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The progression of rheumatoid arthritis (RA) is critically aggravated by synovial M1 macrophage-mediated inflammatory infiltration and excessive reactive oxygen species (ROS) accumulation. While emerging heteronuclear diatomic catalysts show potential in inflammatory modulation, their therapeutic efficacy remains constrained by insufficient control over interatomic synergy and multi-active sites regulatory precision. This work pioneers a spatial confinement strategy to engineer heteronuclear diatomic nanozymes (HDNs) with dual-pathway therapeutic capabilities for RA. We investigate Fe and Co sites embedded in a nitrogen-coordinated carbon matrix, where the heteronuclear pair adopts an asymmetric Fe and Co configuration with tunable interatomic distances, facilitated by N-bridging ligands. This architecture enables spin-state and d-band center alignment, lowering activation barriers for enzymatic ROS scavenging, which demonstrates multi-enzyme mimetic activity, achieving 3.66-fold higher SOD-like enzyme reaction and 3.21-fold enhanced CAT-like catalytic efficiency versus monoatomic controls. HDNs reverse RA by enhancing M2 macrophage polarization to achieve an anti-inflammatory environment. Transcriptome sequencing validates that HDNs modulate immune homeostasis and inhibits the IL-17 and TNF pathways, promoting chondrocyte recovery. Our findings establish insights into the spatial confinement effect of HDNs, establishing a transformative platform for remodeling redox and immune homeostasis in RA-related pathologies.
This study pioneers the incorporation of hydroxyethyl cellulose (HEC) into electrochemiluminescence (ECL) sensing strategy. By modifying a novel velvet-like graphitic carbon nitride (V-g-C3N4) with exceptional conductivity and luminescent properties, we successfully constructed a highly sensitive ECL sensor based on HEC-functionalized V-g-C3N4 (HEC/V-g-C3N4). The incorporation of HEC ensured stable immobilization of V-g-C3N4 on glassy carbon electrode surface. This facilitated the generation of more excited-state species, which significantly enhanced the ECL signal intensity. Compared to the commonly used chitosan-functionalized V-g-C3N4 (CS/V-g-C3N4), HEC/V-g-C3N4 exhibited a 4.35-fold enhancement in ECL intensity. Thus, HEC/V-g-C3N4 was applied in ECL sensors for the ultra-sensitive detection of 3-nitro-l-tyrosine (3-NT) in human saliva. Under optimized conditions, the sensor demonstrated a wide detection range (1 × 10-10 - 1 × 10-5 M) and an exceptionally low detection limit (2.8 × 10-11 M). When applied to the detection of 3-NT in saliva samples, the sensor achieved high accuracy, with recoveries ranging from 96.77% to 106.1% and relative standard deviations between 1.15% and 5.56%. The results highlight the ECL sensor's excellent selectivity, stability, and reproducibility, offering a novel, reliable, and cost-effective platform for the high-sensitivity detection of 3-NT in saliva from healthy individuals.
Parkinson's disease (PD) is a progressive neurodegenerative disorder for which no curative therapy currently exists. Qihuang needle therapy (QNT) is a novel acupuncture technique that has demonstrated clinical promise in alleviating PD symptoms, but its neuroplasticity mechanisms remain unexplored. This trial aims to investigate the efficacy and neurological effects of the QNT via multimodal MRI. This triple-arm randomized controlled trial will enroll 69 PD patients randomized into three groups (1:1:1): verum acupuncture, sham acupuncture, or wait-list control. Patients in the verum and sham groups will receive eight treatment sessions over 4 weeks, followed by an 8-week follow-up period. The control group will not receive any acupuncture treatment throughout the trial. Clinical outcomes included the Unified Parkinson's Disease Rating Scale Part III (UPDRS-III), Non-Motor Symptoms Scale (NMSS), 39-item Parkinson's Disease Questionnaire (PDQ-39), muscle rigidity (shear-wave elastography), and gait/balance parameters (Footscan system). Multimodal MRI will evaluate neuroplasticity markers: gray matter volume, functional connectivity, white matter integrity, nigral iron deposition, and neuromelanin content. This protocol pioneers the integration of the QNT with advanced neuroimaging to elucidate its neuroplasticity mechanisms in PD, providing high-level mechanistic evidence for the integration of the QNT into PD care and optimizing integrative treatment strategies that combine traditional Chinese and Western medicine. (http://itmctr.ccebtcm.org.cn/), Identifier :ITMCTR2025000402.
