Cellulose nanofibrils (CNFs) are strong, flexible biopolymers, whereas producing large-area (centimeter-scale) optical films with tunable, vivid interference colors with them remains difficult. The amorphous regions within the fibrils reduce birefringence and prevent uniform color formation. Here, we develop an integrated salt-assisted assembly (iSAA) strategy that combines metal-ion crosslinking with organic–inorganic coassembly to fabricate nanofibril–crystal composite films with tunable, vibrant colors. By adjusting the concentration of aluminum salt during assembly, we precisely control optical phase retardation from about 400 nm to over 2,500 nm, covering the full range of the interference colors. The resulting films appear naturally transparent while displaying intense colors across the visible spectrum when viewed under polarized light. We further demonstrate the universality of the iSAA strategy by fabricating films from different biopolymer fibrils (e.g., chemically modified CNFs and protein amyloid fibrils) on hydrophilic and hydrophobic substrates. Additionally, coupling the transmitted colors of these films and their intrinsic optical haze produces a novel spectrally selective polychromatic lighting effect. These results establish the iSAA strategy as a general platform for engineering nanofibril-based birefringent materials with programmable polarization optics, expanding their potential in advanced optical and energy-efficient applications.

Liquid biopsy strategies for glioma leveraging metabolic features remain inadequately investigated. Herein, we performed liquid chromatography-mass spectrometry-based metabolomic and proteomic analyses on 189 tissue samples from 122 adult glioma patients, and nuclear magnetic resonance-based targeted metabolomic profiling on plasma samples from 430 participants encompassing 82 adult glioma patients, 53 pediatric primary brain tumor patients, 80 pancreatic cancer patients, and 215 nontumor controls. The results demonstrate that aberrations in “Alanine, aspartate, and glutamate metabolism” and “tricarboxylic acid (TCA) cycle” pathways are ubiquitous across subtypes and progression of glioma. Notably, these signatures could be captured in plasma, thereby reflecting shared metabolic features between tumor tissues and circulation. Based on these findings, we developed a liquid biopsy model comprising 7 plasma metabolites (including creatine, lactic acid, succinic acid, N,N-dimethylglycine, 2-oxoglutaric acid, acetic acid, and glutamic acid). This model achieved high diagnostic accuracy in independent test sets (area under the curve = 0.964 for adult glioma set; and 0.925 for pediatric primary brain tumor set). Meanwhile, the model exhibited a higher sensitivity of 0.885 for glioma compared to 0.800 for pancreatic cancer, providing evidence to support the tumor selectivity of the model. Together, we present a plasma-based metabolomic classifier that faithfully mirrors the core metabolic reprogramming of glioma and can serve as a readily available liquid biopsy tool.

The pathophysiology of ischemic stroke is critically mediated by detrimental neuroinflammation. Tripartite motif-containing 21 (TRIM21) serves as an E3 ubiquitin ligase that regulates important biological functions. Nonetheless, the specific role of TRIM21 in neuroinflammation and ischemic brain injury remains unclear. In this study, we found that TRIM21 expression was up-regulated in astrocytes within the peri-infarct regions of mice subjected to transient middle cerebral artery occlusion (tMCAO) and in an in vitro oxygen–glucose deprivation and reoxygenation (OGD/R) model. TRIM21 deficiency alleviated cerebral ischemia/reperfusion (I/R) injury by attenuating the inflammatory responses and oxidative stress. Mechanistically, our findings demonstrated that TRIM21 interacts with MDA5 and sequentially promotes the K63-linked ubiquitination and stabilization of MDA5, ultimately activating the nuclear factor κB (NF-κB) pathway in astrocytes. Moreover, MDA5 overexpression effectively reversed protective effects of TRIM21 deficiency after cerebral ischemia. Consistently, brain-targeted TRIM21 silencing with nanoparticle delivery considerably ameliorated cerebral I/R injury. Collectively, our findings identify TRIM21 as a novel astrocyte-specific mediator of neuroinflammation in cerebral ischemic injury and highlight its potential as a therapeutic target for ischemic stroke.

Rapid urbanization intensifies hygiene and sustainability challenges in drainage systems, where conventional floor drains suffer from odor backflow, bacterial growth, and pathogen transmission. Existing disinfection methods depend on external power or chemicals, increasing energy consumption and environmental pollution. Herein, we develop an intelligent floor drain system that enables self-powered disinfection by recovering wastewater energy. By synergistically integrating a turbine blade drain valve, a magnetic levitation module, a contactless drive module, and an electromagnetic power generation (EMG) module, the intelligent floor drain system recovers energy from wastewater for power generation while maintaining its traditional functionality. The EMG module is able to produce a peak power output of 0.8 mW at a drainage rate of 4.15 l/min. A voltage-multiplying circuit boosts energy output by 55%. The system was able to achieve 98.2% sterilization efficiency after 50 min of operation. This work contributes to the global goals of sustainability and energy efficiency.

tRNA-derived small RNAs (tsRNAs) or tRNA-derived fragments (tRFs) are an important class of regulatory molecules whose role in cardiac hypertrophy remains largely unknown. Here, we identified a novel tRF contributing to the regulation of cardiac hypertrophy that we termed CHAtRF (cardiac hypertrophy-associated tRF). The CHAtRF level was increased in mice and in patients with cardiac hypertrophy. CHAtRF deficiency attenuated angiotensin II (AngII)-induced cardiac hypertrophy and restored the heart function, while CHAtRF overexpression enhanced hypertrophic responses. Mechanistically, CHAtRF directly interacts with SRSF5 and blocks SRSF5 to bind with Psmg4 pre-mRNA, which mediates alternative splicing of Psmg4 pre-mRNA and promotes exon 2 skipping of Psmg4. CHAtRF-dependent alternative splicing of Psmg4 inhibits the expression of Psmg4 full-length isoform, resulting in progression of pathological hypertrophy. The ability of CHAtRF to regulate hypertrophy was confirmed in hiPSC-CMs, and CHAtRF serum levels are higher in individuals with myocardial hypertrophy or heart failure. Our findings reveal new insights into the previously unrecognized role of tsRNAs during cardiac hypertrophy, which provide potential novel therapeutic targets for pathological hypertrophy and might serve as potential biomarkers for diagnosing cardiac hypertrophy and heart failure.

