Search

In the current manuscript, we systematically investigated the stability, Gilbert damping parameters, electronic and magnetic properties, exchange interactions and Curie temperatures of quaternary Heusler alloys CrTiCoZ (Z=Al, Ga, In). Stability calculations show that the CrTiCoZ alloys meet mechanical, thermodynamic and dynamic stabilities. Gilbert damping parameters of CrTiCoZ alloys calculated via linear response theory are localized in 0.006∼0.054 at 300 K, indicating they have lower energy loss and higher response speed as microwave and spintronic materials. Electronic calculations indicate that the CrTiCoIn is half-metallic ferrimagnet, and its integer total magnetic moment obeys the Slater–Pauling rule: Mt =Zt-18, while the CrTiCoAl and CrTiCoGa are nearly half-metals. After applying the GGA+U and HSE06 methods, it was found that the CrTiCoAl and CrTiCoGa alloys exhibit half-metallic properties. However, the CrTiCoIn alloy loses its half-metallicity. Origin of half-metallic gap is discussed by hybridization, occupation and distribution of electronic states. According to the Heisenberg model, we calculated the exchange coupling parameters of CrTiCoZ alloys, and found that the competition and cooperation between d-d exchange and RKKY exchange lead to the emergence of ferrimagnetic phase. Finally, we estimated the Curie temperatures of CrTiCoZ alloys by using mean-field approximation and Monte Carlo simulation, the calculated Curie temperatures are noticeably higher than room temperature. High spin polarization and Curie temperature as well as lower Gilbert damping parameters make the CrTiCoZ alloys as a promising material for microwave or spintronics applications.

Lack of immunogenicity of cancer cells has been considered a major reason for their failure in induction of a tumor specific T cell response. In this paper, we present evidence that decitabine (DAC), a DNA methylation inhibitor that is currently used for the treatment of myelodysplastic syndrome (MDS), acute myeloid leukemia (AML) and other malignant neoplasms, is capable of eliciting an anti-tumor cytotoxic T lymphocyte (CTL) response in mouse EL4 tumor model. C57BL/6 mice with established EL4 tumors were treated with DAC (1.0 mg/kg body weight) once daily for 5 days. We found that DAC treatment resulted in infiltration of IFN-γ producing T lymphocytes into tumors and caused tumor rejection. Depletion of CD8(+), but not CD4(+) T cells resumed tumor growth. DAC-induced CTL response appeared to be elicited by the induction of CD80 expression on tumor cells. Epigenetic evidence suggests that DAC induces CD80 expression in EL4 cells via demethylation of CpG dinucleotide sites in the promoter of CD80 gene. In addition, we also showed that a transient, low-dose DAC treatment can induce CD80 gene expression in a variety of human cancer cells. This study provides the first evidence that epigenetic modulation can induce the expression of a major T cell co-stimulatory molecule on cancer cells, which can overcome immune tolerance, and induce an efficient anti-tumor CTL response. The results have important implications in designing DAC-based cancer immunotherapy.