Enhancing the conduction and polarization properties of the emerging two-dimensional carbon material graphdiyne (GDY) represents a crucial step in broadening its application in microwave absorption. A novel strategy was proposed to improve the microwave absorption performance of GDY through precise regulation of single-atom structures. Using three-dimensional spherical GDY as a substrate, Two Fe single-atom absorbers were successfully constructed: one anchored by Fe-N-GDY (FeN2C2) via sp-N/sp-C cooperative coordination, and the other anchored by Fe-GDY (FeC4) via sp-C coordination alone. Combined experimental characterization and theoretical calculations revealed that the FeN2C2 configuration induces stronger charge transfer and dipole polarization. This effect synergistically optimizes both the dielectric loss and impedance matching of the material. Consequently, the optimal sample Fe-N-GDY achieved an effective absorption bandwidth of 5.98 GHz at a matched thickness of 2.0 mm, with a minimum reflection loss of -51.2 dB. The strategy was further extended to multiple 3d transition metals (Cr, Mn, Co, Ni, Cu, and Zn). Results indicate that Group VIII elements (Fe, Co, Ni) exhibit superior performance in practical materials due to their electronic structures that favor balancing polarization and conduction losses. Radar cross section simulations confirm the exceptional attenuation capabilities of this series of absorbers in real-world scenarios. This work not only pioneers new applications for GDY in microwave absorption but also establishes a theoretical foundation for rationally designing atomically precise electromagnetic functional materials by revealing the "single-atom structure-property" correlation.
Origami-structured triboelectric nanogenerators have been demonstrated to be effective for harvesting water energy and other natural energy sources. However, achieving both a high power output and seamless integration into daily life applications remains challenging. Here, we present a double-W origami device through multilayer folding of a single substrate, enabling enhanced contact-separation motion within compact spaces for linear and arc motion energy harvesting. Through systematic evaluation of 22 configurations, the optimal structure was identified. When integrated with a voltage multiplier circuit, the device demonstrates a 14.21-fold increase in transferred charge, delivers a peak power of 14.78 mW (the volume power density and average power density are 587.37 W m-3 and 28.51 W m-3 at compressed volume, respectively), and can illuminate 948 LEDs. This work not only pioneers a new approach for an origami triboelectric nanogenerator in harvesting arc motion energy but also advances its seamless integration with real-world applications through integrated co-design of device architecture, power management, and system implementation.
Bone defects remain a significant challenge in bone tissue engineering, driving an urgent need for advanced materials with enhanced therapeutic properties. Additive manufacturing highlights a unique capacity for customization, which enables the precise realization of complex and personalized composite scaffolds. This study innovatively integrates the superior mechanical properties of polycaprolactone (PCL) with the antibacterial characteristics of S53P4 bioactive glass. Utilizing thermal melt extrusion processing and fused deposition modeling (FDM) technology, we fabricated gradient-structured S53P4@PCL composite three-dimensional porous scaffolds with varying doping ratios (5 wt%, 10 wt%, 20 wt%). To further improve the antibacterial efficacy of the scaffold, exosomes (EXO) derived from grouper eggs were functionalized with bacteria-targeting aptamers (APTs), a type of functional DNA capable of binding to bacterial peptidoglycan, and EXO-APT-20%S53P4@PCL was fabricated. The resulting EXO-APT-20%S53P4@PCL scaffold was able to facilitate the targeted capture and subsequent eradication of bacteria. This study pioneers the synergistic integration of aptamer-modified exosomes into 3D composite scaffolds. Our analysis confirmed that the incorporation of APTs enabled targeted bacterial capture, and antibacterial EXO further enhanced the overall bacterial killing capability of the S53P4@PCL scaffolds. The fabrication of porous S53P4@PCL scaffolds through an innovative composite-molding strategy, combined with EXO-APT functionalization, establishes a new paradigm for customized bone repair.
