Tais Romero-Uruñuela

This study shows that Plasmodium falciparum egress products disrupt BBB endothelial junctions and activate JAK-STAT signaling, leading to increased permeability and suggesting therapeutic targets.

This study shows that disrupting the hexosamine biosynthetic pathway in Plasmodium falciparum blocks GPI production, arrests parasite growth, and prevents egress from host cells.

The paper examines variability in breast milk antibody reactivity to bacterial lipopolysaccharides between rural Kenya and urban Switzerland, finding broad reactivity in Kenya and cross-reactivity with parasitic pathogens.