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Abstract: In this work, we reported the microstructure and electromagnetic properties of a series of zirconium substituted yttrium iron garnet ferrites (YCaZrIG) with iron deficiency composition of Y3−x Ca x Zr x Fe4.93−x O12 (x =0.1, 0.2, 0.3, and 0.4, with electrostatic balance by Ca2+ substituted for Y3+ ions) prepared by a solid-reaction method. The addition of ZrO2 shows no obvious influence on the phase, density and dielectric constant of YIG ferrites. When Zr addition x ≤0.3, the substitution of Zr4+ for Fe3+ decreases the amount of Fe ions, increases the lattice parameter and enhances the grain growth of garnet phase. The solubility of zirconium in YCaZrIG ferrite was found to be approximately 0.3, above which excess ZrO2 would lead to the precipitation of a second phase inside the YCaZrIG ferrite. This would inhibit the grain growth of garnet phase and cause an increase in the dielectric loss and coercivity. The observed reduce for saturation magnetization when x =0.4 is possibly due to antiparallel alignment of magnetic moment of Fe3+ in the d site caused by the decrease of a–d exchange interaction. Additionally, we got the optimum electromagnetic properties in the samples with x =0.3: ɛ r =14.1, tan δ e =2.5×10−4, H c =47A/m, 4πM s =1936×10−4 T, ΔH =7.1KA/m. [Copyright &y& Elsevier]

Glucosylceramide synthase (GCS) is a key enzyme engaged in the biosynthesis of glycosphingolipids and in regulating ceramide metabolism. Studies exploring alterations in GCS activity suggest that the glycolase may have a role in chemosensitizing tumor cells to various cancer drugs. The chemosensitizing effect of inhibitors of GCS (e.g. PDMP and selected analogues) has been observed with a variety of tumor cells leading to the proposal that the sensitizing activity of GCS inhibitors is primarily through increases in intracellular ceramide leading to induction of apoptosis. The current study examined the chemosensitizing activity of the novel GCS inhibitor, Genz-123346 in cell culture. Exposure of cells to Genz-123346 and to other GCS inhibitors at non-toxic concentrations can enhance the killing of tumor cells by cytotoxic anti-cancer agents. This activity was unrelated to lowering intracellular glycosphingolipid levels. Genz-123346 and a few other GCS inhibitors are substrates for multi-drug resistance efflux pumps such as P-gp (ABCB1, gP-170). In cell lines selected to over-express P-gp or which endogenously express P-gp, chemosensitization by Genz-123346 was primarily due to the effects on P-gp function. RNA interference studies using siRNA or shRNA confirmed that lowering GCS expression in tumor cells did not affect their responsiveness to commonly used cytotoxic drugs.