ORCID Profile
0000-0001-5113-0700
Current Organisation
The University of Auckland
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Publisher: Elsevier BV
Date: 04-2010
DOI: 10.1016/J.AJOG.2010.01.025
Abstract: The objective of the investigation was to study placental transfer and conjugation of bisphenol A (BPA) across the human placenta. Human placentae obtained from healthy term singleton pregnancies were utilized in a dual recirculating model of ex vivo placental perfusion. Seven placentae were perfused with BPA (10 ng/mL) added to the maternal perfusate for 180 minutes. Antipyrine and fluorescein isothiocyanate dextran were used as positive and negative controls, respectively, to validate integrity of the circuits. Concentrations of BPA and its conjugates were determined by liquid chromatography-mass spectrometry. The transfer percentage for antipyrine and BPA were 25.5 +/- 1.13% and 27.0 +/- 1.88%, respectively, and the transfer index for BPA was 1.1 +/- 0.09 after 180 minutes of perfusion. Only 3.2 +/- 1.6% of BPA in the fetal compartment was in the conjugated form. Bisphenol A at low environmentally relevant levels can transfer across the human placenta, mainly in active unconjugated form.
Publisher: Elsevier BV
Date: 04-2012
DOI: 10.1016/J.PLACENTA.2011.12.018
Abstract: Gangliosides are structural and functional glycosphingolipids, considered to have important roles in neuronal development in fetal and neonatal development and in memory formation. In this report, we have investigated the ability of bovine milk-derived gangliosides GM3 and GD3 to cross the human placenta. We have employed the ex-vivo model of dually-perfused isolated human placental lobules. There was significant uptake of both GD3 and GM3 from the maternal perfusate. There was significant increase of GM3 in the fetal side and a non-statistically significant trend for GD3 to increase on the fetal side. Hence an apparent preference for GM3 release into fetal circulation. We suggest that gangliosides consumed by the mother enter her circulation, can be transferred across the placenta and may be available to the developing fetus for building neural connections.
Publisher: Springer Science and Business Media LLC
Date: 20-07-2018
DOI: 10.1038/S41525-018-0058-3
Abstract: Pancreatic neuroendocrine tumors (pNETs) are uncommon cancers arising from pancreatic islet cells. Here we report the analysis of gene mutation, copy number, and RNA expression of 57 sporadic well-differentiated pNETs. pNET genomes are dominated by aneuploidy, leading to concordant changes in RNA expression at the level of whole chromosomes and chromosome segments. We observed two distinct patterns of somatic pNET aneuploidy that are associated with tumor pathology and patient prognosis. Approximately 26% of the patients in this series had pNETs with genomes characterized by recurrent loss of heterozygosity (LoH) of 10 specific chromosomes, accompanied by bi-allelic MEN1 inactivation and generally poor clinical outcome. Another ~40% of patients had pNETs that lacked this recurrent LoH pattern but had chromosome 11 LoH, bi-allelic MEN1 inactivation, and universally good clinical outcome. The somatic aneuploidy allowed pathogenic germline variants (e.g., ATM ) to be expressed unopposed, with RNA expression patterns showing inactivation of downstream tumor suppressor pathways. No prognostic associations were found with tumor morphology, single gene mutation, or expression of RNAs reflecting the activity of immune, differentiation, proliferative or tumor suppressor pathways. In pNETs, single gene mutations appear to be less important than aneuploidy, with MEN1 the only statistically significant recurrently mutated driver gene. In addition, only one pNET in the series had clearly actionable single nucleotide variants (SNVs) (in PTEN and FLCN ) confirmed by corroborating RNA expression changes. The two clinically relevant patterns of LoH described here define a novel oncogenic mechanism and a plausible route to genomic precision oncology for this tumor type.
Publisher: Informa UK Limited
Date: 08-08-2022
No related grants have been discovered for Kimiora Henare.