Traditional gas sensing systems are facing efficiency challenges due to physically separated von Neumann architectures, making the construction of in-sensor computing neuromorphic olfactory systems urgently needed for low-power and low-latency scenarios. In this study, a reconfigurable neuromorphic heterostructure memristor based on MXene@SnS₂@PANI and an in-sensor computing olfactory system were proposed. Notably, the reconfigurable neuromorphic olfactory electronics differ fundamentally from conventional sensors. Specifically, the memristor’s circuit architecture supports both synaptic and neuronal computational functions, enabling reconfigurable responses to both electrical and gas stimuli within a single device, which substantially minimizes circuit complexity. Through modulation of the energy band under both gas and electrical signals, the device achieves reconfigurable neuromorphic computing features supporting both volatile and nonvolatile conductance updates. Under electrical stimulation, it demonstrates integrate-and-fire neuronal dynamics for gas flow recognition via a spiking neural network. Under gas exposure, neuromorphic synaptic behaviors are realized, enabling gas concentration identification through reservoir computing. The system has been successfully implemented for real-time hazardous gas monitoring and automated ventilation control, paving the way for next-generation neuromorphic intelligent sensing systems.

While sleep disorders are a known correlate of social memory deficits, the underlying neurocircuitry and molecular mechanisms remain poorly understood. Using an oxytocin (OXT)-specific sensor imaging approach, we discovered that chronic sleep deprivation (SD) reduced OXT neuropeptide release in the hippocampal CA2 and prelimbic cortex (PrL), thereby disrupting social memory encoding and retrieval processes, respectively. Using fiber photometry recordings and in vitro electrophysiology, we identified the activity of the predominantly OXT-expressing neurons in the paraventricular hypothalamic nucleus (PVN^OXT) were reduced following SD. Specific optogenetic activation of the PVN^OXT–CA2 pathway during encoding phase or PVN^OXT–PrL pathway during retrieval transiently restored SD-induced social memory deficits. Conversely, optogenetic high-frequency activation of PVN^OXT neurons enhanced the function of both PVN^OXT–CA2 and PVN^OXT–PrL pathways, promoting increased OXT release and providing sustained protection against SD-induced social memory deficits. These findings offer causal evidence that the PVN^OXT–CA2 and PVN^OXT–PrL pathways exert distinct modulatory roles in sleep-related social memory deficits and thereby nominate these pathways as precise targets for neuromodulation in sleep-related cognitive disorders.

Spinal cord injury (SCI) causes extensive neuronal loss, in which ferroptosis is critically involved. Although lipid transport at endoplasmic reticulum-mitochondria contact sites (ERMCSs) has been implicated in facilitating ferroptosis, the neuron-specific regulatory mechanisms remain elusive. Here, we show that neuronal ferroptosis is characterized by excessive ERMCS formation. Mechanistically, a systematic screening revealed the down-regulation of stearoyl-CoA desaturase 1 (SCD1), a critical enzyme in the synthesis of monounsaturated fatty acids (MUFAs) in neurons, following SCI (in vivo) or erastin treatment (in vitro). We demonstrated that SCD1 deficiency is the driving force behind aberrant ERMCS expansion, leading to increased lipid peroxidation and neuronal ferroptosis. Conversely, SCD1 overexpression could reverse these effects. Furthermore, we identified liver X receptor alpha (LXRα) as a direct transcriptional activator of SCD1. Pharmacological activation of LXRα with T0901317 upregulated SCD1 expression, which in turn restrained ERMCS formation, elevated MUFA levels, and ultimately inhibited neuronal ferroptosis. In murine SCI models, both adeno-associated virus-mediated neuronal SCD1 overexpression and LXRα agonist treatment effectively mitigated excessive ERMCS, reduced lesion size, preserved neuronal architecture, and improved functional recovery. Collectively, our study establishes the LXRα–SCD1 axis as a novel and druggable pathway for reducing neuronal loss and improving functional recovery by modulating ERMCS-dependent lipid exchange dynamics, revealing promising therapeutic targets after central nervous system trauma.

