Rory K. M. Long

This study develops an iPSC-based model with enhanced endothelial identity to study malaria parasite interactions and pathogenesis in vitro.

This paper shows that Plasmodium falciparum impairs Ang-1 secretion by pericytes in a 3D brain microvessel model, leading to vascular dysfunction that can be partially reversed with Ang-1 or AKB-9778.

The paper shows that fever increases adhesion of malaria parasites and neutrophils to brain blood vessels by damaging the endothelial glycocalyx, suggesting antipyretics could reduce disease severity.

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.