scholarly journals VP41.01: Assessment of fetal brain vascularisation in fetal growth restriction using 3D power angiography

2020 ◽  
Vol 56 (S1) ◽  
pp. 237-237
Author(s):  
A. Rossi ◽  
C. Braghin ◽  
F. Benazzi ◽  
M. Salemi ◽  
A. Azzena
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Fetal Brain ◽  
Growth Restriction

scholarly journals Quantification of fetal organ sparing in maternal low-protein dietary models

2021 ◽  
Vol 6 ◽  
pp. 218
Author(s):  
Patricia Serpente ◽  
Ying Zhang ◽  
Eva Islimye ◽  
Sarah Hart-Johnson ◽  
Alex P. Gould
Keyword(s):  
Protein Content ◽  
Fetal Growth ◽  
Dietary Protein ◽  
Fetal Growth Restriction ◽  
Fetal Brain ◽  
Growth Restriction ◽  
Maternal Malnutrition ◽  
Fetal Organ ◽  
Low Protein ◽  
Organ Sparing

Background: Maternal malnutrition can lead to fetal growth restriction. This is often associated with organ sparing and long-lasting physiological dysfunctions during adulthood, although the underlying mechanisms are not yet well understood. Methods: Low protein (LP) dietary models in C57BL/6J mice were used to investigate the proximal effects of maternal malnutrition on fetal organ weights and organ sparing at embryonic day 18.5 (E18.5). Results:  Maternal 8% LP diet induced strikingly different degrees of fetal growth restriction in different animal facilities, but adjustment of dietary protein content allowed similar fetal body masses to be obtained. A maternal LP diet that restricted fetal body mass by 40% did not decrease fetal brain mass to the same extent, reflecting positive growth sparing of this organ. Under these conditions, fetal pancreas and liver mass decreased by 60-70%, indicative of negative organ sparing. A series of dietary swaps between LP and standard diets showed that the liver is capable of efficient catch-up growth from as late as E14.5 whereas, after E10.5, the pancreas is not. Conclusions: This study highlights that the reproducibility of LP fetal growth restriction studies between laboratories can be improved by careful calibration of maternal dietary protein content. LP diets that induce 30-40% restriction of prenatal growth provide a good model for fetal organ sparing. For the liver, recovery of growth following protein restriction is efficient throughout fetal development but, for the pancreas, transient LP exposures spanning the progenitor expansion phase lead to an irreversible fetal growth deficit.

scholarly journals OP17.08: Assessment of fetal brain volume by tridimensional ultrasound in fetal growth restriction

2012 ◽  
Vol 40 (S1) ◽  
pp. 107-107
Author(s):  
A. R. Caetano ◽  
A. P. Zamarian ◽  
R. Cavalcante ◽  
D. Soares ◽  
P. M. Nowak ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Brain Volume ◽  
Fetal Brain ◽  
Growth Restriction

scholarly journals Altered neurodevelopmental DNA methylation status after fetal growth restriction with brain-sparing

2021 ◽  
pp. 1-12
Author(s):  
Anne E. Richter ◽  
Iris Bekkering-Bauer ◽  
Rikst Nynke Verkaik-Schakel ◽  
Mariëtte Leeuwerke ◽  
Jozien C. Tanis ◽  
...  
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Child Behavior Checklist ◽  
Epigenetic Modification ◽  
Methylation Status ◽  
Neurodevelopmental Outcome ◽  
Fetal Brain ◽  
Growth Restriction ◽  
Tyrosine Kinase Receptor ◽  
Response Element

Abstract It is under debate how preferential perfusion of the brain (brain-sparing) in fetal growth restriction (FGR) relates to long-term neurodevelopmental outcome. Epigenetic modification of neurotrophic genes by altered fetal oxygenation may be involved. To explore this theory, we performed a follow-up study of 21 FGR children, in whom we prospectively measured the prenatal cerebroplacental ratio (CPR) with Doppler sonography. At 4 years of age, we tested their neurodevelopmental outcome using the Wechsler Preschool and Primary Scale of Intelligence, the Child Behavior Checklist, and the Behavior Rating Inventory of Executive Function. In addition, we collected their buccal DNA to determine the methylation status at predefined genetic regions within the genes hypoxia-inducible factor-1 alpha (HIF1A), vascular endothelial growth factor A (VEGFA), erythropoietin (EPO), EPO-receptor (EPOR), brain-derived neurotrophic factor (BDNF), and neurotrophic tyrosine kinase, receptor, type 2 (NTRK2) by pyrosequencing. We found that FGR children with fetal brain-sparing (CPR <1, n = 8) demonstrated a trend (0.05 < p < 0.1) toward hypermethylation of HIF1A and VEGFA at their hypoxia-response element (HRE) compared with FGR children without fetal brain-sparing. Moreover, in cases with fetal brain-sparing, we observed statistically significant hypermethylation at a binding site for cyclic adenosine monophophate response element binding protein (CREB) of BDNF promoter exon 4 and hypomethylation at an HRE located within the NTRK2 promoter (both p <0.05). Hypermethylation of VEGFA was associated with a poorer Performance Intelligence Quotient, while hypermethylation of BDNF was associated with better inhibitory self-control (both p <0.05). These results led us to formulate the hypothesis that early oxygen-dependent epigenetic alterations due to hemodynamic alterations in FGR may be associated with altered neurodevelopmental outcome in later life. We recommend further studies to test this hypothesis.

scholarly journals Clinical and pathogenetic variants of fetal growth restriction with different periods of manifestation

2021 ◽  
pp. 54-65
Author(s):  
I. S. Lipatov ◽  
Yu. V. Tezikov ◽  
M. S. Amosov ◽  
E. M. Zumorina
Keyword(s):  
Fetal Growth ◽  
Fetal Growth Restriction ◽  
Clinical Laboratory ◽  
Growth Parameters ◽  
Human Life ◽  
Clinical Manifestations ◽  
Fetal Brain ◽  
Growth Restriction ◽  
Growth Potential ◽  
Obstetric Management

The article presents data on the clinical and pathogenetic variants of fetal growth restriction (FGR). FGR is one of the typical clinical manifestations of large obstetric syndromes, is associated with a high perinatal morbidity and has a significant impact on the quality and duration of human life. The emphasis is made on the differences in pathogenesis, the features of prediction, diagnosis, obstetric management and the assessment of perinatal outcomes in the early and late phenotype of the FGR. The review includes materials from domestic and foreign scientific literature that found in eLibrary and PubMed on this topic and published for the last 10 years. This article discusses the role of the formation of the embryo(feto)placental system under the influence of existing periconceptional risk factors in the implementation of various phenotypes of FGR. An analysis of the literature shows that the fetal growth potential, which genetically and epigenetically determined, changes during pregnancydepending on maternal, placental and fetal factors, which ultimately determine the final weight-growth parameters of the newborn. The issues of informativeness of clinical, laboratory and instrumental predictors, diagnostic criteria, the choice of rational obstetric management in case of FGR of various periods of manifestation are discussed in this article. Convincing data on the perinatal and long-term consequences of intrauterine growth restriction are presented. The pathogenetic variant of FGR determines the features of the functioning of the immune system, has a significant impact on the programming of metabolic and endocrine processes, the formation of fetal brain structures. Identification of pregnant women at risk for the development of FGR of various periods of manifestation, timely diagnosis, selection of the timing and method of delivery should correspond to the main directions of the "4P-model" of modern medicine and represent an integral predictive, preventive and personalized system of examination and observation based on evidence-based medicine data and the requirements of practical obstetrics and perinatology.

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