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Ballistic impact response of resistance-spot-welded (RSW) double-layered (2 × 1.6 mm) plates (190 mm × 150 mm) for Q&P980 steel impacted by a round-nosed steel bullet (12 mm diameter and 30 mm length) was investigated by using gas gun and high-speed camera system. The RSW specimens were spot welded using a 6 mm diameter electrode face producing a 7.2 mm diameter fusion zone of the spot weld. The ballistic curve and energy balance for the tests of the spot weld of the RSW specimens at different velocity were analyzed to characterize the ballistic behavior of the RSW specimens under bullet impact. The fracture mechanisms of the RSW specimens under bullet impact were presented. For the tests below the ballistic limit, the cracks initiated from the notch-tip and propagated along the faying surface or obliquely through the thickness depending on the impact velocity. For the tests above the ballistic limit, the plug fracture in the front plate of the RSW specimen could be caused by the thinning-induced necking in the BM near the HAZ, while the plug fracture in the rear plate of the RSW specimens may be consist of the circumferential cracking from the rear surface and the bending fracture of the hinged part of material. The effects of the electrode indentation and the weld interfaces on deformation and fracture of the RSW specimens under bullet impact were revealed. For the tests above the ballistic limit, the circumferential fracture from the rear surface of the RSW specimens was always initiated along the interior periphery of the electrode indentation and the crack paths were along the FZ/CGHAZ or CGHAZ/ FGHAZ interface. When the circumferential crack also formed outside the electrode indentation, the fracture on the BM/HAZ interface could be found. On the front plate of the RSW specimens, the shear/ bending induced cracking from the notch-tip were observed and the crack paths were along the FZ/ CGHAZ or CGHAZ/FGHAZ interface. [ABSTRACT FROM AUTHOR]

The gut microbiota and microRNAs play important roles in the defense against infection. However, the role of miR-146a in L. monocytogenes infection and gut microbiota remains unclear. We tried to determine whether miR-146a controlled L. monocytogenes infection by regulating the gut microbiota. Wild-type and miR-146a-deficient mice or macrophages were used to characterize the impact of miR-146a on animal survival, cell death, bacterial clearance, and gut microbiota following L. monocytogenes challenge. We found that L. monocytogenes infection induced miR-146a expression both in vitro and in vivo. When compared to wild-type mice, miR-146a-deficient mice were more resistant to L. monocytogenes infection. MiR-146a deficiency in macrophages resulted in reduced invasion and intracellular survival of L. monocytogenes. High-throughput sequencing of 16S rRNA revealed that the gut microbiota composition differed between miR-146a-deficient and wild-type mice. Relative to wild-type mice, miR-146a-deficient mice had decreased levels of the Proteobacteria phylum, Prevotellaceae family, and Parasutterella genus, and significantly increased short-chain fatty acid producing bacteria, including the genera Alistipes, Blautia, Coprococcus_1, and Ruminococcus_1. Wild-type mice co-housed with miR-146a-deficient mice had increased resistance to L. monocytogenes, indicating that miR-146a deficiency guides the gut microbiota to alleviate infection. Together, these results suggest that miR-146a deficiency protects against L. monocytogenes infection by regulating the gut microbiota. [ABSTRACT FROM AUTHOR]

Infectious agents can reach the placenta either via the maternal blood or by ascending the genito-urinary tract, and then initially colonizing the maternal decidua. Decidual stromal cells (DSCs) are the major cellular component of the decidua. Although DSCs at the maternal-fetal interface contribute to the regulation of immunity in pregnancy in the face of immunological and physiological challenges, the roles of these DSCs during viral infection remain ill defined. Here, we characterized the response of DSCs to a synthetic double-stranded RNA molecule, polyinosinic-polycytidylic acid [poly(I:C)], which is a mimic of viral infection. We demonstrated that both transfection of cells with poly(I:C) and addition of extracellular (non-transfected) poly(I:C) trigger the necroptosis of DSCs and that this response is dependent on RIG-I-like receptor/IPS-1 signaling and the toll-like receptor 3/TIR-domain-containing adapter-inducing interferon-β pathway, respectively. Furthermore, following poly(I:C) challenge, pregnant mixed lineage kinase domain-like protein-deficient mice had fewer necrotic cells in the mesometrial decidual layer, as well as milder pathological changes in the uterine unit, than did wild-type mice. Collectively, our results establish that necroptosis is a contributing factor in poly(I:C)-triggered abnormal pregnancy and thereby indicate a novel therapeutic strategy for reducing the severity of the adverse effects of viral infections in pregnancy. [ABSTRACT FROM AUTHOR]

Dynamic damage evolution and its influence on the constitutive relation for materials in high strain rate are experimentally and theoretically studied. It is revealed that damage evolution is a rate-dependent process depending on both strain and strain rate, and can be modeled by the thermo-activation mechanism. For polymer PMMA, PP/PA blend and concrete, the coupled damage evolution law and the rate dependent constitutive relation (DM-ZWT model) are obtained and well supported by the experimental data. [ABSTRACT FROM AUTHOR]