BACKGROUND: The coronavirus disease 2019, caused by severe acute respiratory syndrome coronavirus 2, is a global public health emergency. Data on the effect of coronavirus disease 2019 in pregnancy are limited to small case series. OBJECTIVE: To evaluate the clinical characteristics and outcomes in pregnancy and the vertical transmission potential of severe acute respiratory syndrome coronavirus 2 infection.

A modified sessile drop method was developed to obtain the precise density values for liquid nickel and nickel-chromium alloy in liquid and solid-liquid coexistence states. The density of liquid nickel decreases linearly with increasing temperature in the range from the melting point to 1923 K. The density at the melting point and the thermal expansion coefficient of liquid nickel are 7.91 Mg·m −3 and 1.81 × 10 −4 K −1 , respectively. The density of nickel-chromium alloy in liquid or solid-liquid coexistence state decreases linearly with increasing the temperature and chromium concentration in the alloy. The temperature coefficient of density of nickel-chromium alloy changes at the liquidus temperature. The absolute value of the temperature coefficient of density in solid-liquid coexistence state is larger than that in liquid state.

The pathogenesis of preeclampsia remains unclear but placental factors are known to play a crucial role causing maternal endothelial cell dysfunction. One potential factor is placental micro- and nano- vesicles. Antiphospholipid antibodies (aPL) increase the risk of preeclampsia ten-fold, in part by damaging the mitochondria in the syncytiotrophoblast. Since mitochondrial DNA (mtDNA) is a danger- associated molecular pattern (DAMP/alarmin) that may activate endothelial cells, the aims of the current study were to investigate whether aPL affect the number of placental vesicles extruded, their mtDNA content and their ability to activate endothelial cells. Exposure of first trimester human placental explants to aPL affected neither the number nor size of extruded micro- and nano- vesicles (n = 5), however their levels of mtDNA were increased (n = 6). These vesicles significantly activated endothelial cells (n = 5), which was prevented by blocking toll-like receptor 9 (TLR-9), a receptor for extracellular DNA. Thus, aPL may increase the risk of preeclampsia in part by increasing the amount of mtDNA associated with placental vesicles. That mitochondrial DNA is recognised as a DAMP by TLR-9 to cause endothelial cell activation, raises the possibility that placental vesicles or TLR-9 might be a target for pharmaceutical intervention to reduce the consequences of aPL in pregnancy.