As an emerging environmentally friendly material, the biggest advantage of wood-based materials lies in its renewability and green sustainability, which helps reduce the ecological impact on the environment. There have been some studies on room-temperature phosphorescent wood-based materials nowadays, but no one has explored them in the field of organic long persistent luminescence (OLPL). Here, we report the high-performance organic afterglow observed in the pyrylium salt (Pyr) induced photopolymerization system, and combine it with transparent wood to prepare unprecedented OLPL materials with emission maxima at approximately 596 nm and lasting for more than 1 h. The transparent wood matrix can provide a rigid environment for the Pyr system and act as an oxygen barrier, inhibiting non-radiative decay and oxygen quenching. At the same time, the transparent wood also has good transparency and other characteristics, which can be considered one of the most promising alternative materials in the future. We have also prepared OLPL wood coatings, adhesives, and wood-plastic composites. The combination of various wood-based materials and luminescent technology not only enhances aesthetics and practicality of wood products, but also promotes technological innovation and development in the fields of anti-counterfeiting and data encryption, green building materials, and emergency lighting.

Highly efficient synthesis of axially chiral biaryls bearing a beta-aryl ketone framework is achieved by an atroposelective C-H alkylation reaction of 1-aryl isoquinoline derivatives with cyclopropanols. Judiciously choosing SPINOL-derived trisubstituted SCpRh as the catalyst is crucial for the desired asymmetric alkylation reaction over the competitive formation of alkenylation byproducts, delivering the target axially chiral biaryls in 40-99% yields and 48-97% ee. Further mechanistic studies suggested that Rh-catalyzed C-H bond cleavage serves as the turnover-limiting step, while the Cu-mediated transformation of cyclopropyl alcohols into their corresponding enones is established as the key source of the active alkylation reagents.

Organic long persistent luminescence (OLPL) materials, with their hour-long afterglow, hold great promise across numerous applications, yet their performance lags behind that of inorganic counterparts. A deeper understanding of the underlying photophysical mechanisms, particularly the effective control of radical intermediates, is essential for developing high-performance OLPL materials; while systematic studies on the intrinsic stability of radical intermediates and their impact on OLPL performance remain scarce. Here biphenyl groups is introduced into a luminophore-matrix-donor three-component OLPL system. By varying substituents at the ortho-position of the biphenyl groups, the stability of radical cations is systematically modulated, and their influence on OLPL properties is investigated. Combined experimental results and theoretical calculations reveal that increased flexibility of the biphenyl bond and adjustable conformations lead to higher stability of radical cations, thereby significantly enhancing OLPL performance. Based on this understanding, a luminophore with two biphenyl groups is designed to successfully achieve remarkable afterglow brightness close to inorganic Sr2Al14O25/Eu2+, Dy3+ materials. Furthermore, these OLPL materials exhibit time-encoded afterglow properties and promising applications in advanced anti-counterfeiting, as well as background-independent bioimaging functions. This work not only provides a novel strategy for constructing high-performance OLPL materials but also lays a foundation for their widespread application in various fields.

Dysfunctional NF-kappa B signaling is critically involved in inflammatory bowel disease (IBD). We investigated the mechanism by which RIPK1 and TRADD, two key mediators of NF-kappa B signaling, in mediating intestinal pathology using TAK1 IEC deficient model. We show that phosphorylation of TRADD by TAK1 modulates RIPK1-dependent apoptosis. TRADD and RIPK1 act cooperatively to mediate cell death regulated by TNF and TLR signaling. We demonstrate the pathological evolution from RIPK1-dependent ileitis to RIPK1- and TRADD-co-dependent colitis in TAK1 IEC deficient condition. Combined RIPK1 inhibition and TRADD knockout completely protect against intestinal pathology and lethality in TAK1 IEC KO mice. Furthermore, we identify distinctive microbiota dysbiosis biomarkers for RIPK1-dependent ileitis and TRADD-dependent colitis. These findings reveal the cooperation between RIPK1 and TRADD in mediating cell death and inflammation in IBD with NF-kappa B deficiency and suggest the possibility of combined inhibition of RIPK1 kinase and TRADD as a new therapeutic strategy for IBD.

BACKGROUND: Heart failure (HF), which is the terminal stage of many cardiovascular diseases, is associated with low survival rates and a severe financial burden. The mechanisms, especially the molecular mechanism combined with new theories, underlying the pathogenesis of HF remain elusive. We demonstrate that phosphorylation-regulated dynamic liquid-liquid phase separation of HIP-55 (hematopoietic progenitor kinase 1-interacting protein of 55 kDa) protects against HF. METHODS: Fluorescence recovery after photobleaching assay, differential interference contrast analysis, pull-down assay, immunofluorescence, and immunohistochemical analysis were used to investigate the liquid-liquid phase separation capacity of HIP-55 and its dynamic regulation in vivo and in vitro. Mice with genetic deletion of HIP-55 and mice with cardiac-specific overexpression of HIP-55 were used to examine the role of HIP-55 on beta-adrenergic receptor hyperactivation-induced HF. Mutation analysis and mice with specific phospho-resistant site mutagenesis were used to identify the role of phosphorylation-regulated dynamic liquid-liquid phase separation of HIP-55 in HF. RESULTS: Genetic deletion of HIP-55 aggravated HF, whereas cardiac-specific overexpression of HIP-55 significantly alleviated HF in vivo. HIP-55 possesses a strong capacity for phase separation. Phase separation of HIP-55 is dynamically regulated by AKT-mediated phosphorylation at S269 and T291 sites, failure of which leads to impairment of HIP-55 dynamic phase separation by formation of abnormal aggregation. Prolonged sympathetic hyperactivation stress induced decreased phosphorylation of HIP-55 S269 and T291, dysregulated phase separation, and subsequent aggregate formation of HIP55. Moreover, we demonstrated the important role of dynamic phase separation of HIP-55 in inhibiting hyperactivation of the beta-adrenergic receptor-mediated P38/MAPK (mitogen-activated protein kinase) signaling pathway. A phosphorylation-deficient HIP-55 mutation, which undergoes massive phase separation and forms insoluble aggregates, loses the protective activity against HF. CONCLUSIONS: Our work reveals that the phosphorylation-regulated dynamic phase separation of HIP-55 protects against sympathetic/adrenergic system-mediated heart failure.