Review of Research Progress on Mo-Si-B Alloys.

Mo-Si-B alloys are a crucial focus for the development of the next generation of ultra-high-temperature structural materials. They have garnered significant attention over the past few decades due to their high melting point and superior strength and oxidation resistance compared to other refractory metal alloys. However, their low fracture toughness at room temperature and poor oxidation resistance at medium temperature are significant barriers limiting the processing and application of Mo-Si-B alloys. Therefore, this review was carried out to compare the effectiveness of doped metallic elements and second-phase particles in solving these problems in detail, in order to provide clear approaches to future research work on Mo-Si-B alloys. It was found that metal doping can enhance the properties of the alloys in several ways. However, their impact on oxidation resistance and fracture toughness at room temperature is limited. Apart from B-rich particles, which significantly improve the high-temperature oxidation resistance of the alloy, the doping of second-phase particles primarily enhances the mechanical properties of the alloys. Additionally, the application of additive manufacturing to Mo-Si-B alloys was discussed, with the observation of high crack density in the alloys prepared using this method. As a result, we suggest a future research direction and the preparation process of oscillatory sintering, which is expected to reduce the porosity of Mo-Si-B alloys, thereby addressing the noted issues.

Postnatal deletion of Spns2 prevents neuroinflammation without compromising blood vascular functions.

Protein Spinster homolog 2 (Spns2) is a sphingosine-1-phosphate (S1P) transporter that releases S1P to regulate lymphocyte egress and trafficking. Global deletion of Spns2 (Spns2-/-) has been shown to reduce disease severity in several autoimmune disease models. To examine whether Spns2 could be exploited as a drug target, we generated and characterized the mice with postnatal knockout of Spns2 (Spns2-Mx1Cre). Our results showed that Spns2-Mx1Cre mice had significantly low number of lymphocytes in blood and lymphoid organs similar to Spns2-/- mice. Lymph but not plasma S1P levels were significantly reduced in both groups of knockout mice. Our lipidomic results also showed that Spns2 releases different S1P species into lymph. Interestingly, lymphatic vessels in the lymph nodes (LNs) of Spns2-/- and Spns2-Mx1Cre mice exhibited morphological defects. The structures of high endothelial venules (HEV) in the LNs of Spns2-Mx1Cre mice were disorganized. These results indicate that lack of Spns2 affects both S1P secretion and LN vasculatures. Nevertheless, blood vasculature of these Spns2 deficient mice was not different to controls under homeostasis and vascular insults. Importantly, Spns2-Mx1Cre mice were resistant to multiple sclerosis in experimental autoimmune encephalomyelitis (EAE) models with significant reduction of pathogenic Th17 cells in the central nervous system (CNS). This study suggests that pharmacological inhibition of Spns2 may be exploited for therapeutic applications in treatment of neuroinflammation.

Effect of Slurry Thickness on the Quality of Aluminized Coatings.

Diffusion aluminum coating is crucial to protect aero-engine turbine blades from high-temperature oxidation. Slurry aluminizing, as a commonly-used coating preparation technology, has variations in the process parameters that directly affect the quality of the coating. Therefore, this paper investigates the effect of slurry thickness on coating quality. Different forms of aluminized coatings were obtained by coating nine DZ22B nickel-based superalloy plates of the same size with different slurry thicknesses while keeping other parameters constant. These aluminized coatings were characterized using a scanning electron microscope (SEM) with an energy dispersive spectrometer (EDS), an X-ray diffractometer (XRD), and a surface gauge. The results show that the AlNi phase dominates the matrix of the aluminized coating, and the outer layer of the coating has white dotted precipitates of Cr. As the slurry thickness increases, the coating thickness increases, and the proportion of the outer layer in the overall coating increases. In contrast, the thickness of the interdiffusion layer does not change significantly. The thicker the slurry, the higher the Al content of the coating surface. A medium-thickness slurry can form a smooth aluminizing coating with a roughness Ra < 4.5 µm surface. The combined results show that a medium-thick slurry can produce a high-quality coating.

Regulation of Host Immune Responses against Influenza A Virus Infection by Mitogen-Activated Protein Kinases (MAPKs).

Influenza is a major respiratory viral disease caused by infections from the influenza A virus (IAV) that persists across various seasonal outbreaks globally each year. Host immune response is a key factor determining disease severity of influenza infection, presenting an attractive target for the development of novel therapies for treatments. Among the multiple signal transduction pathways regulating the host immune activation and function in response to IAV infections, the mitogen-activated protein kinase (MAPK) pathways are important signalling axes, downstream of various pattern recognition receptors (PRRs), activated by IAVs that regulate various cellular processes in immune cells of both innate and adaptive immunity. Moreover, aberrant MAPK activation underpins overexuberant production of inflammatory mediators, promoting the development of the "cytokine storm", a characteristic of severe respiratory viral diseases. Therefore, elucidation of the regulatory roles of MAPK in immune responses against IAVs is not only essential for understanding the pathogenesis of severe influenza, but also critical for developing MAPK-dependent therapies for treatment of respiratory viral diseases. In this review, we will summarise the current understanding of MAPK functions in both innate and adaptive immune response against IAVs and discuss their contributions towards the cytokine storm caused by highly pathogenic influenza viruses.