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Statements

Subject Item
n2:RIV%2F00209805%3A_____%2F14%3A%230000592%21RIV15-MSM-00209805
rdf:type
skos:Concept n13:Vysledek
rdfs:seeAlso
https://www.novapublishers.com/catalog/product_info.php?products_id=48036&osCsid=b
dcterms:description
The ftal origin of civilization disorders concept favors the idea of prenatal programming of adult age diseases such as hypertension. Patients with advanced chronic heart failure or other and-stage diseases often have increased AngII levels and cachexia, and angiotensin-converting enzyme (ACE) inhibitor treatment improves weight loss. In this cross-sectional association study, we investigated possible associations of ACE ID and AGT M235T polymorphisms with occurence of idiopathic, non-syndromic intrauterine growth restriction (IUGR) and/or preeclampsia. No significant differences in single genotype distributions or allelic frequencies of both ACE ID and AGT M235T polymorphisms were observed between studied cohorts. However, the double heterozygosity (ID/MT) was significantly associated with lower prevalence of IUGR. The single genotypes for ACE ID or AGT M235T genes do not seem to increase the risk of preeclampsia or IUGR in pregnanacy. Despite the small sample size, the present study supports the idea of protective effect of combined heterozygotes (ID/MT) against the IUGR development risk. The ftal origin of civilization disorders concept favors the idea of prenatal programming of adult age diseases such as hypertension. Patients with advanced chronic heart failure or other and-stage diseases often have increased AngII levels and cachexia, and angiotensin-converting enzyme (ACE) inhibitor treatment improves weight loss. In this cross-sectional association study, we investigated possible associations of ACE ID and AGT M235T polymorphisms with occurence of idiopathic, non-syndromic intrauterine growth restriction (IUGR) and/or preeclampsia. No significant differences in single genotype distributions or allelic frequencies of both ACE ID and AGT M235T polymorphisms were observed between studied cohorts. However, the double heterozygosity (ID/MT) was significantly associated with lower prevalence of IUGR. The single genotypes for ACE ID or AGT M235T genes do not seem to increase the risk of preeclampsia or IUGR in pregnanacy. Despite the small sample size, the present study supports the idea of protective effect of combined heterozygotes (ID/MT) against the IUGR development risk.
dcterms:title
Double heterozygotes for ACE ID and AGT M235t polymorphisms are in lower risk of developing non-syndromic intrauterine growth restriction: a possible role of appetite? Double heterozygotes for ACE ID and AGT M235t polymorphisms are in lower risk of developing non-syndromic intrauterine growth restriction: a possible role of appetite?
skos:prefLabel
Double heterozygotes for ACE ID and AGT M235t polymorphisms are in lower risk of developing non-syndromic intrauterine growth restriction: a possible role of appetite? Double heterozygotes for ACE ID and AGT M235t polymorphisms are in lower risk of developing non-syndromic intrauterine growth restriction: a possible role of appetite?
skos:notation
RIV/00209805:_____/14:#0000592!RIV15-MSM-00209805
n3:aktivita
n6:Z n6:P
n3:aktivity
P(ED2.1.00/03.0101), Z(MZ0MOU2005)
n3:dodaniDat
n4:2015
n3:domaciTvurceVysledku
n20:4447719
n3:druhVysledku
n19:C
n3:duvernostUdaju
n9:S
n3:entitaPredkladatele
n15:predkladatel
n3:idSjednocenehoVysledku
12299
n3:idVysledku
RIV/00209805:_____/14:#0000592
n3:jazykVysledku
n16:eng
n3:klicovaSlova
preeclampsia; ACE ID and AGT M235t polymorphisms; pregnancy
n3:klicoveSlovo
n10:preeclampsia n10:pregnancy n10:ACE%20ID%20and%20AGT%20M235t%20polymorphisms
n3:kontrolniKodProRIV
[321E24DC5C6A]
n3:mistoVydani
New York
n3:nazevZdroje
Appetite: regulation, use of stimulants and cultural and biological influences
n3:obor
n18:FD
n3:pocetDomacichTvurcuVysledku
1
n3:pocetStranKnihy
228
n3:pocetTvurcuVysledku
4
n3:projekt
n8:ED2.1.00%2F03.0101
n3:rokUplatneniVysledku
n4:2014
n3:tvurceVysledku
Bienertová-Vašků, Julie
n3:zamer
n17:MZ0MOU2005
s:numberOfPages
11
n12:hasPublisher
Nova Science Publishers
n21:isbn
978-1-63117-241-0