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Developing ultrabroad radar-infrared compatible stealth materials has turned into a research hotspot, which is still a problem to be solved. Herein, the copper sulfide wrapped by reduced graphene oxide to obtain three-dimensional (3D) porous network composite aerogels (CuS@rGO) were synthesized via thermal reduction ways (hydrothermal, ascorbic acid reduction) and freeze-drying strategy. It was discovered that the phase components (rGO and CuS phases) and micro/nano structure (microporous and nanosheet) were well-modified by modulating the additive amounts of CuS and changing the reduction ways, which resulted in the variation of the pore structure, defects, complex permittivity, microwave absorption, radar cross section (RCS) reduction value and infrared (IR) emissivity. Notably, the obtained CuS@rGO aerogels with a single dielectric loss type can achieve an ultrabroad bandwidth of 8.44 GHz at 2.8 mm with the low filler content of 6 wt% by a hydrothermal method. Besides, the composite aerogel via the ascorbic acid reduction realizes the minimum reflection loss (RLmin) of − 60.3 dB with the lower filler content of 2 wt%. The RCS reduction value can reach 53.3 dB m2, which effectively reduces the probability of the target being detected by the radar detector. Furthermore, the laminated porous architecture and multicomponent endowed composite aerogels with thermal insulation and IR stealth versatility. Thus, this work offers a facile method to design and develop porous rGO-based composite aerogel absorbers with radar-IR compatible stealth.

Background and Purpose ANRIL has long been considered as the strongest candidate gene at the 9p21 locus, robustly associated with stroke and coronary artery disease (CAD). However, the underlying molecular mechanism remains unknown. The present study works to elucidate such a mechanism. Methods Utilizing eQTL analysis we identified potential genes whose expression may be influenced by genetic variation in ANRIL. To verify the identified gene(s), knockdown and over-expression of ANRIL was evaluated in HUVECs and HepG2 cells. Ischemic stroke and CAD risk was then evaluated in the gene(s) demonstrated to be mediated by ANRIL in 3 populations of Chinese Han ancestry; two ischemic stroke populations including the Central China cohort (903 cases and 873 controls) and the Northern China cohort (816 cases and 879 controls), and one CAD cohort consisting of 772 patients and 873 controls. Results eQTL analysis identified CARD8 among others, with knockdown of ANRIL expression decreasing CARD8 expression and over-expression of ANRIL increasing CARD8 expression. The minor T allele of a previously identified CARD8 variant (rs2043211) was found to be significantly associated with a protective effect of ischemic stroke under the recessive model in two independent stroke cohorts. No significant association was found between rs2043211 and CAD. Conclusion CARD8 is a downstream target gene regulated by ANRIL. SNP rs2043211 in CARD8 is significantly associated with ischemic stroke. ANRIL may increase the risk of ischemic stroke through regulation of the CARD8 pathway.

Scheme 1. a) Schematic diagram of obtaining MXene nanoflakes by adopting a certain etching strategy. b) Schematic diagram of the potential EMA mechanism analysis of MXene structure. c) Schematic illustration of the multifunctional application of MXene composites.

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