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Triple-layered Sr4Ru3O10 is a unique ferromagnet with the central RuO6 layer behaving differently from two outer layers both crystallographically and magnetically. We report that the partial substitution of Ru by smaller Mn gives rise to modification in crystal structure, electronic and magnetic properties of Sr4(Ru1-xMnx)3O10. Through the single crystal X-ray diffraction refinement, we find that (Ru/Mn)O6 octahedral rotation is no longer detectable at x ≥ 0.23, leading to the tetragonal structure. The magnetization measurements indicate the ferromagnetic transition temperature TC decreases from 105 K for x = 0 to 30 K for x = 0.41, with the reduced magnetic moment as well. Remarkably, Mn doping results in the change of magnetic anisotropy from the easy c axis in x = 0 to the easy ab plane seen in x = 0.34 and 0.41. Such change also removes the ab-plane metamagnetic transition observed in x = 0. Furthermore, the electrical resistivity increases with increasing x showing semiconducting behavior with Δ ~ 10 meV for x = 0.34 and 30 meV for x = 0.41. Under applied magnetic field, the magnetoresistance exhibits negative and linear field dependence in all current and field configurations. These results clearly indicate Sr4(Ru1-xMnx)3O10 is a novel ferromagnetic semiconductor with exotic magnetotransport properties.
Inflammatory cytokines and lncRNAs are closely associated with tumorigenesis. Herein, we reveal inflammatory cytokines IL6 cooperates with long noncoding RNA CUDR to trigger the malignant transformation of human embryonic stem cells-derived hepatocyte-like stem cells. Mechanistically, IL6 cooperates with CUDR to cause MELLT3 to interact with SUV39h1 mRNA3'UTR and promote SUV39h1 expression. Moreover, the excessive SUV39h1 also increases tri-methylation of histone H3 on nineth lysine (H3K9me3). Intriguingly, under inflammatory conditions, H3K9me3 promotes the excessive expression and phosphorylation of NF-κB, and in turn, phorsphorylated NF-κB promotes the expression and phosphorylation of Stat3. Furthermore, that the phosphorylated Stat3 loads onto the promoter region of miRs and lncRNAs. Ultimately, the abnormal expression of miRs and lncRNAs increased telomerase activity, telomere length and microsatellite instability (MSI), leading to malignant transformation of hepatocyte-like stem cells.
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