Epoxy powders offer a low-cost means of manufacturing thick section composite parts, such as those found in wind and tidal turbines. Currently, their processing cycle includes a lengthy drying stage (≥ 15 h) to remove ambient moisture. This prevents void defect formation and, thereby, a reduction in mechanical properties, however, it constitutes up to 60% of the processing time. Little research has been published on the study of this process or its optimisation. Experimental and simulated analyses are used to investigate the effects of hygroscopicity in epoxy powder composites. In particular, focus is given to the drying process, which is used to prevent void defect formation and, thereby, a reduction in mechanical properties. As such, tests are performed to quantify the void content of dried and undried laminates, and to measure its impact on transverse flexural strength. Dynamic vapour sorption analysis is used to study the sorption behaviour of the epoxy powder. Sorption data is fitted to a modified linear driving force model, and then implemented in existing process simulations tools. The drying of a thick epoxy powder composite section is simulated to investigate the influence of powder sintering on the duration required for drying. It is shown that the epoxy powder is slightly hygroscopic (1.36 wt%) and exhibits sorption behaviour that is characteristic of glassy polymers. This results in up to 4.8% voids (by volume) if processed in an undried state, leading to a 43% reduction in transverse flexural strength. Process simulations reveal that a standard drying cycle prematurely sinters the powder; inhibiting moisture release. By maintaining a powder state, simulations show that the drying cycle can be reduced to 5 h.

Despite existing strong evidence on oxidative markers overproduction following ischemia/reperfusion (I/R), the mechanism by which oxidative enzyme Cytochrome P450-2E1 (CYP2E1) contributes to I/R outcomes is not clear. In this study, we sought to evaluate the functional significance of CYP2E1 in I/R. CYP2E1 KO mice and controls were subjected to middle cerebral artery occlusion (MCAo-90min) followed by 24hr of reperfusion to induce focal I/R injury models. Then, histological and chemical analyses were conducted to investigate the role of CYP2E1 in lesion volume, oxidative stress, and inflammation exacerbation. Also, the role of CYP2E1 on the BBB integrity was investigated by measuring 20-Hydroxyecosatetraenoic acid (20-HETE) activity, as well as, in vivo BBB transfer rate. Following I/R, the CYP2E1 KO mice exhibited a significantly lower lesion volume, and neurological deficits compared to controls (p<0.005). Also, ROS production, apoptosis, and the neurodegeneration were significantly lower in the CYP2E1(-/-) I/R group (p<0.001). The BBB damage was significantly lower in CYP2E1(-/-) mice compared to WT (p<0.001), while 20-HETE production was increased by 41%. Besides, inflammatory cytokines expression and the number of activated microglia were significantly lower in CYP2E1(-/-) mice following I/R. CYP2E1 suppression ameliorates I/R injury and protects BBB integrity by reducing both oxidative stress and inflammation.