Focal cortical dysplasia (FCD) is a leading cause of drug-resistant epilepsy, whereas its molecular and cellular mechanisms remain poorly understood. This study aimed to characterize the cellular heterogeneity of FCD and investigate the function of ferroptosis in FCD pathogenesis. Single-nucleus RNA sequencing was carried out on epileptogenic cortical tissues from 18 patients with FCD and 6 perilesional control samples with normal histology. Data were analysed using uniform manifold approximation and projection for dimensionality reduction and visualization. Differentially expressed genes (DEGs) were identified and subjected to Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses. UCell scoring and gene set enrichment analysis (GSEA) were applied to assess pathway activity. Expression levels of ferroptosis-related genes (FRGs) were validated by immunofluorescence, and biochemical assays quantified the levels of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and lipid peroxides (LPO). A total of 170 747 nuclei were profiled, resolving five major cell types, including inhibitory neurons, excitatory neurons, astrocytes, microglia and oligodendrocytes. DEGs across these populations were significantly enriched in ferroptosis and oxidative stress-associated pathways. UCell and GSEA highlighted remarkable alterations in ferroptosis, apoptosis and oxidative stress, particularly in inhibitory neurons and astrocytes. Immunofluorescence confirmed upregulation of key FRGs, including ferritin light chain, ferritin heavy chain 1, poly rC binding protein 1, microtubule-associated protein 1 light chain 3B and prion protein-encoding gene, in FCD tissues. Concordantly, biochemical assays demonstrated reduced SOD and GSH levels, alongside elevated MDA and LPO levels, confirming the transcriptional and histological findings. The results indicated that ferroptosis may play a notable role or act as a concurrent mechanism in the pathogenesis of FCD, potentially contributing to the neuronal and glial dysfunction and epileptogenesis. Integrating transcriptomic, histological and biochemical data, this study demonstrated that targeting ferroptosis-related pathways may hold promise as a potential therapeutic strategy for FCD, providing new insights into the molecular mechanisms underlying this condition. This study pioneers the first single-nucleus transcriptomic atlas for Focal Cortical Dysplasia (FCD) types I and II, deciphering the cellular heterogeneity across five major brain cell types within the epileptogenic cortex. Through integrated multi-omics analysis, it reveals for the first time a significant association between the ferroptosis pathway and FCD pathogenesis. We identify and validate ferroptosis-related genes (e.g., FTH1, FTL, PCBP1) as potential biomarkers and therapeutic targets, supported by congruent biochemical evidence of oxidative stress in this drug-resistant epilepsy.
Lingui Zhugan Decoction (LGZGD), a traditional Chinese medicinal formulation documented in the Golden Cabinet Essentials, is widely employed across East Asia for the treatment of metabolic liver disease. To evaluate the anti - MASH efficacy of LGZGD and its Active blood-entering components and elucidate their mechanisms, with a particular focus on the regulation of bile acid metabolism. A mouse model of MASH was established using a high-fat, high-cholesterol diet (HFHCD). Transcriptomic profiling and blood component analysis were performed on mice after LGZGD intervention. Molecular docking was then employed in combination with these analyses to screen for active constituents. Subsequent analyses focused on examining the effects of Oroxin A on MASH through transcriptomics, bile acid-targeted metabolomics, gut microbiota 16S rRNA sequencing, and Western blotting. LGZGD, Oroxin A all alleviated obesity, hepatic steatosis, inflammatory responses, and liver fibrosis induced by a high-fat diet. Microbial analysis of the ileum via 16S rDNA sequencing revealed that Oroxin A intervention restored gut microbial diversity, increasing the abundance of Paracoccus, Akkermansia, and Bifidobacterium. Targeted metabolomic analysis revealed significant alterations in bile acid composition under Oroxin A intervention, characterised by decreased levels of LCA and other bile acids alongside marked increases in TUDCA and others. Western blotting results indicate that Oroxin A applies its anti-MASH impacts by modulating the FXR/CYP7A1 pathway and TGR5/NLRP3 pathway. Oroxin A can improve pathological conditions in MASH mice through multiple pathways, including restoring gut microbiota balance and regulating bile acid metabolism. Within conventional medical frameworks, Oroxin A pioneers novel therapeutic approaches for MASH. This method overcomes the limitations of synthetic drugs while maintaining metabolic homeostasis.
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This paper delves into the history of the University of al-Qarawiyyin, founded in 859 CE in Fez, Morocco, as an important institution in the global history of higher education. Established by Fatima Al-Fihriya, this university marks a significant phase in the Islamic Golden Age, evolving from a mosque-centered religious institution into a multidisciplinary academic center. This review article emphasizes al-Qarawiyyin's contribution to the preservation and integration of classical Greek and Roman knowledge with Islamic scientific advancements, offering a curriculum that includes theology, mathematics, astronomy, and medicine, among other disciplines. Special emphasis is placed on the university's pioneering role in the formalization of medical education, highlighting the Ijaza as an early model of structured credentialing that serves as a useful parallel to the subsequent development of licensing systems in medieval European universities. While the intellectual contributions of figures such as Ibn Rushd, Ibn Khaldun, and Maimonides spanned the vast landscape of the Islamic world, the University of al-Qarawiyyin served as one important channel through which this knowledge was preserved and transmitted to the West. It functioned as a key node in a wider network of intellectual exchange that linked North Africa, Al-Andalus, the Euro-Mediterranean space, and beyond. This narrative review article highlights the institution's lasting influence on contemporary educational frameworks and the historical significance of female philanthropic leadership in intellectual progress.