Exposures that disrupt the immune system can affect human health. This study aimed to understand immune variability influenced by exposures from the perspectives of systems biology and multiomics. We recruited 1,001 healthy participants and collected 183 exposures, 1,332 immunophenotypes, whole blood transcriptome, and plasma metabolome. Through exposure–immune wide association analysis, we identified 81 significant signals, with sleep and diet emerging as dominant exposures affecting the immunity. Sleep and diet influence the proportions of innate immune cells and the expression levels of immune cell surface proteins such as CD85j and CD16, respectively. Notably, distinct from the increase in interleukin-1β secretion caused by short-term late sleep onset, long-term late sleep onset triggered chronic inflammation with more metabolic changes. On the basis of the intracorrelation structure of exposure data, composite exposures were constructed and were found to have additional effects on immunophenotypes. Bidirectional mediation analysis revealed that sleep effects on immunity are commonly linked to the transcriptome, whereas dietary influences on immunity are primarily associated with the metabolome. We quantified the mediation effects of exposures, omics, and immunophenotypes and further demonstrated that these effects reflect human immune health or chronic diseases. Our study drew a comprehensive map of “exposure–immunome–omics” and is expected to provide guidance for future health assessment and management.

Hepatic encephalopathy (HE), a severe neurological complication of liver dysfunction, has long been regarded as a clinical issue confined to liver disease. However, recent clinical observations and basic research have revealed complex pathophysiological connections between HE and Parkinson’s disease (PD), 2 seemingly independent conditions. Patients with HE often exhibit irreversible extrapyramidal symptoms that closely resemble the motor disorders of PD; meanwhile, epidemiological studies suggest that individuals with liver disease—particularly non-alcoholic fatty liver disease (NAFLD)—may face an increased risk of developing PD. From the perspective of the gut–liver–brain axis, this study systematically explores the molecular mechanisms linking HE and PD, proposing a core hypothesis: HE creates a unique “neurotoxic soil” through ammonia toxicity, systemic neuroinflammation, and gut–liver–brain axis dysfunction. This soil may trigger PD in susceptible individuals, accelerate subclinical PD progression, or mimic PD-like pathology. The study analyzes in depth the direct regulatory role of ammonia in α-synuclein (α-syn) aggregation, the impact of liver disease-driven neuroinflammation on microglial activation and α-syn propagation, and the hypothesis of liver-derived α-syn transmission via the gut–liver–brain axis. It further discusses synergistic mechanisms such as manganese deposition, neurotransmitter imbalance, and gut microbiota metabolites. Based on these mechanisms, the study prospects translational medical applications, including the development of diagnostic biomarkers and novel therapeutic strategies such as “ammonia clearance plus” and gut–liver–brain axis targeting. This work provides new insights into how environmental metabolic factors contribute to neurodegenerative diseases and offers a theoretical basis for the combined prevention and treatment of HE and PD.

Understanding cellular dynamics requires real-time high-resolution imaging. Recent advancements in imaging technologies have provided unprecedented spatial and temporal resolutions, enabling the precise in situ monitoring of live-cell behavior. This review covers 4 advanced imaging modalities: stimulated emission depletion microscopy, structured illumination microscopy, single-molecule localization microscopy, and Raman spectroscopy. We summarize the principles, applications, advantages, and limitations of these methods, highlighting their significance for high-precision spatiotemporal monitoring of cellular structures and biochemical activities. These tools enable precise tracking of molecular interactions and analysis of cellular dynamics at the nanoscale, which is critical for understanding cellular physiology. The integration of these technologies into biomedical research has markedly enhanced our ability to observe live-cell processes, such as division, migration, differentiation, and signaling. The development and application of these high-precision imaging technologies hold substantial promise for improving disease diagnosis, therapeutic strategies, and drug discovery.

Mycotoxins are fungi-derived secondary metabolites that pose ecological and human health hazards. Deoxynivalenol (DON), as one of the most prevalent contaminating mycotoxins, has a detrimental impact on intestinal inflammation. Lycopene (LYC), a strong lipophilic carotenoid, is one of the most vital dietary antioxidants for human health. Thioredoxin-interacting protein (TXNIP), as a thioredoxin inhibitory protein, regulates NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation. We performed this work to probe the mechanisms by which LYC antagonizes DON-induced intestinal epithelium damage and the role of TXNIP in it. In the present study, we demonstrated that LYC relieved DON-induced structural and functional injury. We observed that LYC mitigated DON-induced inhibition of cell proliferation and cell cycle arrest, thereby delaying cellular senescence. LYC also mitigated DON-induced activation of TLR4/NF-κB/TNF-α signaling and inflammatory reaction. In addition, LYC prevented DON-induced up-regulation of TXNIP, thus inhibiting NLRP3 inflammasome activation and pyroptosis. Interestingly, TXNIP overexpression reversed the protective effect of LYC on DON-induced pyroptosis and senescence, but NLRP3 inhibitor restored these impairments. Our study suggested that LYC antagonized DON-induced intestinal epithelial cell senescence by suppressing TXNIP-mediated NLRP3 inflammasome activation. These findings show that TXNIP modulates intestinal function and thereby is a new curative molecule for intestinal diseases.

