Calcium flux and endothelial dysfunction during acute lung injury: a STIMulating target for therapy
Bacterial pathogen-associated molecular pattern molecules (PAMPs) such as LPS activate the endothelium and can lead to lung injury, but the signaling pathways mediating endothelial injury remain incompletely understood. In a recent issue of the JCI, Gandhirajan et al. identify STIM1, an ER calcium sensor, as a key link between LPS-induced ROS, calcium oscillations, and endothelial cell (EC) dysfunction. In addition, they report that BTP2, an inhibitor of calcium channels, attenuates lung injury. This study identifies a novel endothelial signaling pathway that could be a future target for the treatment of lung injury.
A workshop on the diagnostic criteria of adult neuronal ceroid-lipofuscinosis (ANCL) or Kufs'disease represented an unique opportunity to make a critical review of the ANCL material from the files of the Born-Bunge Foundation. Our review included the clinical data when available, the light microscopic sections and the electron micrographs. When the postmortem material had not been immediately fixed in glutaraldehyde, we sampled formalin-fixed material, post-fixed it and used classical electron microscopic techniques to better define the ultrastructure of the stored products. Only one family fulfilled the criteria for ANCL. Neurons and vascular smooth muscle cells contained membrane-bound inclusions with curvilinear, rectilinear and fingerprint profiles.