{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T00:05:49Z","timestamp":1715558749796},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1996,6,15]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            Recently we found that the deletion (D) allele of the insertion\/deletion (I\/D) polymorphism of the ACE gene in 404 children was associated with a history of coronary artery disease (CAD) in their grandparents. This led us to explore polymorphisms in other genes of the renin-angiotensin system in this same population.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            We determined the genotypes for three microsatellite markers located near or in the angiotensinogen, angiotensin II (type-1) receptor, and renin genes in the children and related the allele frequencies to grandparental CAD. We found a significant association between the angiotensinogen marker in children and grandparental CAD (\u03c7\n            <jats:sup>2<\/jats:sup>\n            =42.2,\n            <jats:italic>P<\/jats:italic>\n            =.00001) with these children having an excess of the 125-bp and 129-bp alleles (odds ratio, 2.5; 95% confidence interval, 1.7 to 3.7). Greatest grandparental risk was when their grandchildren had the 125-bp\/125-bp, 129-bp\/129-bp, or 125-bp\/129-bp genotypes (odds ratio, 7.75; 95% confidence interval, 2.2 to 27). There was no association between the microsatellites at either the angiotensin II (type-1) receptor (\n            <jats:italic>P<\/jats:italic>\n            =.8) or renin (\n            <jats:italic>P<\/jats:italic>\n            =.2) genes in children and grandparental CAD and none between the angiotensinogen and ACE polymorphisms in relation to CAD family history.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            This study identifies a significant association between an angiotensinogen marker in children and grandparental CAD. There was no association between the microsatellites at either the angiotensin II (type-1) receptor or renin genes and CAD in this population. We conclude that the angiotensinogen polymorphism as well as the ACE polymorphism may explain a part of the risk related to a family history of CAD.\n          <\/jats:p>","DOI":"10.1161\/01.cir.93.12.2092","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"2092-2096","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Association Between an Angiotensinogen Microsatellite Marker in Children and Coronary Events in Their Grandparents"],"prefix":"10.1161","volume":"93","author":[{"given":"Renee F.","family":"Badenhop","sequence":"first","affiliation":[{"name":"From the Department of Cardiovascular Medicine, University of New South Wales\/Prince Henry Hospital, Sydney, Australia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xing Li","family":"Wang","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, University of New South Wales\/Prince Henry Hospital, Sydney, Australia."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David E.L.","family":"Wilcken","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, University of New South Wales\/Prince Henry Hospital, Sydney, Australia."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/0002-8703(92)90635-9"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.91.6.1655"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/359641a0"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(93)91075-W"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.1993.tb03903.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199503163321103"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(93)92064-Z"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/0140-6736(93)92061-W"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199406093302302"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.89.3.8124834"},{"key":"e_1_3_2_11_2","doi-asserted-by":"crossref","unstructured":"Dzau VJ. 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