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“Methylcellulose (MC) films were prepared by casting from its 1% aqueous solution containing 0.5% vegetable oil, 0.25% glycerol, and 0.025% Tween (R) 80. Poly(caprolactone) (PCL) films were prepared by compression molding from its granules. Biodegradable composite films were fabricated using MC film as reinforcing agent and PCL as the matrix material by compression molding. One layer of MC film was reinforced with two layers of PCL films. The MC content in the composites was varied from 10 to 50% by weight. Mechanical, barrier, and degradation
properties of PCL, MC, and composite films were evaluated. The values of puncture strength (PS), puncture deformation (PD), viscoelasticity (gamma) coefficient, and water vapor permeability (WVP) of the composites (50% MC content) were found to be 124.3 N/mm, 3.2 mm, 31%, and 2.6 g.mm/m(2).day.kPa, respectively. Oxygen transmission rate (OTR) of PCL, MC, and composites (50% MC) were found BEZ235 in vivo to be P005091 175, 25, 22 cc/m(2)/d, respectively, which indicated that composite films showed significantly lower OTR than PCL films. Degradation tests of the composite films (50% MC) were performed for 6 weeks in aqueous medium (at 25 degrees C), and it was found that composites lost its mass slowly with time. After 6 weeks, mass and PS of
the composites were decreased to 13.4 and 12%, respectively. Composite interface was studied by scanning electron microscopy (SEM). The MC film had good adhesion with PCL matrix during compression molding and suggested strong interface of the composite system. SEM image after 6 weeks of degradation showed some openings in the interface and revealed slow degradation of the MC films. (C) 2011 Wiley Periodicals, Inc. J Appl Polym Sci
123: 1690-1697, 2012″
“Haem GSK-J4 oxygenase-1 (HO-1) confers protection against a variety of oxidant-induced cell and tissue injury in animals and plants. In this report, it is confirmed that programmed cell death (PCD) in wheat aleurone layers is stimulated by GA and prevented by ABA. Meanwhile, HO activity and HO-1 protein expression exhibited lower levels in GA-treated layers, whereas the hydrogen peroxide (H(2)O(2)) content was apparently increased. The pharmacology approach illustrated that scavenging or accumulating H(2)O(2) either delayed or accelerated GA-induced PCD. Furthermore, pretreatment with the HO-1 specific inhibitor, zinc protoporphyrin IX (ZnPPIX), before exposure to GA, not only decreased HO activity but also accelerated GA-induced PCD significantly. The application of the HO-1 inducer, haematin, and the enzymatic reaction product of HO, carbon monoxide (CO) aqueous solution, both of which brought about a noticeable induction of HO expression, substantially prevented GA-induced PCD. These effects were reversed when ZnPPIX was added, suggesting that HO in vivo played a role in delaying PCD.