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The present study investigates the tensile behavior and microstructure evolution of the 6082 aluminum alloy aged with high temperature. A universal testing machine was applied to explore the tensile behavior, while features of the fracture surface were characterized via scanning electron microscopy (SEM). The microstructural evolution was assessed through optical microscopy (OM) and transmission electron microscopy (TEM). The findings illustrate that the 6082 alloy sheet achieves peak strength following treatment at 180 °C for 8 h for the 0° orientation specimen, with the yield strength and tensile strength reaching 345 MPa and 373 MPa, respectively. An increase in aging temperature results in a decline in strength, accompanied by an improvement in elongation. After the treatment at 330 °C for 0.5 h, the corresponding yield strength falls below 150 MPa, with elongation exceeding 12%. The alloy sheet consistently exhibits ductile fracture characteristics with various aging treatments. The aging processes have no obvious influence on grain morphology. The fibrous grain structure is responsible for the anisotropic mechanical properties. The alloy aged at 180 °C for 8 h demonstrates the greatest precipitate density with the smallest precipitate size. As the aging temperature increases, the precipitate distribution becomes less uniform, and the precipitates grow coarser, leading to a decline in the precipitate density and corresponding strength of the alloy. Furthermore, it is noted that smaller precipitates are more effective in suppressing the mechanical anisotropy of the alloy. [ABSTRACT FROM AUTHOR]

This study investigates the impact of cryogenic treatment duration on the mechanical properties and microstructural evolution of 6082 aluminum alloy subjected to subsequent artificial aging. Tensile tests were conducted using an electronic universal testing machine, and the microstructure was characterized by employing optical microscopy (OM), scanning electron microscopy (SEM), and transmission electron microscopy (TEM). The results indicate that both the tensile strength and elongation of the alloy first increase and then decrease with the extension of cryogenic treatment duration. The alloy treated with 12 h of cryogenic treatment followed by artificial aging at 180 °C for 8 h achieved a peak strength of 390 MPa. Meanwhile, the alloy treated with 8 h of cryogenic treatment and the same artificial aging process reached a maximum elongation of 13%. All specimens of 6082 aluminum alloy subjected to cryogenic and aging treatments exhibited ductile fracture under room temperature tensile conditions. The size of dimples at the fracture surface first increased and then decreased with increasing cryogenic treatment duration, indicating a transition from deeper to shallower dimples. The cryogenic treatment did not significantly affect the grain size of the alloy, which remained approximately 230 µm on average. Cryogenic treatment facilitated the precipitation of fine, densely distributed precipitates, enhancing the pinning effect of dislocations and thus improving the tensile strength. Additionally, cryogenic treatment increased the dislocation density and promoted the formation of subgrains, while the grain boundary precipitates transitioned from a continuous to a discontinuous distribution, all of which contribute to the enhancement of the plasticity. [ABSTRACT FROM AUTHOR]

Intestinal microbiota (IM) dysbiosis contributes to the development of autoimmune hepatitis (AIH). This study aimed to investigate the potential effect of fecal microbiota transplantation (FMT) in a murine model of experimental AIH (EAH), a condition more similar to that of AIH patients. Changes in the enteric microbiome were determined in AIH patients and EAH mice. Moreover, we established an experimental model of secondary EAH mice harboring dysbiosis (ABx) to analyze the effects of therapeutic FMT administration on follicular regulatory T (TFR) and helper T (TFH) cell imbalances and IM composition in vivo. Alterations of the IM composition and bacterial translocation occurred in AIH patients compared to nonalcoholic fatty liver disease patients and healthy controls (HCs). Therapeutic FMT significantly attenuated liver injury and bacterial translocation and improved the imbalance between splenic TFR cells and TFH cells in ABx EAH mice. Furthermore, therapeutic FMT also partially reversed the increasing trend in serum liver enzymes (ALT and AST) of CXCR5−/−EAH mice on the 28th day. Finally, therapeutic FMT could effectively restore antibiotic-induced IM dysbiosis in EAH mice. Taken together, our findings demonstrated that FMT was capable of controlling hepatitis progression in EAH mice, and the associated mechanism might be involved in the regulation of the TFR/TFH immune imbalance and the restoration of IM composition.

