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Eric Jauniaux

Researcher at University College London

Publications -  521
Citations -  28088

Eric Jauniaux is an academic researcher from University College London. The author has contributed to research in topics: Pregnancy & Placenta. The author has an hindex of 79, co-authored 490 publications receiving 24316 citations. Previous affiliations of Eric Jauniaux include Université libre de Bruxelles & Centre national de la recherche scientifique.

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Onset of Maternal Arterial Blood Flow and Placental Oxidative Stress: A Possible Factor in Human Early Pregnancy Failure

TL;DR: In this article, the authors measured changes in the oxygen tension within the human placenta associated with onset of the maternal arterial circulation at the end of the first trimester of pregnancy, and the impact on placental tissues.
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Rheological and Physiological Consequences of Conversion of the Maternal Spiral Arteries for Uteroplacental Blood Flow during Human Pregnancy

TL;DR: Dilation has a surprisingly modest impact on total blood flow, and so it is suggested the placental pathology associated with deficient conversion is dominated by rheological consequences rather than chronic hypoxia.
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Oxygen measurements in endometrial and trophoblastic tissues during early pregnancy.

TL;DR: It is suggested that the increase of placental PO2 at the end of the first trimester is related to the establishment of continuous maternal blood flow in the intervillous space.
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Placental oxidative stress: from miscarriage to preeclampsia.

TL;DR: Miscarriage, missed miscarriage, and early- and late-onset preeclampsia represent a spectrum of disorders secondary to deficient trophoblast invasion, and high levels of oxidative stress in the periphery may induce formation of the chorion laeve.
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Placental-related diseases of pregnancy: involvement of oxidative stress and implications in human evolution

TL;DR: It is suggested that pre-eclampsia is a three-stage disorder with the primary pathology being an excessive or atypical maternal immune response, which would impair the placentation process leading to chronic oxidative stress in theplacenta and finally to diffuse maternal endothelial cell dysfunction.