The trabecular meshwork (TM) plays a pivotal role in maintaining intraocular pressure (IOP) by regulating aqueous humor outflow. Nuclear factor erythroid 2-related factor 2 (NRF2) was identified as a key transcriptional controller of TM redox balance and mitochondrial function. Transcriptomic profiling of tert-butyl hydroperoxide (tBHP)-induced oxidative injury revealed NRF2 pathway involvement in TM cellular defense. NRF2 knockout (KO) mice exhibited impaired aqueous humor dynamics, elevated IOP, and TM oxidative damage. In vitro, NRF2 knockdown aggravated oxidative stress and mitochondrial dysfunction, whereas NRF2 overexpression mitigated tBHP-induced cytotoxicity. The results of the gene set enrichment analysis (GSEA) indicated enrichment of oxidative phosphorylation pathway in NRF2-deficient cells. Chromatin immunoprecipitation sequencing (ChIP-seq) confirmed NDUFS7 as a direct NRF2 target essential for mitochondrial complex I integrity. Restoration of NDUFS7 expression in NRF2-deficient TM cells or KO mice rescued mitochondrial impairment. Collectively, these findings establish the NRF2/NDUFS7 axis as a central defense mechanism protecting TM from oxidative injury and suggest potential therapeutic strategies for glaucoma-associated ocular hypertension.

Behavior plays a critical role in health and disease. Although molecular omics have advanced the understanding of biological mechanisms, they alone cannot explain the role of behavior in health, and traditional behavioral measurement technologies have struggled to capture the dynamic, multidimensional, and heterogeneous nature of real-world behaviors. With the development of digital technologies such as wearable devices, smartphone sensors, and ecological momentary assessment, behavioromics has emerged as a new research paradigm with a holistic systems perspective, integrating continuous, multimodal behavioral data with molecular, physiological, and environmental information. By organizing behavioral measurement, modeling, and interpretation within a unified analytical framework, behavioromics reveals dynamic behavioral patterns, supports mechanism-informed inference, and identifies actionable targets for early intervention. Despite ongoing challenges in data heterogeneity, causal interpretation, and ethical governance, behavioromics holds promise for reshaping disease prediction, early detection, and precision intervention, and for advancing proactive health through earlier, behavior-centered prevention.

Chemical alterations in metal oxides during manipulation greatly diminish their potential in artificial photosynthesis. Clarifying and overcoming these changes is crucial for realizing the sustainable generation of solar fuels and chemicals. Here, employing multimodal operando techniques, we elucidated the degradation mechanism of copper oxide (CuO_x) photocathodes under operational conditions, revealing an electron-mediated reductive photocorrosion pathway: Cu₂O/CuO → Cu₂O → Cu. These key findings led us to engineer an ultrathin carbon layer encapsulation strategy formed via electrodeposition-coupled self-assembly of carbon nanodots. This protective layer enables efficient photoelectron extraction and spatial isolation. The resulting CuO_x@C exhibits gratifying durability with unaltered phases and steady photocurrent throughout extended operation exceeding 24 h. To enhance activity and selectivity toward ethylene, Ag nanoparticles were integrated onto CuO_x@C. The Ag decoration enhances CO₂ adsorption, stabilizes *CO intermediate, and facilitates the crucial *CO–*CO coupling. The Faraday efficiency for CO₂-to-ethylene conversion on CuO_x@C/Ag reaches up to ~66.4% and retains ~95% of its initial performance after prolonged use. This synergistic strategy of carbon encapsulation and metal decoration exhibits broad applicability, as validated by CuO_x@C/Ru, CuO_x@C/Pd, and BiVO₄@C/Pt. Our work provides a universal design framework for efficient and durable photoelectrodes, accelerating their transition from laboratory prototypes to scalable technologies.

Liver metastasis remains a major challenge in cancer treatment, yet its cellular and molecular landscape remains poorly defined at the pan-cancer level. Here, we construct a single-cell transcriptomic atlas of liver metastases across multiple cancer types by analyzing 100 single-cell RNA sequencing samples, profiling over 460,000 cells, and identifying 121 distinct cellular subtypes. We define 4 representative cellular programs (CPs) associated with liver metastasis, revealing how cellular composition and intercellular interactions within the tumor microenvironment drive metastatic progression and immune modulation. These CPs recapitulate a dynamic transition from immunoactive states, marked by natural-killer-cell-mediated immune surveillance and macrophage-driven angiogenesis, to immunosuppressive environments dominated by regulatory T cell infiltration and immune exclusion. The shift is marked by progressive alterations in immune infiltration, stromal remodeling, and tumor-intrinsic adaptations, elucidating key mechanisms of immune evasion and metastatic niche formation. Our study provides a high-resolution framework for understanding the heterogeneity and evolution of liver metastasis and highlights the potential of CP-based stratification to inform therapeutic strategies targeting the metastatic tumor microenvironment.