ABSTRACT
Most previous attempts on achieving electric-field manipulation of ferromagnetism in complex oxides, such as La0.66Sr0.33MnO3 (LSMO), are based on electrostatically induced charge carrier changes through high-k dielectrics or ferroelectrics. Here, the use of a ferroelectric copolymer, polyvinylidene fluoride with trifluoroethylene [P(VDF-TrFE)], as a gate dielectric to successfully modulate the ferromagnetism of the LSMO thin film in a field-effect device geometry is demonstrated. Specifically, through the application of low-voltage pulse chains inadequate to switch the electric dipoles of the copolymer, enhanced tunability of the oxide magnetic response is obtained, compared to that induced by ferroelectric polarization. Such observations have been attributed to electric field-induced oxygen vacancy accumulation/depletion in the LSMO layer upon the application of pulse chains, which is supported by surface-sensitive-characterization techniques, including X-ray photoelectron spectroscopy and X-ray magnetic circular dichroism. These techniques not only unveil the electrochemical nature of the mechanism but also establish a direct correlation between the oxygen vacancies created and subsequent changes to the valence states of Mn ions in LSMO. These demonstrations based on the pulsing strategy can be a viable route equally applicable to other functional oxides for the construction of electric field-controlled magnetic devices.
ABSTRACT
Single-phase (00 l)-oriented Bi2Te3 topological insulator thin films have been deposited on (111)-oriented ferroelectric 0.71Pb(Mg1/3Nb2/3)O3-0.29PbTiO3 (PMN-PT) single-crystal substrates. Taking advantage of the nonvolatile polarization charges induced by the polarization direction switching of PMN-PT substrates at room temperature, the carrier density, Fermi level, magnetoconductance, conductance channel, phase coherence length, and quantum corrections to the conductance can be in situ modulated in a reversible and nonvolatile manner. Specifically, upon the polarization switching from the positively poled Pr+ state (i.e., polarization direction points to the film) to the negatively poled Pr- (i.e., polarization direction points to the bottom electrode) state, both the electron carrier density and the Fermi wave vector decrease significantly, reflecting a shift of the Fermi level toward the Dirac point. The polarization switching from Pr+ to Pr- also results in significant increase of the conductance channel α from -0.15 to -0.3 and a decrease of the phase coherence length from 200 to 80 nm at T = 2 K as well as a reduction of the electron-electron interaction. All these results demonstrate that electric-voltage control of physical properties using PMN-PT as both substrates and gating materials provides a simple and a straightforward approach to realize reversible and nonvolatile tuning of electronic properties of topological thin films and may be further extended to study carrier density-related quantum transport properties of other quantum matter.
ABSTRACT
Angiotensin II has progressively been considered to play an important role in the development of liver fibrosis, although the mechanism isn't fully understood. The aim of this study was to investigate a possible pro-fibrotic mechanism, by which angiotensin II would enhance the pro-fibrotic effect of transforming growth factor beta 1 (TGF-ß1) through up-regulation of toll-like receptor 4 (TLR4) and enhancing down-regulation of TGF-ß1 inhibitory pseudo-receptor-BAMBI caused by LPS in hepatic stellate cells (HSCs). Firstly, the synergistic effects of angiotensin II, TGF-ß1 and LPS on collagen 1α production were confirmed in vitro by ELISA, in which angiotensin II, LPS and TGF-ß1 were treated sequentially, and in vivo by immunofluorescence, in the experiments single or multiple intra-peritoneally implanted osmotic mini-pumps administrating angiotensin II or LPS combined with intra-peritoneal injections of TGF-ß1 were used. We also found that only LPS and TGF-ß1 weren't enough to induce obvious fibrogenesis without angiotensin II. Secondly, to identify the reason of why angiotensin II is so important, the minute level of TLR4 in activated HSCs - T6 and primary quiescent HSCs of rat, up-regulation of TLR4 by angiotensin II and blockage by different angiotensin II receptor type 1 (AT1) blockers in HSCs were assayed by western blotting in vitro and immunofluorescence in vivo. Finally, BAMBI expression level, which is regulated by LPS-TLR4 pathway, was detected by qRT-PCR and results showed angiotensin II enhanced the down-regulation of BAMBI mRNA caused by LPS in vitro and in vivo, and TLR4 neutralization antibody blocked this interactive effect. These data demonstrated that angiotensin II enhances LPS-TLR4 pathway signaling and further down-regulates expression of BAMBI through up-regulation of TLR4, which results in facilitation of pro-fibrotic activity of TGF-ß1. Angiotensin II, LPS and TGF-ß1 act synergistically during hepatic fibrogenesis, showing crosstalks between angiotensin II-AT1, LPS-TLR4 and TGF-ß1-BAMBI signal pathways in rat HSCs.
