Dimensional Accuracy of Acrylic Resin Denture Bases : Literature Review

The more contact there is between the denture base and the cast, the better the fit, resulting in a close adaptation of the denture surface to the oral mucosa and a more retentive denture. Many prosthodontists, however, feel that compression-molded dentures processed with acrylic resins become ill fitting in the mouth because they warp severely during processing and while in service. One of the reasons for this problem is shrinkage of the acrylic resin due to polymerization. This article reviews the studies on accuracy of denture bases using various activation methods for polymerization of acrylic resin

Regulation of energy metabolism by interleukin-1 β, but not by interleukin-6, is mediated by nitric oxide in primary cultured rat hepatocytes

AbstractThe effects of inflammatory cytokines (interleukin-1 β, interleukin-6, and tumor necrosis factor-α) on energy metabolism were studied in primary cultured rat hepatocytes. Adenine nucleotide (ATP, ADP, and AMP) content, lactate production, the ketone body ratio (acetoacetate/β-hydroxybutyrate) reflecting the liver mitochondrial redox state (NAD+/NADH), and nitric oxide formation were measured. Insulin increased ATP content in hepatocytes and had a maximal effect after 8–12 h of culture. Both interleukin-1β and interleukin-6, but not tumor necrosis factor-α, significantly inhibited the ATP increase time- and dose-dependently. Interleukin-1β and interleukin-6 also stimulated lactate production. During the same period, interleukin-1 β but not interleukin-6 decreased the ketone body ratio. Furthermore, interleukin-1 β markedly stimulated nitric oxide formation in hepatocytes, and this increase was blocked by NG-monomethyl-L-arginine (a nitric oxide synthase inhibitor) and by interleukin-1 receptor antagonist. NG-monomethyl-l-arginine reversed inhibition of the ATP increase, decrease in the ketone body ratio, and increase in lactate production, which were induced by interleukin-lβ. Interleukin-1 receptor antagonist completely abolished all of the effects induced by interleukin-1 β. These results demonstrated that interleukin-1 β and interleukin-6 affect the insulin-induced energy metabolism in rat hepatocytes by different mechanisms. Specifically, interleukin-1 β inhibits ATP synthesis by causing the mitochondrial dysfunction, a process which may be mediated by nitric oxide