Search

Extreme-high-speed laser cladding (EHLA), as a novel surface treatment technique, has attracted great attention because of its high cladding rate and good performance of cladding coatings. However, when depositing coatings with high cracking susceptibility, such as Ni60 coatings, cracks are difficult to avoid. Therefore, an extreme-high-speed laser-induction hybrid cladding technology (EH-LIHC) was innovatively proposed in this study. The effects of different preheating temperatures on the surface morphology, internal defects, microstructure, and mechanical properties of Ni60 coatings that were deposited by EHLA and EH-LIHC were analyzed. The results show that the roughness of the coating deposited by EHLA is 26.228 μm. However, the surface roughness of the coating deposited by EH-LIHC at 400 ℃ decreases to 14.316 μm. Simultaneously, the pores- and cracks-free Ni60 coating was deposited at 400 ℃. The coating dilution rate obviously increases as the preheating temperature rises. When the preheating temperature rises, the size of the grains and precipitates also increases. However, although Fe elemental diffusion is increased, there is no significant effect on the properties of the coating. The hardness of the coating fluctuates between 700 and 900 HV, nearly three times that of the substrate. As the preheating temperature rises, the coating's wear mechanism shifts from abrasive to abrasive and adhesive wear, and eventually back to abrasive wear. The improvement of wear resistance of the Ni60 coating deposited at 400 ℃ was mainly attributed to its high hardness and uniform and dense microstructure. The proposed EH-LIHC technique provides a promising method for the efficient deposit of crack-free coatings with good properties. [ABSTRACT FROM AUTHOR]

Objective: We aimed to reveal a spatial proteomic and immune signature of kidney function regions in lupus nephritis (LN). Material and methods: The laser capture microdissection (LCM) was used to isolate the glomerulus, tubules, and interstitial of the kidney from paraffin samples. The data-independent acquisition (DIA) method was used to collect proteomics data. The bioinformatic analysis was performed. Results: A total of 49,658 peptides and 4056 proteins were quantitated. Our results first showed that a high proportion of activated NK cells, naive B cells, and neutrophils in the glomerulus, activated NK cells in interstitial, and resting NK cells were accumulated in tubules in LN. The immune-related function analysis of differential expression proteins in different regions indicated that the glomerulus and interstitial were major sites of immune disturbance and regulation connected with immune response activation. Furthermore, we identified 7, 8, and 9 hub genes in LN's glomerulus, renal interstitial, and tubules. These hub genes were significantly correlated with the infiltration of immune cell subsets. We screened out ALB, CTSB, LCN2, A2M, CDC42, VIM, LTF, and CD14, which show higher performance as candidate biomarkers after correlation analysis with clinical indexes. The function within three regions of the kidney was analyzed. The differential expression proteins (DEGs) between interstitial and glomerulus were significantly enriched in the immune-related biological processes, and myeloid leukocyte-mediated immunity and cellular response to hormone stimulus. The DEGs between tubules and glomerulus were significantly enriched in cell activation and leukocyte-mediated immunity. While the DEGs between tubules and interstitial were enriched in response to lipid, antigen processing, and presentation of peptide antigen response to oxygen-containing compound, the results indicated a different function within kidney regions. Conclusions: Collectively, we revealed spatial proteomics and immune signature of LN kidney regions by combined using LCM and DIA. [ABSTRACT FROM AUTHOR]

Objective: This study aims to provide a new perspective of determining the pathophysiology of chronic hepatitis B (CHB) development by analyzing the gene regulatory network in CHB patients using single-cell ATAC sequencing. Background: Hepatitis B virus (HBV)-related liver disease induces liver damage by hepatic immune and inflammatory responses. The exact mechanism is unknown. As such, there is an urgent need to address this problem and study the relationship between aberrant peripheral blood mononuclear cell (PBMC) immune response and progression of liver disease. Method: The sequencing of the chromatin accessibility of 8016 cells from the whole venous blood of normal control (NC) individuals and CHB patients was performed through assay for transposase-accessible chromatin in single-cell sequencing (ScATAC-seq). Unsupervised clustering and annotation analyses were performed by Signac (version 1.7.0) and Seurat clustering to identify different cell types. Then, TF motif enrichment analysis and differentially expressed peak analysis were performed to identify cell-type-specific candidate open chromatins related to CHB. Result: We identified 12 leukocytic clusters corresponding to five cell types. The specific cell types associated with CHB were found to be located in B-0 and T-3. We have drawn the regulatory network of the hepatitis B signal pathway composed of genes linked to the differentially expressed peaks of these two CHB disease-specific cell types. Further, we profoundly explored the potential mechanisms of B-0-associated TF motif IRF2 and T-3-associated TF motif FOXC2 in the occurrence of CHB. Conclusion: We have drawn a systematic and distinguishing gene regulatory network of CHB-related PBMCs. Key Points • Peripheral blood mononuclear cells were robustly clustered based on their types without using antibodies. • We draw a systematic and distinctive gene regulatory network of CHB-related PBMC through ScATAC-seq. [ABSTRACT FROM AUTHOR]