Simultaneous Enhancement of Strength and Sulfide Stress Cracking Resistance of Hot-Rolled Pressure Vessel Steel Q345 via a Quenching and Tempering Treatment.

Sulfide stress cracking (SSC) failure is a main concern for the pressure vessel steel Q345 used in harsh sour oil and gas environments containing hydrogen sulfide (H2S). Methods used to improve the strength of steel usually decrease their SSC resistance. In this work, a quenching and tempering (Q&T) processing method is proposed to provide higher strength combined with better SSC resistance for hot-rolled Q345 pressure vessel steel. Compared to the initial hot-rolled plates having a yield strength (YS) of ~372 MPa, the Q&T counterparts had a YS of ~463 MPa, achieving a remarkable improvement in the strength level. Meanwhile, there was a resulting SSC failure in the initial hot-rolled plates, which was not present in the Q&T counterparts. The SSC failure was not only determined by the strength. The carbon-rich zone, residual stress, and sensitive hardness in the banded structure largely determined the susceptibility to SSC failure. The mechanism of the property amelioration might be ascribed to microstructural modification by the Q&T processing. This work provides an approach to develop improved strength grades of SSC-resistant pressure vessel steels.

Relationship between Biodegradation Rate and Grain Size Itself Excluding Other Structural Factors Caused by Alloying Additions and Deformation Processing for Pure Mg.

This work studied the relationship between biodegradation rate and grain size itself, excluding other structural factors such as segregations, impure inclusions, second phase particles, sub-structures, internal stresses and textures caused by alloying additions and deformation processing for pure Mg. A spectrum of grain size was obtained by annealing through changing the annealing temperature. Grain boundary influenced the hardness and the biodegradation behavior. The hardness was grain size-dependent, following a typical Hall-Petch relation: HV=18.45+92.31d-12. The biodegradation rate decreased with decreasing grain size, following a similar Hall-Petch relation: Pi=0.17-0.68d-12 or Pw=1.34-6.17d-12. This work should be helpful for better controlling biodegradation performance of biodegradable Mg alloys through varying their grain size.

Xanthine dehydrogenase as a prognostic biomarker related to tumor immunology in hepatocellular carcinoma.

BACKGROUND: Xanthine dehydrogenase (XDH) is a critical enzyme involved in the oxidative metabolism of purines, pterin and aldehydes and a central component of the innate immune system. However, the prognostic value of XDH in predicting tumor-infiltrating lymphocyte abundance, the immune response, and survival in different cancers, including hepatocellular carcinoma (HCC), is still unclear. METHODS: XDH expression was analyzed in multiple databases, including Oncomine, the Tumor Immune Estimation Resource (TIMER), the Kaplan-Meier plotter database, the Gene Expression Profiling Interactive Analysis (GEPIA) database, and The Cancer Genome Atlas (TCGA). XDH-associated transcriptional profiles were detected with an mRNA array, and the levels of infiltrating immune cells were validated by immunohistochemistry (IHC) of HCC tissues. A predictive signature containing multiple XDH-associated immune genes was established using the Cox regression model. RESULTS: Decreased XDH mRNA expression was detected in human cancers originating from the liver, bladder, breast, colon, bile duct, kidney, and hematolymphoid system. The prognostic potential of XDH mRNA expression was also significant in certain other cancers, including HCC, breast cancer, kidney or bladder carcinoma, gastric cancer, mesothelioma, lung cancer, and ovarian cancer. In HCC, a low XDH mRNA level predicted poorer overall survival, disease-specific survival, disease-free survival, and progression-free survival. The prognostic value of XDH was independent of the clinical features of HCC patients. Indeed, XDH expression in HCC activated several immune-related pathways, including the T cell receptor, PI3K-AKT, and MAPK signaling pathways, which induced a cytotoxic immune response. Importantly, the microenvironment of XDHhigh HCC tumors contained abundant infiltrating CD8 + T cells but not exhausted T cells. A risk prediction signature based on multiple XDH-associated immune genes was revealed as an independent predictor in the TCGA liver cancer cohort. CONCLUSION: These findings suggest that XDH is a valuable prognostic biomarker in HCC and other cancers and indicate that it may function in tumor immunology. Loss of XDH expression may be an immune evasion mechanism for HCC.

