Magnetic doping is the most common method for breaking time-reversal-symmetry surface states of topological insulators (TIs) to realize novel physical phenomena and to create beneficial technological applications. Here we present a study of the magnetic coupling of a prototype magnetic TI, that is, Cr-doped Bi2Se3, in its ultrathin limit which is expected to give rise to quantum anomalous Hall (QAH) effect. The high quality Bi2-xCrxSe3 epitaxial thin film was prepared using molecular beam epitaxy (MBE), characterized with scanning transimission electron microscopy (STEM), electrical magnetotransport, and X-ray magnetic circularly dichroism (XMCD) techniques, and the results were simulated using density functional theory (DFT) with spin-orbit coupling (SOC). We observed a sizable spin moment mspin = (2.05 ± 0.20) μB/Cr and a small and negative orbital moment morb = (-0.05 ± 0.02) μB/Cr of the Bi1.94Cr0.06Se3 thin film at 2.5 K. A remarkable fraction of the (CrBi-CrI)(3+) antiferromagnetic dimer in the Bi2-xCrxSe3 for 0.02 < x < 0.40 was obtained using first-principles simulations, which was neglected in previous studies. The spontaneous coexistence of ferro- and antiferromagnetic Cr defects in Bi2-xCrxSe3 explains our experimental observations and those based on conventional magnetometry which universally report magnetic moments significantly lower than 3 μB/Cr predicted by Hund's rule.

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One of the core issues for multiferroicity is the strongly coupled ferroelectric polarization and magnetization, while so far most multiferroics have antiferromagnetic order with nearly zero magnetization. Magnetic spinel compounds with ferrimagnetic order may be alternative candidates offering large magnetization when ferroelectricity can be activated simultaneously. In this work, we investigate the ferroelectricity and magnetism of spinel FeCr2S4 in which the Fe2+ sublattice and Cr3+ sublattice are coupled in antiparallel alignment. Well defined ferroelectric transitions below the Fe2+ orbital ordering termperature Too = 8.5 K are demonstrated. The ferroelectric polarization has two components. One component arises mainly from the noncollinear conical spin order associated with the spin-orbit coupling, which is thus magnetic field sensitive. The other is probably attributed to the Jahn-Teller distortion induced lattice symmetry breaking, occuring below the orbital ordering of Fe2+. Furthermore, the coupled ferroelectric polarization and magnetization in response to magnetic field are observed. The present work suggests that spinel FeCr2S4 is a multiferroic offering both ferroelectricity and ferrimagnetism with large net magnetization.

Background: The receptor-interacting protein kinase 3 (RIP3/RIPK3) was recently found to be a critical regulator of programmed necrosis/necroptosis. However, the biological role and clinical significance of RIP3 in prostate cancer remain obscure. Methods: Western blotting and QRT-PCR were performed to detect the level of RIP3 in prostate cancer cells. Fixed cancer tissue and normal tissue specimens were subjected to immunohistochemical analysis of RIP3. Cell migration and invasion abilities were evaluated by transwell assays. In vitro proliferative ability was examed by MTS. And in vivo nude mice model were used to evaluate the effect of RIP3 ectopic expression on proliferative capability. Cell cycle of prostate cancer cells were analyzed by flow cytometry. Changes in some related proteins caused by RIP3 overexpression were explored using Western blotting. Results: RIP3 was significantly down-regulated in prostate cancer cell lines and clinical prostate tumor samples. And over-expressing RIP3 suppressed the migration and invasion of prostate cancer cells. Two important matrix metalloproteinases MMP2, MMP9 which enables the destruction of the histological barrier of tumor cell invasion and three mesenchymal markers Vimentin, fibronectin, and N-cadherin were underexpressed due to the overexpression of RIP3, but the E-cadherin level which is the epithelial marker was increased. Furthermore, our results also showed that RIP3 can inhibit the proliferation and tumorigenicity of prostate cancer cells both in vitro and in vivo by phosphorylating MLKL, which were reversed by MLKL inhibitor treatment, indicating that necroptosis was involved in cell death. Conclusion: Taken together, these findings indicated that RIP3 is responsible for the progression of prostate cancer, suggesting that RIP3 might have the potential to be a prognostic marker or a therapeutic target against prostate cancer.

BackgroundKnee osteoarthritis (KOA) is the most common form of chronic degenerative joint disease worldwide. Its incidence has increased in recent years. Aberrant expression profile of lncRNAs in damaged bone and cartilage of KOA patients has been reported recently, indicating its potential contributions in KOA development and a promising target for disease diagnosis and treatment. The aim of this study was to identify the association between genetic variation in lncRNA and KOA.MethodsWe retrieved relevant articles from the PubMed, Medline and Embase databases up to Jul 2017 investigating the association between lncRNA and the risk of osteoarthritis. There are 15 lncRNAs which show connection with osteoarthritis. We selected potential functional polymorphisms identified by RegulomeDB database in these lncRNAs. A case-control study was conducted which contained 278 KOA patients and 289 OA-free controls.ResultsLogistic regression analyses revealed that H19 rs2067051 T allele was significantly associated with decreased risk of KOA after adjusted for age, gender and BMI in recessive genetic model (OR = 0.63, P = 0.03) and additive genetic model (OR = 0.79, P = 0.03). MEG3 rs4378559 T allele was significantly associated with increased risk of KOA in additive genetic model (OR = 1.32, P = 0.04). Heterogeneity tests proved that H19 rs2067051, MEG3 rs4378559 and HOTTIP rs202384’s risk effects on KOA were more remarkable for female, BMI ≥ 25 and younger age (age < 60), respectively.ConclusionThe results indicate that potential functional genetic variation in lncRNA plays an important role in the pathogenesis of KOA.