A major bottleneck delaying the further commercialization of thin-film solar cells based on hybrid organohalide lead perovskites is interface loss in state-of-the-art devices. We present a generic interface architecture that combines solution-processed, reliable, and cost-efficient hole-transporting materials without compromising efficiency, stability, or scalability of perovskite solar cells. Tantalum-doped tungsten oxide (Ta-WO )/conjugated polymer multilayers offer a surprisingly small interface barrier and form quasi-ohmic contacts universally with various scalable conjugated polymers. In a simple device with regular planar architecture and a self-assembled monolayer, Ta-WO -doped interface-based perovskite solar cells achieve maximum efficiencies of 21.2% and offer more than 1000 hours of light stability. By eliminating additional ionic dopants, these findings open up the entire class of organics as scalable hole-transporting materials for perovskite solar cells.

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The performance of organic solar cells is determined by the delicate, meticulously optimized bulk-heterojunction microstructure, which consists of finely mixed and relatively separated donor/acceptor regions. Here we demonstrate an abnormal strong burn-in degradation in highly efficient polymer solar cells caused by spinodal demixing of the donor and acceptor phases, which dramatically reduces charge generation and can be attributed to the inherently low miscibility of both materials. Even though the microstructure can be kinetically tuned for achieving high-performance, the inherently low miscibility of donor and acceptor leads to spontaneous phase separation in the solid state, even at room temperature and in the dark. A theoretical calculation of the molecular parameters and construction of the spinodal phase diagrams highlight molecular incompatibilities between the donor and acceptor as a dominant mechanism for burn-in degradation, which is to date the major short-time loss reducing the performance and stability of organic solar cells.

Rotavirus, a leading cause of severe gastroenteritis and diarrhoea in young children, accounts for around 215,000 deaths annually worldwide1. Rotavirus specifically infects the intestinal epithelial cells in the host small intestine and has evolved strategies to antagonize interferon and NF-κB signalling2–5, raising the question as to whether other host factors participate in antiviral responses in intestinal mucosa. The mechanism by which enteric viruses are sensed and restricted in vivo, especially by NOD-like receptor (NLR) inflammasomes, is largely unknown. Here we uncover and mechanistically characterize the NLR Nlrp9b that is specifically expressed in intestinal epithelial cells and restricts rotavirus infection. Our data show that, via RNA helicase Dhx9, Nlrp9b recognizes short double-stranded RNA stretches and forms inflammasome complexes with the adaptor proteins Asc and caspase-1 to promote the maturation of interleukin (Il)-18 and gasdermin D (Gsdmd)-induced pyroptosis. Conditional depletion of Nlrp9b or other inflammasome components in the intestine in vivo resulted in enhanced susceptibility of mice to rotavirus replication. Our study highlights an important innate immune signalling pathway that functions in intestinal epithelial cells and may present useful targets in the modulation of host defences against viral pathogens.

We analyze how to realize Rec. 2020 wide color gamut with quantum dots. For photoluminescence, our simulation indicates that we are able to achieve over 97% of the Rec. 2020 standard with quantum dots by optimizing the emission spectra and redesigning the color filters. For electroluminescence, by optimizing the emission spectra of quantum dots is adequate to render over 97% of the Rec. 2020 standard. We also analyze the efficiency and angular performance of these devices, and then compare results with LCDs using green and red phosphors-based LED backlight. Our results indicate that quantum dot display is an outstanding candidate for achieving wide color gamut and high optical efficiency.

Highlights d Screening of gut microbiota metabolomes against hundreds of G protein-coupled receptors d Phylogenetically diverse gut microbes produce agonists for many GPCRs including orphans d Bioactivity-based screening reveals diet-microbe-host and microbe-microbe-host axes d Microbiota-derived GPCR ligands impact local and systemic host physiology

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Interferon-stimulated gene 56 (ISG56) family members play important roles in blocking viral replication and regulating cellular functions, however, their underlying molecular mechanisms are largely unclear. Here, we present the crystal structure of ISG54, an ISG56 family protein with a novel RNA-binding structure. The structure shows that ISG54 monomers have 9 tetratricopeptide repeat-like motifs and associate to form domain-swapped dimers. The Cterminal part folds into a super-helical structure and has an extensively positively-charged nucleotide-binding channel on its inner surface. EMSA results show that ISG54 binds specifically to some RNAs, such as adenylate uridylate (AU)-rich RNAs, with or without 5′ triphosphorylation. Mutagenesis and functional studies show that this RNAbinding ability is important to its antiviral activity. Our results suggest a new mechanism underlying the antiviral activity of this interferon-inducible gene 56 family member.