Does blockade of vascular endothelial growth factor activity suppress wear debris-induced inflammatory osteolysis?
The observation that VEGF inhibitor treatment prevented UHMWPE particle-induced inflammatory osteolysis opens new possibilities for treatment of aseptic loosening, especially at an early stage.
Chronic CBZ administration to rats blocks increments in the AA signal k*, and in PGE(2) and TXB(2) concentrations that are produced by NMDA in vehicle-treated rats. The clinical action of antimanic drugs might involve inhibition of brain NMDAR-mediated signaling involving AA and its metabolites.