Study on a Novel Biodegradable and Antibacterial Fe-Based Alloy Prepared by Microwave Sintering.

This research produced a porous Fe-8 wt.% Cu alloy by microwave sintering in order to achieve (i) an increased biodegradation rate, and (ii) an antibacterial function. The Fe-8Cu alloy had higher density, hardness and degradation rate (about 2 times higher) but smaller and fewer surface pores, compared to the pure Fe. The Fe-8Cu alloy had a strong antibacterial function (the antibacterial rates against E. coli were up to 99.9%) and good biocompatibility. This work provides a novel approach of alloy design and processing to develop novel antibacterial Fe-based alloys.

Biodegradation, Antibacterial Performance, and Cytocompatibility of a Novel ZK30-Cu-Mn Biomedical Alloy Produced by Selective Laser Melting.

In the present study, an antibacterial biomedical magnesium (Mg) alloy with a low biodegradation rate was designed, and ZK30-0.2Cu-xMn (x = 0, 0.4, 0.8, 1.2, and 1.6 wt%) was produced by selective laser melting, which is a widely applied laser powder bed fusion additive manufacturing technology. Alloying with Mn evidently influenced the grain size, hardness, and biodegradation behavior. On the other hand, increasing Mn content to 0.8 wt% resulted in a decrease of biodegradation rate which is attributed to the decreased grain size and relatively protective surface layer of manganese oxide. Higher Mn contents increased the biodegradation rate attributed to the presence of the Mn-rich particles. Taken together, ZK30-0.2Cu-0.8Mn exhibited the lowest biodegradation rate, strong antibacterial performance, and good cytocompatibility.

Fra-2/AP-1 regulates melanoma cell metastasis by downregulating Fam212b.

Metastatic melanoma remains a challenging disease. Understanding the molecular mechanisms how melanoma becomes metastatic is therefore of interest. Herein we show that downregulation of the AP-1 transcription factor member Fra-2 in melanoma cells is associated with an aggressive melanoma phenotype in vitro and in vivo. In vitro, Fra-2 knockdown in melanoma cells promoted cell migration and invasion associated with increased Snail-1, Twist-1/2, and matrix metalloproteinase-2 (MMP-2) expression. In vivo, Fra-2 knockdown in a melanoma cell line led to increased metastasis into the lungs and liver. The increased metastatic potential of Fra-2 knockdown melanoma cells was likely due to an accelerated cell cycle transition and increased tissue angiogenesis. Using Fra-2 knockdown cell lines microarray analysis, we identified the protein Fam212b (family with sequence similarity 212 member B) as a downstream target of Fra-2. By additional knockdown of Fam212b in Fra-2 mutant cells, we mitigated the cell migration, invasion, and cell cycle transition phenotype induced by Fra-2 knockdown. Furthermore, Fam212b overexpression enhanced ß-catenin pathway. Finally, Fam212b expression is correlated with increased melanoma metastasis and poor clinical outcomes in human patients. In summary, these findings reveal the Fra-2-Fam212b axis as a new pathway of melanoma metastasis, which can be in the future used as potential marker of the metastatic properties of melanoma.

Adipogenic niches for melanoma cell colonization and growth in bone marrow.

Bone marrow (BM) adipocytes are abundant in BM and may be involved in the process of bone metastasis. However, their behaviors in metastatic BM niches during bone metastasis have not been fully explored. In this study, intracardiac transplantation of B16-F10 melanoma cells into immunocompetent C57BL/6 mice was performed. Tibial marrow sections were stained with hematoxylin and eosin, Masson's trichrome, tartrate-resistant acid phosphatase, and fatty acid-binding protein 4 (FABP4) and analyzed using a histomorphometric system. The results showed that the number of BM adipocytes rapidly increased in melanoma metastatic BM niches, which were in direct contact with metastasizing melanoma cells and acted as a tumor stromal population in the BM-melanoma niche. Melanoma cell-derived factors could enhance BM adipogenesis, which promotes melanoma cell proliferation and cell cycle transitions. Moreover, BM adipocytes might aid in the modification of the osteolytic BM microenvironment. These results indicate that an increase in the number of BM adipocytes in a metastatic BM niche may facilitate melanoma cell colonization and growth in BM. BM adipocytes might therefore support the development of bone metastases.