(C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Supercritical carbon dioxide (SC-CO(2)) has been successfully employed in a variety of applications due to its numerous advantages. Despite extensive investigations on the relationship between the activity of enzymes treated with supercritical fluids and supercritical operating conditions, there are no experimental studies that have addressed the effects of supercritical pretreatment on enzyme denaturation. in this study,

we have Nepicastat ic50 explored the impact Of SC-CO(2) pretreatment on the activity and stability of hen egg-white lysozyme during its course of denaturation. Our data indicated no noticeable enhancement in enzyme activity and stability in the presence of SC-CO(2) pretreatment for lysozyme samples denatured in 8 M urea at 50 degrees C and pH 6.2. However, SC-CO(2) pretreated lysozyme samples in 0.067 M phosphate buffer containing dithiothreitol (DTT) (0.1 M DTT, pH 6.2, 25 degrees C or 0.01 M DTT, pH 6.2, 50 degrees C) at 2500 psi and 50 degrees C had better residual activity relative to samples that were not pretreated. In addition, when denaturing at 65 degrees C and pH 9.0, the pretreatment in SC-CO(2) at 2500 psi and 50 degrees C resulted in the best stability of lysozyme. The result of this study may provide supporting evidence

that supercritical fluids serve as Selleckchem PU-H71 potential media for enhancing the activity of enzymes used in a variety of biochemical applications. (C) 2009, The Society for Biotechnology, Japan. All rights reserved.”
“Hyperplasia of airway smooth muscle (ASM) within the bronchial wall of asthmatic patients has been well documented and is likely due to increased muscle proliferation. We have shown that ASM cells obtained from asthmatic patients proliferate selleck compound faster than those obtained from non-asthmatic patients. In ASM from non-asthmatics, mitogens act via dual signaling pathways (both ERK- and PI 3-kinase-dependent) to control growth. In this study we are the first to examine

whether dual pathways control the enhanced proliferation of ASM from asthmatics. When cells were incubated with 0.1% or 1% FBS, ERK activation was significantly greater in cells from asthmatic subjects (P < 0.05). In contrast, when cells were stimulated with 10% FBS, ERK activity was significantly greater in the non-asthmatic cells. However, cell proliferation in asthmatic cells was still significantly higher in cells stimulated by both I% and 10% FBS. Pharmacological inhibition revealed that although dual proliferative pathways control ASM growth in cells from non-asthmatics stimulated with 10% FBS to an equal extent ([H-3]-thymidine incorporation reduced to 57.2 +/- 6.9% by the PI 3-kinase inhibitor LY294002 and 57.8 +/- 1.