Background and aim: As the first identified m6A demethylase, FTO has been implicated in the progression of various cancers. However, the specific mechanism of FTO in clear cell renal cell carcinoma (ccRCC) remains incompletely understood. In this study, we aimed to explore the potential molecular mechanisms influencing the progression of ccRCC. Methods: We initially assessed the expression of FTO in tumor and adjacent tissues using TCGA database, RT-qPCR, and Western blot. We then conducted CCK-8, cell cycle analysis, and colony formation assay to investigate the impact of FTO on ccRCC cell proliferation. MeRIP-seq and RNA-seq were employed to identify potential downstream targets of FTO in ccRCC, and these findings were further validated through dual-luciferase reporter assays and MeRIP-qPCR. Then, DNA damage and cell death were assessed separately through gammaH2AX immunofluorescence detection and the LIVE/DEAD Fixable Dead Cell Stain assay, respectively. Subsequently, we identified downstream pathways influenced by FTO's regulation of POLQ through TCGA database analysis and GSEA enrichment analysis. Validation was carried out through Western blot. Results: FTO is highly expressed in ccRCC tissues and cell lines. Furthermore, ROC curve demonstrates that FTO contributes to the diagnosis of ccRCC. FTO modulates m6A modification, consequently influencing the expression of POLQ, thus facilitating cell proliferation and maintaining genome stability in ccRCC. Conclusion: FTO could potentially serve as a diagnostic marker for ccRCC. FTO promotes the progression of ccRCC by regulating m6A modification, making the inhibition of FTO a potential novel therapeutic strategy in ccRCC. [ABSTRACT FROM AUTHOR]

The occurrence of early esophageal cancer located within an area of leiomyoma is extremely rare, and its clinical features and treatment methods have not been well described. We herein report the clinical characteristics, diagnosis, and treatment methods of early esophageal cancer that developed on top of a leiomyoma in the upper third of the esophagus in a 78-year-old woman. All tumor marker concentrations were normal. The leiomyoma was correctly diagnosed as a submucosal tumor by endoscopy and endoscopic ultrasonography. Endoscopic biopsy revealed esophageal squamous cell carcinoma. Both lesions were successfully treated by endoscopic submucosal dissection. The patient was followed up for 6 months without recurrence. Endoscopic submucosal dissection was a successful initial treatment method for esophageal carcinoma coexisting with esophageal leiomyoma in this case.

Background: Tissue-resident CD8+T cells (CD103+CD8+T cells) are the essential effector cell population of anti-tumor immune response in tissue regional immunity. And we have reported that IL-33 can promote the proliferation and effector function of tissue-resident CD103+CD8+T cells. As of now, the immunolocalization and the prognostic values of tissue-resident CD8+T cells in human hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) still remain to be illustrated. Methods: In our present study, we used the tissue microarrays of HCC and ICC, the multicolor immunohistochemistry (mIHC), and imaging analysis to characterize the tissue-resident CD8+T cells in HCC and ICC tissues. The prognostic values and clinical associations were also analyzed. We also studied the biological functions and the cell–cell communication between tumor-infiltrating CD103+CD8+T cells and other cell types in HCC and ICC based on the published single-cell RNA sequencing (scRNA-seq) data. Results: Our work unveiled the expressions of CD8 and CD103 and immunolocalization of tissue-resident CD8+T cells in human HCC and ICC. Elevated CD8+T cells indicated a better overall survival (OS) rate, implying that tumor-infiltrating CD8+T cells in HCC and ICC could serve as an independent prognostic factor. Moreover, the number of CD103+CD8+T cells was increased in HCC and ICC tissues compared with adjacent normal tissues. HCC patients defined as CD8highCD103high had a better OS, and the CD8lowCD103low group tended to have a poorer prognosis in ICC. Evaluation of the CD103+CD8+T-cell ratio in CD8+T cells could also be a prognostic predictor for HCC and ICC patients. A higher ratio of CD103+CD8+T cells over total CD8+T cells in HCC tissues was negatively and significantly associated with the advanced pathological stage. The percentage of higher numbers of CD103+CD8+T cells in ICC tissues was negatively and significantly associated with the advanced pathological stage. In contrast, the higher ratio of CD103+CD8+T cells over total CD8+T cells in ICC tissues was negatively and significantly associated with the advanced pathological stage. In addition, single-cell transcriptomics revealed that CD103+CD8+T cells were enriched in genes associated with T-cell activation, proliferation, cytokine function, and T-cell exhaustion. Conclusion: The CD103+ tumor-specific T cells signified an important prognostic marker with improved OS, and the evaluation of the tissue-resident CD103+CD8+T cells might be helpful in assessing the on-treatment response of liver cancer. [ABSTRACT FROM AUTHOR]