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Melt size‐dependent physical property variation is examined in a multicomponent GeSe2‐As2Se3‐PbSe chalcogenide glass developed for gradient refractive index applications. The impact of melting conditions on small (40 g) prototype laboratory‐scale melts extended to commercially‐relevant melt sizes (1.325 kg) have been studied and the role of thermal history variation on physical and optical property evolution in parent glass, the glass’ crystallization behavior and postheat‐treated glass ceramics, is quantified. As‐melted glass morphology, optical homogeneity and heat treatment‐induced microstructure following a fixed, two‐step nucleation and growth protocol exhibit marked variation with melt size. These attributes are shown to impact crystallization behavior (growth rates, resulting crystalline phase formation) and induced effective refractive index change, neff, in the resulting optical nanocomposite. The magnitude of these changes is discussed based on thermal history related melt conditions.

Recent studies from our laboratory demonstrated the involvement of endothelial cell reactive oxygen species (ROS) formation and activation of apoptotic signaling in vascular hyperpermeability following hemorrhagic shock (HS). The objective of this study was to determine if (-)-deprenyl, an antioxidant with anti-apoptotic properties would attenuate HS-induced vascular hyperpermeability. In rats, HS was induced by withdrawing blood to reduce the MAP to 40 mmHg for 60 minutes followed by resuscitation for 60 minutes. To study hyperpermeability, the rats were injected with FITC-albumin (50 mg/kg) and the changes in integrated optical intensity of the mesenteric postcapillary venules were obtained intra and extra vascularly utilizing intravital microscopy. Mitochondrial ROS formation and mitochondrial transmembrane potential (ΔΨm) were studied using dihydrorhodamine 123 and JC-1 respectively. Mitochondrial release of cytochrome c was determined using ELISA and caspase-3 activity by a fluorometric assay. Parallel studies were performed in rat lung microvascular endothelial cells (RLMEC) utilizing pro-apoptotic BAK as inducer of hyperpermeability. Hemorrhagic shock induced vascular hyperpermeability, mitochondrial ROS formation, decrease in ΔΨm, release of cytochrome c and caspase-3 activation (p < 0.05). (-)-Deprenyl (0.15 mg/Kg) attenuated all these effects (p < 0.05). Similarly in RLMEC, (-)-deprenyl attenuated BAK peptide induced monolayer hyperpermeability (p < 0.05), ROS formation, decrease in ΔΨm, cytochrome c release (p < 0.05) and activation of caspase-3 (p < 0.05). The protective effects of (-)-deprenyl on vascular barrier functions may be due to its protective effects on ΔΨm thereby preventing mitochondrial release of cytochrome c and caspase-3 mediated disruption of endothelial adherens junctions.