Amniotic fluid deficiency and congenital abnormalities both influence fluctuating asymmetry in developing limbs of human deceased fetuses

ten Broek, Clara Mariquita Antoinette; Bots, Jessica; Varela-Lasheras, Irma; Bugiani, Marianna; Galis, Frietson; Van Dongen, Stefan

Publication

Amniotic fluid deficiency and congenital abnormalities both influence fluctuating asymmetry in developing limbs of human deceased fetuses

2013-11-27Journal article

dc.contributor.author	ten Broek, Clara Mariquita Antoinette
dc.contributor.author	Bots, Jessica
dc.contributor.author	Varela-Lasheras, Irma
dc.contributor.author	Bugiani, Marianna
dc.contributor.author	Galis, Frietson
dc.contributor.author	Van Dongen, Stefan
dc.date.accessioned	2015-10-23T12:14:50Z
dc.date.available	2015-10-23T12:14:50Z
dc.date.issued	2013-11-27
dc.description.abstract	Fluctuating asymmetry (FA), as an indirect measure of developmental instability (DI), has been intensively studied for associations with stress and fitness. Patterns, however, appear heterogeneous and the underlying causes remain largely unknown. One aspect that has received relatively little attention in the literature is the consequence of direct mechanical effects on asymmetries. The crucial prerequisite for FA to reflect DI is that environmental conditions on both sides should be identical. This condition may be violated during early human development if amniotic fluid volume is deficient, as the resulting mechanical pressures may increase asymmetries. Indeed, we showed that limb bones of deceased human fetuses exhibited increased asymmetry, when there was not sufficient amniotic fluid (and, thus, space) in the uterine cavity. As amniotic fluid deficiency is known to cause substantial asymmetries and abnormal limb development, these subtle asymmetries are probably at least in part caused by the mechanical pressures. On the other hand, deficiencies in amniotic fluid volume are known to be associated with other congenital abnormalities that may disturb DI. More specifically, urogenital abnormalities can directly affect/reduce amniotic fluid volume. We disentangled the direct mechanical effects on FA from the indirect effects of urogenital abnormalities, the latter presumably representing DI. We discovered that both factors contributed significantly to the increase in FA. However, the direct mechanical effect of uterine pressure, albeit statistically significant, appeared less important than the effects of urogenital abnormalities, with an effect size only two-third as large. We, thus, conclude that correcting for the relevant direct factors allowed for a representative test of the association between DI and stress, and confirmed that fetuses form a suitable model system to increase our understanding in patterns of FA and symmetry development.	pt_PT
dc.description.sponsorship	Research Fund of the University of Antwerp, mobility grant from the Research Foundation – Flanders (FWO).	pt_PT
dc.identifier	10.1371/journal.pone.0081824
dc.identifier.citation	ten Broek CMA, Bots J, Varela-Lasheras I, Bugiani M, Galis F, et al. (2013) Amniotic Fluid Deficiency and Congenital Abnormalities both Influence Fluctuating Asymmetry in Developing Limbs of Human Deceased Fetuses. PLoS ONE 8(11): e81824. doi:10.1371/journal.pone.0081824	pt_PT
dc.identifier.doi	10.1371/journal.pone.0081824
dc.identifier.uri	http://hdl.handle.net/10400.7/435
dc.language.iso	eng	pt_PT
dc.peerreviewed	yes	pt_PT
dc.publisher	PLOS	pt_PT
dc.relation.publisherversion	http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0081824	pt_PT
dc.rights.uri	http://creativecommons.org/licenses/by/4.0/	pt_PT
dc.subject	Amniotic Fluid	pt_PT
dc.subject	Congenital Abnormalities	pt_PT
dc.subject	Fetus	pt_PT
dc.title	Amniotic fluid deficiency and congenital abnormalities both influence fluctuating asymmetry in developing limbs of human deceased fetuses	pt_PT
dc.type	journal article
dspace.entity.type	Publication
oaire.citation.endPage	9	pt_PT
oaire.citation.issue	11	pt_PT
oaire.citation.startPage	1	pt_PT
oaire.citation.title	PLOS One	pt_PT
oaire.citation.volume	8	pt_PT
rcaap.rights	openAccess	pt_PT
rcaap.type	article	pt_PT