Molecular Beam Epitaxy Growth of Superconducting LiFeAs Film on SrTiO3(001) Substrate

The stoichiometric "111" iron-based superconductor, LiFeAs, has attacted great research interest in recent years. For the first time, we have successfully grown LiFeAs thin film by molecular beam epitaxy (MBE) on SrTiO3(001) substrate, and studied the interfacial growth behavior by reflection high energy electron diffraction (RHEED) and low-temperature scanning tunneling microscope (LT-STM). The effects of substrate temperature and Li/Fe flux ratio were investigated. Uniform LiFeAs film as thin as 3 quintuple-layer (QL) is formed. Superconducting gap appears in LiFeAs films thicker than 4 QL at 4.7 K. When the film is thicker than 13 QL, the superconducting gap determined by the distance between coherence peaks is about 7 meV, close to the value of bulk material. The ex situ transport measurement of thick LiFeAs film shows a sharp superconducting transition around 16 K. The upper critical field, Hc2(0)=13.0 T, is estimated from the temperature dependent magnetoresistance. The precise thickness and quality control of LiFeAs film paves the road of growing similar ultrathin iron arsenide films.Comment: 7 pages, 6 figure

Simultaneous electrical-field-effect modulation of both top and bottom Dirac surface states of epitaxial thin films of three-dimensional topological insulators

It is crucial for the studies of the transport properties and quantum effects related to Dirac surface states of three-dimensional topological insulators (3D TIs) to be able to simultaneously tune the chemical potentials of both top and bottom surfaces of a 3D TI thin film. We have realized this in molecular beam epitaxy-grown thin films of 3D TIs, as well as magnetic 3D TIs, by fabricating dual-gate structures on them. The films could be tuned between n-type and p-type by each gate alone. Combined application of two gates can reduce the carrier density of a TI film to a much lower level than with only one of them and enhance the film resistance by 10000 %, implying that Fermi level is tuned very close to the Dirac points of both top and bottom surface states without crossing any bulk band. The result promises applications of 3D TIs in field effect devices.Comment: 19 pages, 4 figures, accepted by Nano Letters, forthcomin

Biodegradation behavior of micro-arc oxidation coating on magnesium alloy-from a protein perspective

Protein exerts a critical influence on the degradation behavior of absorbable magnesium (Mg)-based implants. However, the interaction mechanism between protein and a micro-arc oxidation (MAO) coating on Mg alloys remains unclear. Hereby, a MAO coating was fabricated on AZ31 Mg alloy. And its degradation behavior in phosphate buffer saline (PBS) containing bovine serum albumin (BSA) was investigated and compared with that of the uncoated alloy. Surface morphologies and chemical compositions were studied using Field-emission scanning electron microscope (FE-SEM), Fourier transform infrared spectrophotometer (FT-IR) and X-ray diffraction (XRD). The degradation behavior of the bare Mg alloy and its MAO coating was studied through electrochemical and hydrogen evolution tests. Cytotoxicity assay was applied to evaluate the biocompatibility of Mg alloy substrate and MAO coating. Results indicated that the presence of BSA decreased the degradation rate of Mg alloy substrate because BSA (RCH(NH2)COO‾) molecules combined with Mg2+ ions to form (RCH(NH2)COO)2Mg and thus inhibited the dissolution of Mg(OH)2 by impeding the attack of Cl‾ ions. In the case of MAO coated Mg alloy, the adsorption of BSA on MAO coating and the formation of (RCH(NH2)COO)2Mg exhibited a synergistic effect and enhanced the corrosion resistance of the coated alloy significantly. Furthermore, cell bioactive assay suggested that the MAO coating had good viability for MG63 cells due to its high surface area

Wnt4 Signaling Prevents Skeletal Aging and Inflammation by Inhibiting Nuclear Factor-κB

Aging-related bone loss and osteoporosis affect millions of people worldwide. Chronic inflammation associated with aging promotes bone resorption and impairs bone formation. Here we show that Wnt4 attenuates bone loss in osteoporosis and skeletal aging mouse models by inhibiting nuclear factor-κB (NF-κB) via noncanonical Wnt signaling. Transgenic mice expressing Wnt4 from osteoblasts were significantly protected from bone loss and chronic inflammation induced by ovariectomy, tumor necrosis factor or natural aging. In addition to promoting bone formation, Wnt4 inhibited osteoclast formation and bone resorption. Mechanistically, Wnt4 inhibited NF-κB activation mediated by transforming growth factor-β–activated kinase-1 (Tak1) in macrophages and osteoclast precursors independently of β-catenin. Moreover, recombinant Wnt4 alleviated bone loss and inflammation by inhibiting NF-κB in vivo in mouse models of bone disease. Given its dual role in promoting bone formation and inhibiting bone resorption, our results suggest that Wnt4 signaling could be an attractive therapeutic target for treating osteoporosis and preventing skeletal aging