At room temperature, glasses are known to be brittle and fracture upon deformation. Zheng et al. show that, by exposing amorphous silica nanostructures to a low-intensity electron beam, it is possible to achieve dramatic shape changes, including a superplastic elongation of 200% for nanowires.

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Background: The molecular mechanisms of endotoxin tolerance remain not well elucidated. Results: IRG1, up-regulated by LPS and during sepsis, can feedback suppress the Toll-like receptor-triggered inflammatory response by increasing A20 expression via reactive oxygen species (ROS) in LPS-tolerized macrophages. Conclusion: Inducible IRG1 promotes endotoxin tolerance by increasing A20 expression through ROS. Significance: Providing new molecular mechanisms regulating hypoinflammation of sepsis and endotoxin tolerance.

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Effective recognition of viral infections and subsequent triggering of antiviral innate immune responses are essential for the host antiviral defense, which is tightly regulated by multiple regulators, including microRNAs (miRNAs). A previous study showed that miR-466l upregulates IL-10 expression in macrophages by antagonizing RNA-binding protein tristetraprolin-mediated IL-10 mRNA degradation. However, the ability of miR-466l to regulate antiviral immune responses remains unknown. Here, we found that interferon-alpha (IFN-a) expression was repressed in Sendai virus (SeV)-and vesicular stomatitis virus (VSV)-infected macrophages and in dendritic cells transfected with miR-466l expression. Moreover, multiple IFN-a species can be directly targeted by miR-466l through their 39 untranslated region (39UTR). This study has demonstrated that miR-466l could directly target IFN-a expression to inhibit host antiviral innate immune response.