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Kai F. Yu

Researcher at National Institutes of Health

Publications -  48
Citations -  6865

Kai F. Yu is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Preeclampsia & Pregnancy. The author has an hindex of 21, co-authored 46 publications receiving 6443 citations. Previous affiliations of Kai F. Yu include United States Department of Health and Human Services & Tsinghua University.

Papers
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Circulating Angiogenic Factors and the Risk of Preeclampsia

TL;DR: Alterations in the levels of sFlt-1 and free PlGF were greater in women with an earlier onset of preeclampsia and in women in whom preeClampsia was associated with a small-for-gestational-age infant.
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Soluble endoglin and other circulating antiangiogenic factors in preeclampsia.

TL;DR: Rising circulating levels of soluble endoglin and ratios of sFlt1:PlGF herald the onset of preeclampsia, which was greatest among women in the highest quartile of the control distributions for both biomarkers but not for either biomarker alone.
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Urinary placental growth factor and risk of preeclampsia.

TL;DR: Testing the hypothesis that urinary PlGF is reduced prior to onset of hypertension and proteinuria and that this reduction predicts preeclampsia found decreased urinary Pl GF at mid gestation is strongly associated with subsequent early development of preeClampsia.
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Soluble endoglin and other circulating antiangiogenic factors in preeclampsia

TL;DR: It is suggested that circulating soluble endoglin and spil-which cause endothelial dysfunction by different mechanisms-may contribute to the development of preeclampsia.
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Two-stage elevation of cell-free fetal DNA in maternal sera before onset of preeclampsia

TL;DR: A nested case control study was performed within the Calcium for Preeclampsia Prevention trial cohort of healthy nulliparous women as discussed by the authors, which was used to determine whether pre-term pregnancy is caused by microfragments of syncytial trophoblast shed into the maternal circulation that stimulate an exaggerated inflammatory response.