Traumatic spinal cord injury (SCI) induces a robust local inflammatory response that can both facilitate repair and exacerbate pathology. Hydroxycarboxylic acid receptor 2 (Hcar2) is known to exert immunomodulatory effects; however, its role in SCI and its potential for targeting Hcar2 to alleviate motor deficits remain unclear. The spinal cord transcriptome following SCI, with a focus on Hcar2, was analysed via publicly available single-cell RNA sequencing datasets from mice and rhesus macaques. Additionally, an in vivo SCI mouse model with Hcar2 knockout and an in vitro LPS-induced BV2 microglial model were established to assess Hcar2 gene and protein expression, microglial activation and inflammatory responses via bulk RNA sequencing, immunofluorescence staining, Western blotting, and real-time polymerase chain reaction. To evaluate the protective effects of Hcar2 activation, niacin, a known Hcar2 agonist, was administered to mice or BV2 cells, followed by assessments of the inflammatory response and motor function. Hcar2 gene expression, which was enriched predominantly in spinal cord microglia, was upregulated following SCl, peaking at 7 days post-SCl. Genetic knockout of Hcar2 decreased the percentage of impaired anti-inflammatory polarized microglia and increased the inflammatory response. In contrast, Hcar2 activation with niacin in LPS-stimulated microglia BV cell models reversed mitochondrial dysfunction, increased the oxygen consumption rate and reduced the expression of the cytokines IL-6 and IL-1β. The administration of niacin to SCl mice upregulated anti-inflammatory microglia, reduced the expression of multiple proinflammatory cytokines, increased the number of motor neurons and improved motor function recovery. Notably, all these protective effects were abolished by genetic loss of Hcar2. Hcar2 serves as a critical regulator of microglial polarization, promoting the switch from a proinflammatory phenotype to an anti-inflammatory phenotype through immunometabolic reprogramming. Targeting Hcar2 with niacin may offer a translatable therapeutic strategy to improve functional recovery after SCl. Hcar2 is identified as a conserved, injury-induced metabolic checkpoint specifically enriched in microglia following spinal cord injury. Hcar2 activation reprogrammes microglial metabolism from glycolysis to oxidative phosphorylation to drive reparative anti-inflammatory polarization. Pharmacological targeting of Hcar2 with niacin resolves neuroinflammation and promotes functional motor recovery in an Hcar2-dependent manner.
The 25th International Congress on Reproductive Biomedicine and the 20th International Congress on Stem Cell Biology and Technology, held in Iran, brought together leading global experts to discuss pioneering advances in stem cell research and reproductive medicine. Key topics included recent progress in somatic and pluripotent stem cells toward clinical applications, developments in regenerative medicine for diverse diseases, innovations in tissue engineering, the integration of artificial intelligence (AI) in biology research, and novel strategies for treating infertility. The congresses fostered collaboration and knowledge exchange across these rapidly evolving fields, highlighting the transformative potential of stem cells in regenerative medicine and their applications in reproductive health. Participation of 33 scientists from the United States, the United Kingdom, Germany, Austria, Italy, Belgium, Turkey, China, Russia, Japan, Sweden, Switzerland, Qatar, and India facilitated a rich exchange of ideas and broadened international perspectives. The insights and outcomes from these congresses are expected to shape ongoing research initiatives and clinical practices worldwide, emphasizing the importance of continued investment in these critical areas of medicine.
