Pregnancy outcome following frozen embryo transfer after artificial cycle or treatment by clomiphene citrate.

The optimal method to prepare endometrium before frozen embryo transfer (FET) is not yet established. We retrospectively studied 4496 FET and detailed pregnancy and miscarriage rates in three groups of patients according to the endometrium preparation they have followed before their successive FET: clomifene citrate (CC, group 1), artificial cycle (AC, group 2) or switch between CC and AC (group 3). The overall pregnancy rates per transfer were 24.

Differential expression of Vegfr-2 and its soluble form in preeclampsia.

Background: Several studies have suggested that the main features of preeclampsia (PE) are consequences of endothelial dysfunction related to excess circulating anti-angiogenic factors, most notably, soluble sVEGFR-1 (also known as sFlt-1) and soluble endoglin (sEng), as well as to decreased PlGF. Recently, soluble VEGF type 2 receptor (sVEGFR-2) has emerged as a crucial regulator of lymphangiogenesis. To date, however, there is a paucity of information on the changes of VEGFR-2 that occur during the clinical onset of PE.

Aetiology and physiopathology of preeclampsia and related forms.

Preeclampsia, a pregnancy-specific syndrome characterized by hypertension, proteinuria and oedema, resolves on placental delivery. Its pathogenesis is thought to be associated to a hypoxic placenta. Placental hypoxia is responsible for the maternal vascular dysfunction via the increased placental release of anti-angiogenic factors such as soluble flt1 and endoglin.

Soluble forms of VEGF receptor-1 and -2 promote vascular maturation via mural cell recruitment.

Two soluble forms of vascular endothelial growth factor (VEGF) receptors, sVEGFR-1 and sVEGFR-2, are physiologically released and overproduced in some pathologies. They are known to act as anti-VEGF agents. Here we report that these soluble receptors contribute to vessel maturation by mediating a dialogue between endothelial cells (ECs) and mural cells that leads to blood vessel stabilization.

[Defective placental implantation and its effects on maternal endothelial function].

Preeclampsia, a pregnancy-specific syndrome characterized by hypertension, edema and proteinuria, resolves spontaneously on placental delivery. Its pathogenesis is thought to involve placental hypoxia, which leads to maternal vascular dysfunction through increased placental release of anti-angiogenic factors such as the soluble form of VEGF receptor-1 (VEGFR1). VEGFR1 binds VEGF and PIGF, which are also produced by villous trophoblastic cells.