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Journal ArticleDOI

Latest advances in understanding preeclampsia.

Christopher W.G. Redman, +1 more
- 10 Jun 2005 - 
- Vol. 308, Iss: 5728, pp 1592-1594
TLDR
Recent work on the causes of preeclampsia is summarized, which reveals a new mode of maternal immune recognition of the fetus, relevant to the condition, and circulating factors derived from the placenta are now better understood.
Abstract
Preeclampsia is a relatively common pregnancy disorder that originates in the placenta and causes variable maternal and fetal problems. In the worst cases, it may threaten the survival of both mother and baby. We summarize recent work on the causes of preeclampsia, which reveals a new mode of maternal immune recognition of the fetus, relevant to the condition. The circulating factors derived from the placenta, which contributes to the clinical syndrome, are now better understood. This brief review on preeclampsia does not cover all aspects of this intriguing condition but focuses on some new and interesting findings.

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Citations
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Journal ArticleDOI

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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Mesenchymal Stem Cell-Derived Microvesicles Protect Against Acute Tubular Injury

TL;DR: It is found that microvesicles derived from human bone marrow MSCs stimulated proliferation in vitro and conferred resistance of tubular epithelial cells to apoptosis, suggesting RNA-dependent biologic effects.
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Endothelial cells and VEGF in vascular development

TL;DR: New insights into non-vascular roles of vascular endothelial growth factor and the requirement for endothelial cells in adult organs and stem-cell niches highlight possible side effects of anti-angiogenic therapy and the need for new targets.
References
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Journal ArticleDOI

Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia

TL;DR: It is confirmed that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia, leading to increased systemic levels of sFlt 1 that fall after delivery, and observations suggest that excess circulating sFelt1 contributes to the pathogenesis of preeClampsia.
Journal ArticleDOI

Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies

TL;DR: Factors that may be present at antenatal booking and the underlying evidence base can be used to assess risk at booking so that a suitable surveillance routine to detect pre-eclampsia can be planned for the rest of the pregnancy.
Journal ArticleDOI

Natural killer cells and pregnancy.

TL;DR: No convincing evidence of uterine maternal T-cell recognition of placental trophoblast cells has been found, but instead, there might be maternal allorecognition mediated by uterine natural killer cells that recognize unusual fetal trophOBlast MHC ligands.
Journal ArticleDOI

MHC class I molecules and kirs in human history, health and survival

TL;DR: In this paper, the interplay between KIR and MHC class I polymorphisms has facilitated human survival in the presence of epidemic infections and has influenced both reproduction and population growth.
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