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Heidi Partanen

Researcher at University of Eastern Finland

Publications -  5
Citations -  256

Heidi Partanen is an academic researcher from University of Eastern Finland. The author has contributed to research in topics: Placenta & Transplacental. The author has an hindex of 5, co-authored 5 publications receiving 226 citations.

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Journal ArticleDOI

Aflatoxin B1 transfer and metabolism in human placenta.

TL;DR: Results from placental perfusions provide the first direct evidence of the actual transfer of AFB1 and its metabolism to aflatoxicol (AFL) by human placenta, and in vitro incubations with placental cytosolic fraction confirmed the capacity of human Placenta to form AFL.
Journal ArticleDOI

Fate of the teratogenic and carcinogenic ochratoxin A in human perfused placenta.

TL;DR: This study is the first to pursue the transfer of OTA through perfused human placenta and clearly contradict the existing epidemiological studies reporting higher OTA levels in fetal than in maternal circulation in vivo.
Journal ArticleDOI

Meta-analysis of data from human ex vivo placental perfusion studies on genotoxic and immunotoxic agents within the integrated European project NewGeneris

TL;DR: As the variance in all parameters within a study decreased after antipyrine normalization, it is concluded that this normalization approach at least partially corrects the bias caused by the small methodological differences between studies.
Journal ArticleDOI

Transplacental Transfer of Nitrosodimethylamine in Perfused Human Placenta

TL;DR: This study demonstrates that the human fetus can be exposed to NDMA from the maternal circulation and shows that NDMA is not metabolized in full-term human placenta from healthy non-smoking, non-drinking mothers.
Book ChapterDOI

The significance of ABC transporters in human placenta for the exposure of the fetus to xenobiotics

TL;DR: Estimating the contribution of an ABC transporter for fetal exposure localization has to be taken into account in addition to the level of expression, functional status and substrate specificity, because interference in the function of transporters may significantly increase the fetal exposure to xenobiotics or drugs.