Toll-like receptors (TLRs) are a family of pattern recognition receptors (PRR) with a crucial function in innate immune responses. Activation of TLR4 signaling at the plasma membrane by lipopolysaccharide (LPS) stimulates proinflammatory signaling pathways dependent on the E3 ubiquitin ligase TRAF6. Here we show the LPS-induced long non-coding RNA (lncRNA) Mirt2 functions as a checkpoint to prevent aberrant activation of inflammation, and is a potential regulator of macrophage polarization. Mirt2 associates with, and attenuates Lys63 (K63)-linked ubiquitination of, TRAF6, thus inhibiting activation of NF-κB and MAPK pathways and limiting production of proinflammatory cytokines. Adenovirus mediated gene transfer of Mirt2 protects mice from endotoxemia induced fatality and multi-organ dysfunction. These findings identify lncRNA Mirt2 as a negative feedback regulator of excessive inflammation.

The proposed working mechanism of the electrochemical CO2 reduction reaction on Fe1N4, Fe1N4–N1, and Fe1N4–O1 active sites.

Emerging sodium-ion batteries (SIBs) have attracted a great attention as promising energy storage devices because of their low cost and resource abundance. Nevertheless, it is still a major challenge to develop anode materials with outstanding rate capability and excellent cycling performance. Compared to intercalation-type anode materials, conversion-type anode materials are very potential due to their high specific capacity and low cost. A new insight and summary on the recent research advances on nanostructured conversion-type anode materials for SIBs is provided herein. The corresponding synthesis methods, sodium storage properties, electrochemical mechanisms, advanced techniques on studying the crystal structures, and optimization strategies for high-performance batteries are presented. Finally, the remaining challenges and perspectives for the future development of conversion-type anode materials in the energy storage fields are proposed. Figure 17. a) Time-lapse images showing the evolution of morphology of a CuO NW at an applied voltage of −3 V during the first sodiation process. b,c) In situ TEM images showing the 1st sodiation and the 1st desodiation of the single SnO 2 nanowire, respectively. d) Time-resolved TEM images from video frames show morphology and structure evolution as a function of sodiation time and its electron diffraction (ED) patterns. Schematic and structural evolution of e,f) the V 2 O 3 ⊂C-NTs and g,h) V 2 O 3 ⊂C-NTs⊂rGO electrodes observed by in situ TEM experiments, respectively, during constant potential discharge at 5 V. i,k) The morphology evolution of two α-MoO 3 nanobelts during the first sodiation process in a low magnification, in which the red arrows denote the reaction front. j) The measured relationship between the sodiation front position and the sodiation time for above two α-MoO 3 nanobelts. l) Time-resolved TEM images from video frames show the sodiation process of an individual Co 9 S 8 -filled CNT with an open end. All scale bars are 200 nm. m) Time-resolved TEM images from video frames reveal the appearance of fractures during the electrochemical sodiation process of an individual Co 9 S 8 -filled CNT with closed ends. All scale bars are 100 nm. n) Schematic showing the setup of the in situ experiment. HAADF-STEM images showing o) pristine and p) sodiated FeF 2 NPs and q) cropped time-lapse frames throughout the sodiation process. a) Reproduced with permission. [131]

The new porcine epidemic diarrhea (PED) has caused devastating economic losses to the swine industry worldwide. Despite extensive research on the relationship between autophagy and virus infection, the concrete role of autophagy in porcine epidemic diarrhea virus (PEDV) infection has not been reported. In this study, autophagy was demonstrated to be triggered by the effective replication of PEDV through transmission electron microscopy, confocal microscopy, and Western blot analysis. Moreover, autophagy was confirmed to benefit PEDV replication by using autophagy regulators and RNA interference. Furthermore, autophagy might be associated with the expression of inflammatory cytokines and have a positive feedback loop with the NF-κB signaling pathway during PEDV infection. This work is the first attempt to explore the complex interplay between autophagy and PEDV infection. Our findings might accelerate our understanding of the pathogenesis of PEDV infection and provide new insights into the development of effective therapeutic strategies.