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Sara L. Hillman

Researcher at University College London

Publications -  22
Citations -  383

Sara L. Hillman is an academic researcher from University College London. The author has contributed to research in topics: Medicine & Pregnancy. The author has an hindex of 5, co-authored 13 publications receiving 278 citations. Previous affiliations of Sara L. Hillman include University College Hospital.

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Maternal gestational diabetes is associated with genome-wide DNA methylation variation in placenta and cord blood of exposed offspring

TL;DR: Replication studies should integrate genomics and transcriptomics with longitudinal sampling to elucidate stability, determine causality for translation into biomarker and prevention studies, and integrateGenetic variation in foetal tissue may have a mechanistic role in metabolic disease programming through interaction of the pregnancy environment with gene function.
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Novel DNA methylation profiles associated with key gene regulation and transcription pathways in blood and placenta of growth-restricted neonates

TL;DR: DNA from umbilical cord blood of FGR born at term had 839 differentially methylated positions (DMPs) that reached genome-wide significance compared with AGA, and Gene Ontology analysis of DMPs supported their involvement in gene regulation and transcription pathways related to organ development and metabolic function.
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CD161 contributes to prenatal immune suppression of IFNγ-producing PLZF+ T cells.

TL;DR: A fetal-specific program of protective immunity whose dysregulation is associated with fetal and neonatal inflammatory pathologies is revealed.
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Paternal Metabolic and Cardiovascular Risk Factors for Fetal Growth Restriction: A case-control study

TL;DR: Men who recently fathered growth-restricted offspring have preclinical evidence of the insulin resistance syndrome and are more likely to smoke than fathers of normal grown offspring, and paternal lifestyle may influence heritable factors important for fetal growth.
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Placenta-specific Slc38a2/SNAT2 knockdown causes fetal growth restriction in mice.

TL;DR: In this article, the role of placental Slc38a2/SNAT2 deficiency in the development of restricted fetal growth was investigated in mice, and the placenta-specific Slc 38a2 deficiency was found to cause late-onset fetal growth restriction.