the endothelial isoform of NO synthase (eNOS). Thus, polymorphisms of the
eNOS gene, by altering production of NO within the vascular endothelium, are potential risk factors for IHD. Several groups have investigated the role of the G894T polymorphism of the
eNOS gene in IHD by using case-control association studies; however, its role is unclear because of contradictory results from these studies. We applied family-based association tests to investigate the role of this polymorphism in IHD in a well-defined Irish population.
A total of 1023 individuals from 388 families (discordant sibships and parent-offspring trios) were recruited. Linkage disequilibrium between the polymorphism and IHD was tested for by using the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test.
Both the combined transmission disequilibrium test/sib–transmission disequilibrium test and pedigree disequilibrium test analyses found no statistically significant excess transmission of either allele to affected individuals (
P = .57 and
P = .38, respectively).
Using robust family-based association tests specifically designed for the study of complex diseases, we found no evidence that the G894T polymorphism of the
eNOS gene has a significant role in the development of IHD in our population.</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>15523316</pmid><doi>10.1016/j.ahj.2004.05.019</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Access via ScienceDirect (Elsevier); ProQuest Central UK/Ireland |
| subjects | Biological and medical sciences Cardiology. Vascular system Cardiovascular disease Female Genes Genotype Health risk assessment Heart attacks Humans Linkage Disequilibrium Male Medical sciences Myocardial Ischemia - enzymology Myocardial Ischemia - genetics Nitric Oxide Synthase - genetics Nitric Oxide Synthase Type III Pedigree Polymorphism, Genetic Siblings Studies |
| title | Endothelial nitric oxide synthase gene polymorphism and ischemic heart disease |
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