<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-02T16:17:26Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/35670" metadataPrefix="qdc">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/35670</identifier><datestamp>2026-02-03T11:07:32Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37953</setSpec></header><metadata><qdc:qualifieddc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:qdc="http://dspace.org/qualifieddc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://purl.org/dc/elements/1.1/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dc.xsd http://purl.org/dc/terms/ http://dublincore.org/schemas/xmls/qdc/2006/01/06/dcterms.xsd http://dspace.org/qualifieddc/ http://www.ukoln.ac.uk/metadata/dcmi/xmlschema/qualifieddc.xsd">
   <dc:title>Identification of Reference Genes for Quantitative RT-PCR in Ascending Aortic Aneurysms.</dc:title>
   <dc:creator>Henn, Dominic</dc:creator>
   <dc:creator>Bandner-Risch, Doris</dc:creator>
   <dc:creator>Perttunen, Hilja</dc:creator>
   <dc:creator>Schmied, Wolfram</dc:creator>
   <dc:creator>Porras-Martín, Carlos</dc:creator>
   <dc:creator>Rodríguez-Losada, Noela</dc:creator>
   <dc:creator>Schäfers, Hans-Joachim</dc:creator>
   <dc:subject>Aneurismas aórticos</dc:subject>
   <dcterms:abstract>Hypertension and congenital aortic valve malformations are frequent causes of ascending aortic aneurysms. The molecular&#xd;
mechanisms of aneurysm formation under these circumstances are not well understood. Reference genes for gene activity&#xd;
studies in aortic tissue that are not influenced by aortic valve morphology and its hemodynamic consequences, aortic&#xd;
dilatation, hypertension, or antihypertensive medication are not available so far. This study determines genes in ascending&#xd;
aortic tissue that are independent of these parameters. Tissue specimens from dilated and undilated ascending aortas were&#xd;
obtained from 60 patients (age #70 years) with different morphologies of the aortic valve (tricuspid undilated n = 24,&#xd;
dilated n = 11; bicuspid undilated n = 6, dilated n = 15; unicuspid dilated n = 4). Of the studied individuals, 36 had&#xd;
hypertension, and 31 received ACE inhibitors or AT1 receptor antagonists. The specimens were obtained intraoperatively&#xd;
from the wall of the ascending aorta. We analyzed the expression levels of 32 candidate reference genes by quantitative RTPCR (RT-qPCR). Differential expression levels were assessed by parametric statistics. The expression analysis of these 32&#xd;
genes by RT-qPCR showed that EIF2B1, ELF1, and PPIA remained constant in their expression levels in the different&#xd;
specimen groups, thus being insensitive to aortic valve morphology, aortic dilatation, hypertension, and medication with&#xd;
ACE inhibitors or AT1 receptor antagonists. Unlike many other commonly used reference genes, the genes EIF2B1, ELF1, and&#xd;
PPIA are neither confounded by aortic comorbidities nor by antihypertensive medication and therefore are most suitable for&#xd;
gene expression analysis of ascending aortic tissue.</dcterms:abstract>
   <dcterms:dateAccepted>2024-12-13T11:43:57Z</dcterms:dateAccepted>
   <dcterms:available>2024-12-13T11:43:57Z</dcterms:available>
   <dcterms:created>2024-12-13T11:43:57Z</dcterms:created>
   <dcterms:issued>2013</dcterms:issued>
   <dc:type>journal article</dc:type>
   <dc:identifier>https://hdl.handle.net/10630/35670</dc:identifier>
   <dc:identifier>10.1371/journal.pone.0054132</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:rights>http://creativecommons.org/licenses/by/4.0/</dc:rights>
   <dc:rights>open access</dc:rights>
   <dc:rights>Attribution 4.0 Internacional</dc:rights>
   <dc:publisher>PLOS</dc:publisher>
</qdc:qualifieddc>
</metadata></record></GetRecord></OAI-PMH>