Excellent electromagnetic interference (EMI) shielding ability, light weight, and good heat resistance are highly required for practical applications of EMI shielding materials, such as in areas of aerospace, aircraft, and automobiles. Herein, a lightweight and robust carbon nanotube (CNT)/polyimide (PI) foam was developed for efficient and heat-resistant EMI shielding. Thanks to poly­(vinyl pyrrolidone) (PVP) as a surfactant that not only promotes the uniform dispersion of CNTs to form perfect CNT conductive networks but also can be removed in situ during the polymerization process, the density of resultant CNT/PI foam is only 32.1 mg·cm–3, and the EMI shielding effectiveness (EMI SE) is up to 41.1 dB, which represents one of the highest EMI SE values compared to previously reported polymer-based foams. The CNT/PI foam also achieves the absorption coefficient (A) of up to 82.3%, which is very impressive in CNT/polymer foams at comparable EMI SE levels. The PI matrix endows the foam with excellent heat resistance. The as-prepared CNT/PI foam presents a higher EMI SE than 35 dB even after being subjected to the flame of an alcohol burner. Moreover, the compressive strength and compressive modulus are up to 240.9 and 323.9 kPa. These results indicate its certain application potential in the harsh requirement of aeronautics and aerospace industries as a highly efficient and lightweight EMI shielding material.

The NLR family pyrin domain containing 3 (NLRP3) inflammasome is one of the best-characterized inflammasomes in humans and other mammals. However, knowledge about the NLRP3 inflammasome in nonmammalian species remains limited. Here, we report the molecular and functional identification of an NLRP3 homolog (DrNLRP3) in a zebrafish (Danio rerio) model. We found that DrNLRP3's overall structural architecture was shared with mammalian NLRP3s. It initiates a classical inflammasome assembly for zebrafish inflammatory caspase (DrCaspase-A/-B) activation and interleukin 1β (DrIL-1β) maturation in an apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC)-dependent manner, in which DrNLRP3 organizes DrASC into a filament that recruits DrCaspase-A/-B by homotypic pyrin domain (PYD)–PYD interactions. DrCaspase-A/-B activation in the DrNLRP3 inflammasome occurred in two steps, with DrCaspase-A being activated first and DrCaspase-B second. DrNLRP3 also directly activated full-length DrCaspase-B and elicited cell pyroptosis in a gasdermin E (GSDME)-dependent but ASC-independent manner. These two events were tightly coordinated by DrNLRP3 to ensure efficient IL-1β secretion for the initiation of host innate immunity. By knocking down DrNLRP3 in zebrafish embryos and generating a DrASC-knockout (DrASC−/−) fish clone, we characterized the function of the DrNLRP3 inflammasome in anti-bacterial immunity in vivo. The results of our study disclosed the origin of the NLRP3 inflammasome in teleost fish, providing a cross-species understanding of the evolutionary history of inflammasomes. Our findings also indicate that the NLRP3 inflammasome may coordinate inflammatory cytokine processing and secretion through a GSDME-mediated pyroptotic pathway, uncovering a previously unrecognized regulatory function of NLRP3 in both inflammation and cell pyroptosis.

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Due to a long history of improper and excessive use, Penicillin G (Pen G) and erythromycin (Ery) are regularly detected in environmental samples and pose a great threat to human health. Here, we set out to investigate effects of Pen G, Ery or their mixture on lipid metabolism and gut microbiota in order to better understand their toxicological mechanisms. Male C57BL/6J mice were exposed either to 60 μg/ml Pen G, Ery or a half mixture of both for 6 weeks or to 10 μg/ml Pen G, Ery or a half mixture of both for 14 weeks. In a recovery experiment, male mice were exposed to 60 μg/ml Pen G or Ery for 2 weeks and then maintained without antibiotics for up to 8 weeks. It was observed that oral exposure to Pen G, Ery or their mixture induced lipid metabolism dysfunction, characterized by significantly increased lipid accumulations, triglycerides (TG) levels and expression of key genes involved in free fatty acid (FFA) synthesis, FFA transport and TG synthesis in the liver. In addition, Pen G and Ery exposure induced an inflammatory response as indicated by the increase of serum lipopolysaccharide levels and the up-regulation of key genes that regulate immune responses in the liver, fat, colon and ileum. Moreover, Pen G and Ery exposure rapidly and dramatically altered the composition of the microbiota in feces and cecum. Furthermore, high throughput sequencing of V3-V4 region of bacterial 16S rRNA gene revealed additional significant changes in the cecal microbiota of antibiotics-treated mice. Importantly, it took a very long time to reconstitute the normal composition of the gut microbiota after it was imbalanced by antibiotics exposure. Orally administered Pen G and Ery (especially to the latter) can induce gut microbiota dysbiosis, which may indirectly link antibiotic exposure to host metabolic disorders and inflammation.