Magnetic Properties and Microstructure of FeCoNi(CuAl)0.8Snx (0 ≤ x ≤ 0.10) High-Entropy Alloys

The present work exhibits the effects of Sn addition on the magnetic properties and microstructure of FeCoNi(CuAl)0.8Snx (0 ≤ x ≤ 0.10) high-entropy alloys (HEAs). The results show all the samples consist of a mixed structure of face-centered-cubic (FCC) phase and body-centered-cubic (BCC) phase. The addition of Sn promotes the formation of BCC phase, and it also affects the shape of Cu-rich nano-precipitates in BCC matrix. It also shows that the Curie temperatures (Tc) of the FCC phase and the saturation magnetization (Ms) of the FeCoNi(CuAl)0.8Snx (0 ≤ x ≤ 0.10) HEAs increase greatly while the remanence (Br) decreases after the addition of Sn into FeCoNi(CuAl)0.8 HEA. The thermomagnetic curves indicate that the phases of the FeCoNi(CuAl)0.8Snx (0 ≤ x ≤ 0.10) HEAs will transform from FCC with low Tc to BCC phase with high Tc at temperature of 600–700 K. This work provides a new idea for FeCoNi(CuAl)0.8Snx (0 ≤ x ≤ 0.10) HEAs for their potential application as soft magnets to be used at high temperatures

miR-142-3p encapsulated in T lymphocyte-derived tissue small extracellular vesicles induces Treg function defect and thyrocyte destruction in Hashimoto’s thyroiditis

Abstract Background Hashimoto’s thyroiditis (HT) is an organ-specific autoimmune disease characterized by lymphocyte infiltration that destroys thyrocyte cells. The aim of the present study was to elucidate the role and mechanisms of tissue small extracellular vesicle (sEV) microRNAs (miRNAs) in the pathogenesis of HT. Methods Differentially expressed tissue sEV miRNAs were identified between HT tissue and normal tissue by RNA sequencing in the testing set (n = 20). Subsequently, using quantitative real-time polymerase chain reaction (qRT‒PCR) assays and logistic regression analysis in the validation set (n = 60), the most relevant tissue sEV miRNAs to HT were verified. The parental and recipient cells of that tissue sEV miRNA were then explored. In vitro and in vivo experiments were further performed to elucidate the function and potential mechanisms of sEV miRNAs that contribute to the development of HT. Results We identified that miR-142-3p encapsulated in T lymphocyte-derived tissue sEVs can induce Treg function defect and thyrocyte destruction through an intact response loop. Inactivation of miR-142-3p can effectively protect non-obese diabetic (NOD).H-2h4 mice from HT development display reduced lymphocyte infiltration, lower antibody titers, and higher Treg cells. Looking at the mechanisms underlying sEV action on thyrocyte destruction, we found that the strong deleterious effect mediated by tissue sEV miR-142-3p is due to its ability to block the activation of the ERK1/2 signaling pathway by downregulating RAC1. Conclusions Our findings highlight the fact that tissue sEV-mediated miR-142-3p transfer can serve as a communication mode between T lymphocytes and thyrocyte cells in HT, favoring the progression of HT