We report on the discovery of a lead-free morphotropic phase boundary in Sm doped BiFeO 3 with a simple perovskite structure using the combinatorial thin film strategy. The boundary is a rhombohedral to pseudo-orthorhombic structural transition which exhibits a ferroelectric (FE) to antiferroelectric (AFE) transition at approximately Bi 0.86 Sm 0.14 FeO 3 with dielectric constant and out-of-plane piezoelectric coefficient comparable to those of epitaxial (001) oriented Pb(Zr,Ti)O 3 (PZT) thin films at the MPB. The discovered composition may be a strong candidate of a Pb-free piezoelectric replacement of PZT.

Skin cancer is currently the most common type of human cancer in Americans. Myricetin, a naturally occurring phytochemical, has potent anticancer-promoting activity and contributes to the chemopreventive potential of several foods, including red wine. Here, we show that myricetin suppresses UVB-induced cyclooxygenase-2 (COX-2) expression in mouse skin epidermal JB6 P+ cells. The activation of activator protein-1 and nuclear factor-KB induced by UVB was dose-dependently inhibited by myricetin treatment. Western blot and kinase assay data revealed that myricetin inhibited Fyn kinase activity and subsequently attenuated UVB-induced phosphorylation of mitogen-activated protein kinases. Pull-down assays revealed that myricetin competitively bound with ATP to suppress Fyn kinase activity. Importantly, myricetin exerted similar inhibitory effects compared with 4-amino-5-(4-chloro-phenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimiidine, a well-known pharmacologic inhibitor of Fyn. In vivo mouse skin data also revealed that myricetin inhibited Fyn kinase activity directly and subsequently attenuated UVB-induced COX-2 expression. Mouse skin tumorigenesis data clearly showed that pretreatment with myricetin significantly suppressed UVB-induced skin tumor incidence in a dose-dependent manner. Docking data suggest that myricetin is easily docked to the ATP-binding site of Fyn, which is located between the N and C lobes of the kinase domain. Overall, these results indicated that myricetin exerts potent chemopreventive activity mainly by targeting Fyn in skin carcinogenesis. [Cancer Res 2008;68(14):6021-30]

We have investigated structural phase transitions across a ferroelectric-to-antiferroelectric phase boundary in epitaxial ͑001͒ oriented Bi ͑1−x͒ Sm x FeO 3 thin films. For the Sm 3+ concentration of 0.1Յ x Յ 0.14, we observe short-range antiparallel cation displacements, verified by the appearance of localized 1 4 ͕011͖ weak reflections in the selected area electron diffraction patterns. At the critical composition of x = 0.14, the system adopts a complex nanoscale domain mixture with appearance of 1 4 ͕011͖, 1 2 ͕011͖, 1 2 ͕010͖, and 1 2 ͕111͖ reflections and an incommensurate phase bridging the rhombohedral and orthorhombic phases. For compositions 0.14Ͻ x Ͻ 0.2, orientational twin domains coupled with antiphase oxygen octahedral tilts, identified by 1 2 ͕hkl͖ weak superstructure are observed. The above systematic changes in the microstructure as a function of Sm 3+ doping are linked to the macroscopic functional properties.

Luteolin, a flavonoid present in various vegetables including onion and broccoli, has been reported to possess anticarcinogenic effects. However, its chemopreventive effect on UV-induced skin cancer and its mechanism are not fully understood. Herein, we examined the chemopreventive effect and associated mechanisms of luteolin in the JB6 P+ cell line and the SKH-1 hairless mouse model. Luteolin suppressed UVB-induced cyclooxygenase-2 expression and activator protein-1 and nuclear factor-κB activity in JB6 P+ cells. Immunoblot and kinase assay data showed that luteolin attenuated protein kinase Cε (PKCε) and Src kinase activities and subsequently inhibited UVB-induced phosphorylation of mitogen-activated protein kinases and the Akt signaling pathway. In addition, pull-down assays revealed that luteolin binds directly to PKCε and Src in an ATP-competitive manner. Importantly, luteolin suppressed tumor incidence, multiplicity, and overall size in SKH-1 hairless mice. Analysis of the skin by immunohistochemistry and immunoblotting showed that luteolintreated groups had a substantial reduction in the levels of cyclooxygenase-2, tumor necrosis factor-α, and proliferating cell nuclear antigen compared with groups treated with only UVB. Further analysis using skin lysates showed that luteolin inhibited PKCε and Src kinase activity. Together, these data suggest that luteolin exerts potent chemopreventive activity against UVB-induced skin cancer mainly by targeting PKCε and Src.