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Mary E. Wlodek

Researcher at University of Melbourne

Publications -  202
Citations -  4893

Mary E. Wlodek is an academic researcher from University of Melbourne. The author has contributed to research in topics: Offspring & Pregnancy. The author has an hindex of 35, co-authored 189 publications receiving 4251 citations. Previous affiliations of Mary E. Wlodek include University of Western Australia & St. Vincent's Institute of Medical Research.

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Exercise initiated during pregnancy in rats born growth restricted alters placental mTOR and nutrient transporter expression.

TL;DR: Maternal exercise during pregnancy differentially regulated mTOR and nutrient transporters in a diet‐ and sex‐specific manner, which likely aimed to improve late gestational placental growth and neonatal survival.
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Uteroplacental insufficiency in rats induces renal apoptosis and delays nephrogenesis completion

TL;DR: This study aimed to determine whether the reduced nephron endowment in Restricted offspring is due to delayed glomerular formation and dysregulation of renal genes regulating branching morphogenesis, apoptosis or leptin signalling and to investigate whether cross‐fostering growth‐restricted offspring onto Control mothers could improveglomerular maturation and restore renal gene abundance.
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A Systematic Review of Collection and Analysis of Human Milk for Macronutrient Composition

TL;DR: This review describes the first systematic evaluation of sampling methodologies used in studies reporting HM composition and highlights the wide range of collection methods applied in the field.
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Effect of pregnancy for females born small on later life metabolic disease risk.

TL;DR: The data suggests that pregnancy ameliorates the enhanced peripheral insulin sensitivity in growth restricted females and has deleterious effects for hepatic insulin sensitivity, regardless of maternal birth weight.
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Intrauterine Growth Restriction Alters the Postnatal Development of the Rat Cerebellum.

TL;DR: Damage to the migratory scaffold (Bergmann glial fibers) and alterations in the genes that influence migration (Trop2 and Astn1) may underlie the deficits in postnatal cerebellar development following IUGR.