{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T03:52:02Z","timestamp":1791345122055,"version":"4.3.1"},"reference-count":33,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2010,2,11]],"date-time":"2010-02-11T00:00:00Z","timestamp":1265846400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/2.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["BMC Med Genet"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n          <jats:sec>\n            <jats:title>Background<\/jats:title>\n            <jats:p>Several studies have shown overexpression of leptin in microarray experiments in pre-eclampsia (PE) and in hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome. We decided to study four leptin receptor (<jats:italic>LEPR<\/jats:italic>) SNP polymorphisms in HELLP syndrome patients by using quantitative real-time PCR and melting curve analysis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>DNA was isolated from blood samples from 83 normotensive pregnant women and 75 HELLP syndrome patients. Four SNPs, <jats:italic>LEPR c.326A&gt;G<\/jats:italic> (K109), <jats:italic>LEPR c.668A&gt;G<\/jats:italic> (Q223R), <jats:italic>LEPR c.1968G&gt;C<\/jats:italic> (K656N) and <jats:italic>LEPR c.3024A&gt;G<\/jats:italic> (S1008) were determined by quantitative real-time PCR and melting curve analysis. Investigators were blinded to clinical outcomes.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>\n              <jats:italic>LEPR c.326A&gt;G<\/jats:italic>, <jats:italic>LEPR c.668A&gt;G<\/jats:italic>, <jats:italic>LEPR c.1968G&gt;C<\/jats:italic> and <jats:italic>LEPR c.3024A&gt;G<\/jats:italic> allele, genotype and haplotype polymorphisms were not different in HELLP syndrome patients and normotensive healthy pregnants. There were strong linkage disequilibrium (LD) between loci <jats:italic>c.326A&gt;G<\/jats:italic> and <jats:italic>c.6687A&gt;G<\/jats:italic> (D' = 0.974), and <jats:italic>c.668A&gt;G<\/jats:italic> and <jats:italic>c.1968G&gt;C<\/jats:italic> (D' = 0.934), and <jats:italic>c.326A&gt;G<\/jats:italic> and <jats:italic>c.1968G&gt;C<\/jats:italic> (D' = 0.885), and <jats:italic>c.1968G&gt;C<\/jats:italic> and <jats:italic>c.3024A&gt;G<\/jats:italic> (D' = 1.0). However, linkages of <jats:italic>c.3024A&gt;G<\/jats:italic> with <jats:italic>c.668A&gt;G<\/jats:italic> (D' = 0.111) and <jats:italic>c.326A&gt;G<\/jats:italic> (D' = 0.398) were weak. The Hardy-Weinberg equilibrium was observed for all polymorphisms. However the <jats:italic>LEPR c.326A&gt;G AG<\/jats:italic> genotype was twice more frequent and the (AG AG GG AG) haplotype was three times more frequent in HELLP syndrome patients. The introduced quantitative real-time PCR combined with melting curve analysis is a fast and reliable method for the determination of <jats:italic>LEPR<\/jats:italic> SNPs.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>Although certain <jats:italic>LEPR<\/jats:italic> haplotypes are more frequent in HELLP syndrome, we conclude that there is no compelling evidence that the four studied <jats:italic>LEPR<\/jats:italic> SNP polymorphisms associated with the development of HELLP syndrome.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2350-11-25","type":"journal-article","created":{"date-parts":[[2010,2,11]],"date-time":"2010-02-11T19:15:18Z","timestamp":1265915718000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Leptin receptor (LEPR) SNP polymorphisms in HELLP syndrome patients determined by quantitative real-time PCR and melting curve analysis"],"prefix":"10.1186","volume":"11","author":[{"given":"Tibor","family":"V\u00e1rkonyi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Levente","family":"L\u00e1z\u00e1r","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Attila","family":"Molvarec","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N\u00e1ndor G\u00e1bor","family":"Than","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"J\u00e1nos","family":"Rig\u00f3","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B\u00e1lint","family":"Nagy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,2,11]]},"reference":[{"key":"586_CR1","doi-asserted-by":"publisher","first-page":"1263","DOI":"10.1016\/0092-8674(95)90151-5","volume":"83","author":"LA Tartaglia","year":"1995","unstructured":"Tartaglia LA, Dembski M, Weng X, Deng N, Culpepper J, Devos R: Identification and expression cloning of a leptin receptor, OB-R. 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