Solid Platelet Rich Plasma in Corneal Surgery.

UNLABELLED: Solid eye platelet-rich plasma (E-PRP) concentrates platelets in a small volume of plasma which contains a high concentration of important growth factors and cell adhesion molecules. These cell adhesion molecules and growth factors occupy a major role in wound healing and enhance the physiological procedure at the site of the injury or the surgery. There are different materials used to tectonically maintain the solid clot attached at the site where treatment is necessary. Although AM may be used for this purpose, other biomaterials such a bovine pericardium or autologous fibrin membrane are at least as effective with less interdonor variations, no biological hazards, providing a better surgical alternative than the biologically so variable amniotic membrane patch. Solid platelet-rich plasma in the form obtained in ophthalmology, E-PRP, is a reliable and effective surgical coadjuvant to promote corneal wound healing in severe corneal ulcers and corneal perforations, and may be associated with other ocular surface reconstruction procedures. FUNDING: Supported in part by a grant from the Spanish Ministry of Science and Innovation, Centro para el Desarrollo Tecnológico Industrial (CDTI), CENIT: "Customized Eye Care", CeyeC (CEN-20091021).

Reelin-dependent ApoER2 downregulation uncouples newborn neurons from progenitor cells.

Reelin and its receptor machinery are well known to be required for the migration and positioning of neocortical projection neurons. More recently, reelin has been shown both necessary and sufficient to determine the rate of neocortical neurogenesis. The molecular links underlying its seemingly distinct proliferative and post-proliferative functions remain unknown. Here we reveal an enriched expression of functional reelin receptors, largely of Apolipoprotein E Receptor 2 (ApoER2), in radial glia basal processes and intermediate progenitor cells during mid/late cortical development. In vivo, ApoER2 overexpression inhibits neuronal migration. In contrast, precluding excessive levels of ApoER2 in reelin-deficient cortices, by either ApoER2 knock-down or the transgenic expression of reelin in neural progenitor cells, improves neuronal migration and positioning. Our study provides groundwork for the highly orchestrated clearance of neocortical neurons from their birth site, suggesting that a reelin-dependent ApoER2 downregulation mechanism uncouples newborn neurons from progenitor cells, thereby enabling neurons to migrate.