We report an experimental investigation of the two-dimensional J eff = 1/2 antiferromagnetic Mott insulator by varying the interlayer exchange coupling in [(SrIrO3)1, (SrTiO3)m] (m = 1, 2 and 3) superlattices. Although all samples exhibited an insulating ground state with long-range magnetic order, temperature-dependent resistivity measurements showed a stronger insulating behavior in the m = 2 and m = 3 samples than the m = 1 sample which displayed a clear kink at the magnetic transition. This difference indicates that the blocking effect of the excessive SrTiO3 layer enhances the effective electron-electron correlation and strengthens the Mott phase. The significant reduction of the Neel temperature from 150 K for m = 1 to 40 K for m = 2 demonstrates that the long-range order stability in the former is boosted by a substantial interlayer exchange coupling. Resonant x-ray magnetic scattering revealed that the interlayer exchange coupling has a switchable sign, depending on the SrTiO3 layer number m, for maintaining canting-induced weak ferromagnetism. The nearly unaltered transition temperature between the m = 2 and the m = 3 demonstrated that we have realized a two-dimensional antiferromagnet at finite temperatures with diminishing interlayer exchange coupling.
We report the observation of multiple phonon satellite features in ultra thin superlattices of form nSrIrO3/mSrTiO3 using resonant inelastic x-ray scattering. As the values of n and m vary the energy loss spectra show a systematic evolution in the relative intensity of the phonon satellites. Using a closed-form solution for the RIXS cross section, we extract the variation in the electronphonon coupling strength as a function of n and m. Combined with the negligible carrier doping into the SrTiO3 layers, these results indicate that tuning of the electron-phonon coupling can be effectively decoupled from doping. This work showcases both a feasible method to extract the electron-phonon coupling in superlattices and unveils a potential route for tuning this coupling which is often associated with superconductivity in SrTiO3-based systems.Despite the discovery of several new classes of superconductors, a comprehensive understanding of superconductivity continues to evade the community, preventing attempts to systamtically control its behavior. The discovery of superconductivity at the interface of two insulating compounds, SrTiO 3 (STO) and LaAlO 3 , is particularly promising for expanding our understanding of superconductivity due to the myriad of control parameters introduced by the heterostructure morphology [1][2][3][4]. Furthermore, superconductivity in monolayer FeSe was recently found to be remarkably enhanced by an order of magnitude when interfaced with STO [5-7]. These findings point to heterostructuring as a promising route towards the rational engineering of the superconducting ground state.While debate remains, the coupling of the conduction electrons to the longitudinal optical (LO 4 ) phonon branch is routinely regarded as an essential ingredient in STO-based superconductors [8][9][10][11][12][13]. Recent angleresolved photoemission spectroscopy (ARPES) experiments observed the systematic tuning of the electron- * dmeyers@bnl.gov † tberlijn@gmail.com ‡
Tick-borne encephalitis virus (TBEV) is one of the flaviviruses that targets the CNS and causes encephalitis in humans. The mechanism of TBEV that causes CNS destruction remains unclear. It has been reported that RANTES-mediated migration of human blood monocytes and T lymphocytes is specifically induced in the brain of mice infected with TBEV, which causes ensuing neuroinflammation and may contribute to brain destruction. However, the viral components responsible for RANTES induction and the underlying mechanisms remain to be fully addressed. In this study, we demonstrate that the NS5, but not other viral proteins of TBEV, induces RANTES production in human glioblastoma cell lines and primary astrocytes. TBEV NS5 appears to activate the IFN regulatory factor 3 (IRF-3) signaling pathway in a manner dependent on RIG-I/MDA5, which leads to the nuclear translocation of IRF-3 to bind with RANTES promoter. Further studies reveal that the activity of RNA-dependent RNA polymerase (RdRP) but not the RNA cap methyltransferase is critical for TBEV NS5-induced RANTES expression, and this is likely due to RdRP-mediated synthesis of dsRNA. Additional data indicate that the residues at K359, D361, and D664 of TBEV NS5 are critical for RdRP activity and RANTES induction. Of note, NS5s from other flaviviruses, including Japanese encephalitis virus, West Nile virus, Zika virus, and dengue virus, can also induce RANTES expression, suggesting the significance of NS5-induced RANTES expression in flavivirus pathogenesis. Our findings provide a foundation for further understanding how flaviviruses cause neuroinflammation and a potential viral target for intervention.
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