Effect of Heat Input on Microstructure and Properties of Laser-Welded 316L/In601 Dissimilar Overlap Joints in High-Temperature Thermocouple.

Heat input, a crucial factor in the optimization of high-temperature thermocouple laser welding, has a significant impact on the appearance and mechanical properties of dissimilar welded joints involving stainless-steel- and nickel-based alloys. This study focuses on laser overlay welding of austenitic stainless steels and nickel-based alloys. The findings indicate that an increase in heat input has a more pronounced effect on the penetration depth and dilution rate. Under high heat input, the weld has cracks, spatter, and other defects. Additionally, considerable amounts of chromium (Cr) and nickel (Ni) elements are observed outside the grain near the crack, and their presence increases with higher heat input levels. Phase analysis reveals the presence of numerous Cr2Fe14C and Fe3Ni2 phases within the weld. The heat input increases to the range of 30-35 J/mm, and the weld changes from shear fracture to tensile fracture. In the center of the molten pool, the Vickers hardness is greater than that of the base metal, while in the fusion zone, the Vickers hardness is lower than that of the base metal. The overall hardness is in a downward trend with the increase of heat input, and the minimum hardness is only 159 HV0.3 at 40 J/mm. The heat input falls within the range of 28-30 J/mm, and the temperature shock resistance is at its peak.

Avian Tembusu virus infection effectively triggers host innate immune response through MDA5 and TLR3-dependent signaling pathways.

Avian Tembusu virus (ATMUV) is a newly emerged flavivirus that belongs to the Ntaya virus group. ATMUV is a highly pathogenic virus causing significant economic loss to the Chinese poultry industry. However, little is known about the role of host innate immune mechanism in defending against ATMUV infection. In this study, we found that ATMUV infection significantly up-regulated the expression of type I and type III interferons (IFN) and some critical IFN-stimulated genes (ISG) in vivo and in vitro. This innate immune response was induced by genomic RNA of ATMUV. Furthermore, we observed that ATMUV infection triggered IFN response mainly through MDA5 and TLR3-dependent signaling pathways. Strikingly, shRNA-based disruption of IPS-1, IRF3 or IRF7 expression significantly reduced the production of IFN in the 293T cell model. Moreover, NF-κB was shown to be activated in both chicken and human cells during the ATMUV infection. Inhibition of NF-κB signaling also resulted in a clear decrease in expression of IFN. Importantly, experiments revealed that treatment with IFN significantly impaired ATMUV replication in the chicken cell. Consistently, type I IFN also exhibited promising antiviral activity against ATMUV replication in the human cell. Together, these data indicate that ATMUV infection triggers host innate immune response through MDA5 and TLR3-dependent signaling that controls IFN production, and thereby induces an effective antiviral immunity.

Muscovy duck reovirus infection rapidly activates host innate immune signaling and induces an effective antiviral immune response involving critical interferons.

Muscovy duck reovirus (MDRV) is a highly pathogenic virus in waterfowl and causes significant economic loss in the poultry industry worldwide. Because the host innate immunity plays a key role in defending against virus invasion, more and more attentions have been paid to the immune response triggered by viral infection. Here we found that the genomic RNA of MDRV was able to rapidly induce the production of interferons (IFNs) in host. Mechanistically, MDRV infection induced robust expression of IFNs in host mainly through RIG-I, MDA5 and TLR3-dependent signaling pathways. In addition, we observed that silencing VISA expression in 293T cells could significantly inhibit the secretion of IFNs. Remarkably, the production of IFNs was reduced by inhibiting the activation of NF-κB or knocking down the expression of IRF-7. Furthermore, our study showed that treatment of 293T cells and Muscovy duck embryo fibroblasts with IFNs markedly impaired MDRV replication, suggesting that these IFNs play an important role in antiviral response during the MDRV infection. Importantly, we also detected the induced expression of RIG-I, MDA5, TLR3 and type I IFN in Muscovy ducks infected with MDRV at different time points post infection. The results from in vivo studies were consistent with those in 293T cells infected with MDRV. Taken together, our findings reveal that the host can resist MDRV invasion by activating innate immune response involving RIG-I, MDA5 and TLR3-dependent signaling pathways that govern IFN production.