Role of anthropogenic forcing in Antarctic sea ice variability simulated in climate models.

Antarctic sea ice extent has seen a slight increase over recent decades, yet since 2016, it has undergone a sharp decline, reaching record lows. While the precise impact of anthropogenic forcing remains uncertain, natural fluctuations have been shown to be important for this variability. Our study employs a series of coupled model experiments, revealing that with constant anthropogenic forcing, the primary driver of interannual sea ice variability lies in deep convection within the Southern Ocean, although it is model dependent.

Small RNAs in the pathogenesis of preeclampsia.

Preeclampsia is a major contributor to maternal and fetal morbidity and mortality. The disorder can be classified into early- and late-onset subtypes, both of which evolve in two stages. The first stage comprises the development of pre-clinical, utero-placental malperfusion.

A method to isolate syncytiotrophoblast-derived medium-large extracellular vesicle small RNA from maternal plasma.

Syncytiotrophoblast-derived extracellular vesicles (STB-EVs) have an important role in placental research: both as mediators of feto-maternal signalling and as liquid biopsies reflecting placental health. Recent evidence highlights the importance of STB-EV RNA. Isolation of STB-EV RNA from maternal blood is therefore an important challenge.

Protein Profiling of Placental Extracellular Vesicles in Gestational Diabetes Mellitus.

Throughout pregnancy, some degree of insulin resistance is necessary to divert glucose towards the developing foetus. In gestational diabetes mellitus (GDM), insulin resistance is exacerbated in combination with insulin deficiency, causing new-onset maternal hyperglycaemia. The rapid reversal of insulin resistance following delivery strongly implicates the placenta in GDM pathogenesis.

Differential 5'-tRNA Fragment Expression in Circulating Preeclampsia Syncytiotrophoblast Vesicles Drives Macrophage Inflammation.

Background: The relationship between placental pathology and the maternal syndrome of preeclampsia is incompletely characterized. Mismatch between placental nutrient supply and fetal demands induces stress in the syncytiotrophoblast, the layer of placenta in direct contact with maternal blood. Such stress alters the content and increases the release of syncytiotrophoblast extracellular vesicles (STB-EVs) into the maternal circulation.