ORCID Profile
0000-0001-8281-2878
Current Organisation
University of Western Australia
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Elsevier BV
Date: 06-2021
Publisher: Wiley
Date: 06-02-2020
DOI: 10.1002/JGH3.12306
Publisher: Elsevier BV
Date: 09-2017
DOI: 10.1016/J.PLACENTA.2017.06.009
Abstract: A significant proportion of children born preterm will experience some level of neurodevelopmental impairment. Changes in placental function have been observed with many antenatal conditions that are risk factors for preterm birth and/or poor neurodevelopment including fetal growth restriction and in-utero inflammation. This review will highlight placental factors that have been studied to understand the underlying mechanisms and identify biomarkers that lead to poor child neurodevelopmental outcomes. These include changes in gross morphological and histopathological structure and the placental inflammatory response to prenatal infection. Further, we will describe the placenta's role as both a barrier to maternally-derived bioactive substances critical for normal fetal brain development, such as cortisol, and a source of neuroactive steroids and neurotrophins known to have critical functions in neuronal proliferation, axonal growth, myelination and the regulation of apoptosis. Finally, emerging data supporting the potential utility of novel placental biomarkers in the early prediction of poor neurodevelopmental outcome in infants born both preterm and term will be discussed. These include the assessment of genetic variants (e.g. single nucleotide polymorphisms in placental tissue) and epigenetic biomarkers (e.g. placental microRNAs and placental DNA methylation). With the placenta the key tissue regulating the fetal environment, integration of observed changes in placental function with genetic and epigenetic variations may advance our ability to predict future infant health. Ultimately, this may facilitate targeted allocation of health resources with the aim of improving lifelong neurodevelopmental capability.
Publisher: Springer International Publishing
Date: 2020
Publisher: Springer Science and Business Media LLC
Date: 04-10-2018
Publisher: Physicians Postgraduate Press, Inc
Date: 20-11-2018
DOI: 10.4088/JCP.18M12472
Publisher: Wiley
Date: 14-09-2022
Abstract: To test the equivalence of two doses of intravenous iron (ferric carboxymaltose) in pregnancy. Parallel, two‐arm equivalence randomised controlled trial with an equivalence margin of 5%. Single centre in Australia. 278 pregnant women with iron deficiency. Participants received either 500 mg ( n = 152) or 1000 mg ( n = 126) of intravenous ferric carboxymaltose in the second or third trimester. The proportion of participants requiring additional intravenous iron (500 mg) to achieve and maintain ferritin microg/L (diagnostic threshold for iron deficiency) at 4 weeks post‐infusion, and at 6 weeks, and 3‐, 6‐ and 12‐months postpartum. Secondary endpoints included repeat infusion rate, iron status, birth and safety outcomes. The two doses were not equivalent within a 5% margin at any time point. At 4 weeks post infusion, 26/73 (36%) participants required a repeat infusion in the 500‐mg group compared with 5/67 (8%) in the 1000‐mg group: difference in proportions, 0.283 (95% confidence interval [CI] 0.177–0.389). Overall, participants in the 500‐mg arm received twice the repeat infusion rate (0.81 [SD = 0.824] versus 0.40 [SD = 0.69], rate ratio 2.05, 95% CI 1.45–2.91). Administration of 1000 mg ferric carboxymaltose in pregnancy maintains iron stores and reduces the need for repeat infusions. A 500‐ mg dose requires ongoing monitoring to ensure adequate iron stores are reached and sustained.
Location: Australia
No related grants have been discovered for Natalie Aboustate.