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Thermally induced spin control is one of the main directions for future spin devices. In this study, we synthesized single-phase polycrystalline ErFe[Formula: see text]CrxO3 and combined the magnetization curves and Mössbauer spectra to determine the macroscopic magnetism at room temperature (RT). The magnetization of the system at various temperatures is well simulated by molecular field theory. And it is found that under the Dzyaloshinskii–Moriya (DM) interaction, not only the B-site ions undergo a reorientation process, but the spins of the A-site ions also change at the same time. The effective spin is defined as the projection of Er[Formula: see text] on the Fe[Formula: see text]/Cr[Formula: see text] spin plane, and the whole reorientation process is obtained by fitting. This study will complement the actual process of ErFe[Formula: see text]CrxO3 spin reorientation and will lay a theoretical foundation for the fabrication of future spin-controlled devices.

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IntroductionLung cancer is the leading cause of cancer death worldwide, and lung adenocarcinoma (LADC) is the most common lung cancer. Lung cancer has a distinct microbiome composition correlated with patients’ smoking status. However, the causal evidence of microbial impacts on LADC is largely unknown.MethodsWe investigated microbial communities’ differences in Formalin-Fixed Paraffin-Embedded tissues of ever-smoke (n = 22) and never-smoke (n = 31) patients with LADC through bacterial 16S rRNA gene high-throughput sequencing. Then nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung cancer mouse model and A549 cells were used to study the effect of Stenotrophomonas maltophilia (S. maltophilia) in LADC.Results and DiscussionWe found a significant increase of genus Stenotrophomonas in LADC tissues of patients with primary tumor size greater than 3 cm and never-smoker patients. We further found that intratracheal infection with S. maltophilia promoted tumor progression in the NNK-induced lung cancer mouse model. We performed RNA-seq analysis on lung tissues and found that S. maltophilia treatment drove inflammation and upregulated tumor associated cell signaling, including Apelin signaling pathway. Mechanistically, histone deacetylase 5 (HDAC5) gene expression was significantly upregulated in S. maltophilia treated groups, and was required for S. maltophilia induced cell proliferation and migration in LADC cell line A549. Therefore, we provide in vivo and in vitro evidence to demonstrate that S. maltophilia promotes LADC progression, in part, through HDAC5.