Subhabrata Basu

TL;DR: The chronic inflammation state of pre-gravid obesity is extending to in utero life with accumulation of a heterogeneous macrophage population and pro-inflammatory mediators in the placenta.

TL;DR: It is demonstrated that subclinical endotoxemia is associated with systemic and AT inflammation in obese pregnant women and recognition of bacterial pathogens may contribute to the combined dysfunction of innate immunity and the metabolic systems in AT.

TL;DR: Results point to fatty acids as preferential lipogenic substrates for placental cells and suggest that genes for fetoplacental lipid metabolism are enhanced selectively in GDM, which may be instrumental in increasing transplacental triglyceride fluxes and the delivery of lipid substrate for fetal use.

TL;DR: The data suggest that the active remodeling of adipose tissue of obese pregnant women results in an increased release of cell‐free DNA of maternal origin into the circulation.

TL;DR: It is shown that digestive enzyme treatment of sporadic CJD brain homogenate generates a C-terminal fragment similar to the proteinase K-resistant PrPSc core of 27-30 kDa implicated in prion disease transmission and pathogenesis, which suggests that PrP scrapie-associated proteins, in particular ferritin, may facilitate PrP Sc uptake in the intestine from distant species, leading to a carrier state in humans.