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For studying the deposition behaviour of dual-carbides cermet particles on coating microstructure and properties，the surface morphology and cross-sectional microstructure of the original powder and the flat particle on the low-carbide steel substrate were analyzed，and the microstructure，phase constitution and properties of HVOF sprayed micro-nano WC-Cr3C2-CoNi coating were investigated systemically.Results showed that the particles deposited on the substrate showed a caky shape with smooth and convex surface，radial sputtering streaks appeared around the particles，and the thickness of flat particles was much smaller than their radial dimensions.In addition，the section microstructure of the coating presented certain lamellar characteristics，and the interfaces between flat particles，hard phase and bond phase，flat particle and substrate and different hard phases bonded well.The coating had the main phase of WC，some decarburized phases，and the amorphous phase of Cr2O5.Moreover，the microhardness，elastic modulus，fracture toughness，adhesive strength and wear weight loss of the coating were (13.19±0.52) GPa，(145.17±3.89) GPa，(2.59±0.64) MPa·m1/2，(38.41±0.51) MPa and (6.08±0.68) mg respectively.Compared to WC-Co12 coating，the decomposition of WC and the decarburized phases decreased significantly in the HVOF sprayed micro-nano WC-Cr3C2-CoNi coating and the coating’s mechanical properties were obviously improved.

Background: Lung cancer is the second most commonly diagnosed cancer and the leading cause of cancer-related death. Malignant pleural effusion (MPE) is a special microenvironment for lung cancer metastasis. Alternative splicing, which is regulated by splicing factors, affects the expression of most genes and influences carcinogenesis and metastasis. Methods: mRNA-seq data and alternative splicing events in lung adenocarcinoma (LUAD) were obtained from The Cancer Genome Atlas (TCGA). A risk model was generated by Cox regression analyses and LASSO regression. Cell isolation and flow cytometry were used to identify B cells. Results: We systematically analyzed the splicing factors, alternative splicing events, clinical characteristics, and immunologic features of LUAD in the TCGA cohort. A risk signature based on 23 alternative splicing events was established and identified as an independent prognosis factor in LUAD. Among all patients, the risk signature showed a better prognostic value in metastatic patients. By single-sample gene set enrichment analysis, we found that among tumor-infiltrating lymphocytes, B cells were most significantly correlated to the risk score. Furthermore, we investigated the classification and function of B cells in MPE, a metastatic microenvironment of LUAD, and found that regulatory B cells might participate in the regulation of the immune microenvironment of MPE through antigen presentation and promotion of regulatory T cell differentiation. Conclusions: We evaluated the prognostic value of alternative splicing events in LUAD and metastatic LUAD. We found that regulatory B cells had the function of antigen presentation, inhibited naïve T cells from differentiating into Th1 cells, and promoted Treg differentiation in LUAD patients with MPE. [ABSTRACT FROM AUTHOR]

Lung adenocarcinoma (LUAD) is the most prevalent histological type of lung cancer. Previous studies have reported that specific long noncoding RNAs (lncRNA) are involved in cancer development and progression. The phenotype and mechanism of ENST00000440028, named MSL3P1, an lncRNA referred to as a cancer-testis gene with potential roles in tumorigenesis and progression, have not been reported. MSL3P1 is overexpressed in LUAD tumor tissues, which is significantly associated with clinical characteristics, metastasis, and poor clinical prognosis. MSL3P1 promotes the metastasis of LUAD in vitro and in vivo. The enhancer reprogramming in LUAD tumor tissue is the major driver of the aberrant expression of MSL3P1. Mechanistically, owing to the competitive binding to CUL3 mRNA with ZFC3H1 protein (a protein involved in targeting polyadenylated RNA to exosomes and promoting the degradation of target mRNA), MSL3P1 can prevent the ZFC3H1-mediated RNA degradation of CUL3 mRNA and transport it to the cytoplasm. This activates the downstream epithelial-to-mesenchymal transition signaling pathway and promotes tumor invasion and metastasis. Implications: This study indicates that lncRNA MSL3P1 regulates CUL3 mRNA stability and promotes metastasis and holds potential as a prognostic biomarker and therapeutic target in LUAD., (©2024 American Association for Cancer Research.)