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This study aimed to investigate Item s associated with treatment response to a phone-based, CBT-I-centered digital intervention in patients with depressive disorders, with a primary focus on sleep-related improvement and its association with changes in depressive symptoms. A total of 307 outpatients with depressive disorders were enrolled from a sleep disorders clinic and received a phone-based, CBT-I-centered digital intervention delivered via a mobile application, in addition to routine pharmacotherapy. The intervention primarily targeted sleep disturbances and incorporated CBT techniques and psychoeducation. Participants completed demographic questionnaires and were assessed using the Pittsburgh Sleep Quality Index (PSQI), Patient Health Questionnaire-9(PHQ-9), Patient Health Questionnaire-15 (PHQ-15), and Epworth Sleepiness Scale (ESS).Treatment response was defined as a ≥ 50% reduction in total PHQ-9 score. Item s influencing treatment response at weeks 8 and 12, as well as Item s associated with residual symptoms at week 12, were analyzed. Univariate analyses showed that age and education level were significantly associated with treatment response at both weeks 8 and 12 (P < 0.05), whereas gender was not. Multivariate logistic regression indicated that younger age (< 30 years) and longer disease duration (> 3 years) were independently associated with poorer treatment outcomes at both follow-up points.At week 12, residual symptoms were significantly associated with younger age, longer disease duration, poorer sleep quality (higher PSQI scores), greater somatic symptom burden (PHQ-15), and increased daytime sleepiness (ESS).Multivariate analyses identified younger age, longer disease duration, and family history of depression as independent risk Item s for residual symptoms. This real-world study suggests that a CBT-I-centered digital intervention primarily targeting sleep disturbances may be associated with concurrent improvements in depressive symptoms among patients with depression. Younger patients and those with longer illness duration appear to be at higher risk for poorer outcomes and persistent residual symptoms. ChiCTR2500103629.
Functional assessment of insulin secretion is essential for the development and application of stem cell-derived β-cell products. Conventional glucose-stimulated insulin secretion (GSIS) assays rely on end-point, batch-averaged enzyme-linked immunosorbent assays (ELISA), limiting temporal resolution and masking functional heterogeneity at the level of individual islet-like clusters. Here, we present a label-free, non-invasive impedance spectroscopy-based approach for real-time monitoring of insulin secretion from individual stem cell-derived islets (SC-islets) cultured on microcavity microelectrode array (MEA) chips. Human induced pluripotent stem cells were differentiated into SC-islets and integrated into microcavity MEAs, enabling three-dimensional confinement and parallel electrical recordings. Impedance measurements during on-chip GSIS revealed characteristic glucose-responsive dynamics that correlated with insulin secretion quantified by ELISA and were suppressed by pharmacological inhibition. Impedance spectroscopy resolved functional responses at the level of individual SC-islets, uncovering cluster-to-cluster variability that was obscured by pooled secretion assays. High-density microcavity MEAs further enabled spatially resolved impedance measurements, revealing intra-cluster heterogeneity of insulin secretion. While impedance spectroscopy provides an indirect readout and glucose stimulation was applied as stepwise changes, this platform enables real-time, scalable, and cluster-resolved functional assessment of three-dimensional islet tissues. The approach establishes a foundation for functional screening of SC-islets, differentiation optimization, drug testing, and future potency assessment workflows.
eIF4G2 (DAP5/NAT1) is a non-canonical translation initiation factor, but its role in homeostasis is unclear. Using inducible Eif4g2 knockout mice and intestinal organoids, we show that eIF4G2 loss collapses Lgr5+ intestinal stem cell (ISC) and secretory maturation programs while preserving villus architecture. Transcriptomic and single-nucleus multiome analyses reveal a durable fetal-like/regenerative state with YAP-TEAD activation and regenerative absorptive cells. Ribosome profiling identifies selective translation-efficiency loss among chromatin regulators, especially the KAT3 coactivators CREBBP and EP300, resulting in reduced KAT3 abundance and global histone acetylation; chemical KAT3 inhibition phenocopies this state. CUT&Tag and assay for transposase-accessible chromatin sequencing (ATAC-seq) demonstrate that reduced eIF4G2-KAT3 output drives locus-selective enhancer remodeling, with loss of adult ISC/Wnt-Notch elements and activation of TEAD-enriched fetal loci, without inflammatory or integrated stress response programs driving the transition. Fetal intestinal spheroids remain viable despite similar biochemical defects, highlighting a stage-specific requirement for translational buffering in maintaining adult identity.