High-precision sensors are of fundamental importance in modern society and technology. Although there are various schemes for the construction of sensors relying on different physical mechanisms, obtaining sensors with higher levels of sensitivity and stronger robustness has always been expected. In particular, non-Hermitian quantum sensors have recently attracted substantial attention due to their unique properties. So far, 2 types of non-Hermitian sensors based on exceptional points and topological zero modes have been realized. Here, high-order exceptional bound states with robust properties are constructed for the first time. Based on these states, we propose theoretically and demonstrate experimentally another new type of non-Hermitian quantum sensors. Such sensors not only are robust against disorders but also have unprecedented sensitivity. Their sensing performance can display the improvement of many orders of magnitude over the previous non-Hermitian sensors. Furthermore, we design and fabricate such sensors based on circuit networks. Taking weak magnetic field detection as an example, we also experimentally demonstrate their sensing capabilities. Our work opens up new avenues for the development of highly sensitive sensors, which have a wide range of applications in various fields.

The growing demand for orthopedic implants, driven by an aging global population and the rising occurrence of bone abnormalities and defects, relies heavily on biocompatible titanium (Ti) and its alloys. However, their inherent biological inertness often results in poor osseointegration and increased vulnerability to bacterial infections, particularly those caused by biofilm-forming pathogens. Traditional antibiotic treatments frequently fail against biofilms and contribute to the escalating problem of antibiotic resistance, emphasizing the need for alternative therapies that do not foster resistance. Photodynamic therapy (PDT), which uses light-activated photosensitizers to generate reactive oxygen species (ROS) for effective bacterial eradication, presents a promising noninvasive strategy with high precision and low likelihood of resistance development. This review thoroughly explores the mechanisms of PDT and its application to Ti implants, focusing on both organic and inorganic photosensitizers. Moreover, considering current challenges, the study investigates approaches to improve PDT’s effectiveness in combating implant-related infections. These include optimizing PDT systems, developing new AIE-active photosensitizers, increasing oxygen supply to boost ROS production, combining multi-modal antibacterial treatments, and designing dual-functional implants. The review aims to identify current limitations and propose future directions, offering valuable insights to advance PDT-based strategies that enhance the antibacterial performance of Ti implants in the post-antibiotic era.

Autoimmune diseases (AIDs) are a group of immune-related disorders primarily affecting joints and surrounding tissues, often marked by chronic inflammation and autoimmune activation. Common types include systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, autoimmune cardiovascular diseases, and skin conditions. While their pathogenesis is unclear, recent studies suggest that abnormal gut microbiota may contribute. Previous research has shown that various patients with rheumatic disease exhibit altered gut microbiota, characterized by decreased microbial diversity, overall compositional changes, and microbiota-mediated functional alterations. Bacterial species closely associated with AIDs include Prevotella copri, Ruminococcus gnavus, and Ligilactobacillus salivarius. Dysregulated gut microbiota activates host immune responses through multiple mechanisms, including compromised intestinal barrier, systemic translocation, molecular mimicry of self-antigen epitopes, and changes in microbiota-derived metabolites, thereby substantially contributing to the development and progression of AIDs. Microbial metabolites, including short-chain fatty acids, tryptophan metabolites, and bile acid metabolites, are actively involved in driving disease progression. In addition, the therapeutic outcomes and adverse effects of immunotherapeutic agents can be modulated by gut microbiota through their impact on drug biotransformation processes. Clinically, analyzing gut microbiota characteristics can aid in disease diagnosis and prognosis prediction. Therapeutic strategies such as fecal microbiota transplantation, probiotics, prebiotics, and the Mediterranean diet may become effective measures for managing AIDs. This article reviews recent research progress, future directions, and the potential of microbiota-based interventions in treating AIDs.