Operational robots have demonstrated significant potential in complex scenarios such as live-line maintenance and medical surgery. Existing research on Mixed Reality (MR) and Digital Twin (DT) systems has primarily focused on unidirectional data visualization and passive state monitoring. Existing research on Mixed Reality (MR) and Digital Twin (DT) systems has primarily focused on unidirectional data visualization and passive state monitoring, acting as "open-loop" observation tools that fail to address low operational precision and inefficient human-robot synergy in dynamic, high-risk environments. For the first time, we integrate an MR-based closed-loop digital twin operating system for human-robot collaborative operation into the task execution of live-line operation equipment to address the above challenges. Moving beyond simple visualization, the proposed framework establishes an integrated operational paradigm that bridges the gap between immersive perception and real-time interventional control. This framework comprises three integral components: (1) the construction of a high-fidelity virtual digital twin; (2) the development of a human-computer interaction paradigm based on MR technology; and (3) the establishment of an MR-based human-machine collaborative operation mode. Building upon this framework, a system was implemented for live-line working robots. Experimental results indicate that, compared with traditional control methods, the proposed system reduces the task completion time of live-line equipment tasks by 14.3% on average, verifying the feasibility and effectiveness of the pioneering application of the closed-loop digital twin operating system in live-line operation equipment.
The Hippo pathway is a tumor suppressor pathway, and most related studies have indicated that its inhibition leads to tumorigenesis. However, recent studies have suggested that the activated Hippo pathway can promote tumorigenesis in certain contexts. Here, we demonstrate that the activated Hippo pathway induces non-cell-autonomous tumorigenesis, characterized by tumor markers in the Drosophila wing epithelium. This suggests that Hippo-activated cells behave similarly to "oncogenic niche cells." We find that Hippo-activated cells induce Dronc-Wingless/Spitz signaling in the hinge/ventral notum region, which causes tumorigenesis. Moreover, we identify the amino acid transporters Sat1/2, which are implicated in amino acid incorporation and function redundantly with the growth factors Wingless and Spitz to facilitate non-cell-autonomous tumorigenesis.
Androgen receptor (AR) signaling is central to prostate cancer progression, yet resistance to AR-targeted therapies remains a major clinical challenge. Understanding the molecular consequences of AR pathway inhibition is therefore essential for improving therapeutic outcomes. Here, we identify a previously unrecognized link between AR antagonism and cuproptosis, a copper-dependent form of regulated cell death. Using integrated genomic profiling, we find that AR-targeted agents transcriptionally activate the key cuproptosis regulator Ferredoxin-1 (FDX1), thereby rendering prostate cancer cells markedly more susceptible to copper-induced lethality. Mechanistically, ligand-bound AR directly engages FDX1 cis-regulatory elements, which are rendered accessible by the pioneer factor GATA2, and drives FDX1 upregulation upon AR antagonist exposure. Consistent with this mechanism, FDX1 expression is elevated in clinical prostate cancer samples following androgen deprivation therapy or AR antagonist treatment. Increased FDX1 enhances intracellular Cu+ accumulation, destabilizes Fe-S cluster proteins, and disrupts mitochondrial metabolism, establishing a procuproptotic state. Functionally, combining AR antagonists with copper ionophores synergistically induces cuproptosis and potently suppresses tumor growth in AR-positive prostate cancer cells, three-dimensional (3D) spheroids, patient-derived organoids, and xenograft models, with minimal systemic toxicity. This synergy is abolished by FDX1 loss or copper chelation, confirming dependence on AR-FDX1 axis activation. Together, these findings uncover FDX1 as a mechanistic effector of AR pathway inhibition and propose a well-tolerated combination strategy that exploits cuproptosis to improve therapeutic responses in prostate cancer.
Microbial communities function as dynamic societies where intercellular communication governs collective behaviors. However, mapping these interaction networks has remained a fundamental challenge in microbiology. This study aims to decode the social networks of complex bacterial communities at single-cell resolution by developing BACON, a computational framework that infers quorum sensing-mediated communication from single-microbe transcriptomic data. The approach combines a curated database of signaling systems with a statistical model that quantifies communication strength through coordinated expression of signal synthesis and receptor genes. Validation in model systems demonstrated BACON's precision in reconstructing density-dependent communication trajectories in Bacillus subtilis and capturing rapid network reorganization in Escherichia coli under antibiotic stress, revealing distinct sender-receiver subpopulations. Applied to human gut microbiomes, BACON unveiled diurnal fluctuations in cross-species signaling that transcend enterotype boundaries and uncovered conserved metabolic specialization in signal-responsive bacteria. In a clinical context, analysis of an ICU patient's gut microbiome revealed how Pseudomonas aeruginosa establishes a self-reinforcing communication circuit that upregulates virulence pathways. This work provides a unified framework for analyzing bacterial social interactions across diverse ecosystems. It opens new avenues for understanding microbial sociology, combating antimicrobial resistance, and engineering synthetic communities.