Medical misinformation propagates rapidly across digital platforms, posing substantial risks to public health decision-making. Traditional content-based detection approaches exhibit limited effectiveness when confronting the nuanced language and domain-specific terminology inherent in health-related claims. While foundation language models demonstrate remarkable semantic understanding capabilities, their direct application to medical misinformation detection encounters two fundamental obstacles: hallucination-induced evidence unreliability and insufficient explainability in high-stakes health contexts. Rather than treating foundation models as monolithic end-to-end predictors, we reconceptualize them as modular evidence generators and verifiers within a collaborative reasoning architecture. We propose Medical misinformation GUard via multi-model Adversarial Reasoning and Dimensional evidence (MedGUARD), a two-stage framework that leverages foundation model collaboration for explainable detection. The evidence generation stage employs adaptive in-context learning and multi-model adversarial negotiation to synthesize reliable multidimensional evidence, effectively mitigating hallucination artifacts. The semantic fusion stage integrates claim representations with evidence-augmented features through multimodal factorized bilinear pooling. Experiments across four medical misinformation benchmarks demonstrate that MedGUARD achieves improvements of 3.2 to 4.5 F1 points over 25 baseline methods, with all advantages confirmed by McNemar’s significance test. Adversarial negotiation reduces hallucination rates by 66% to 70% while generating transparent reasoning trails across seven evidential dimensions. Computational efficiency analysis quantifies MedGUARD’s cost-performance trade-off against all baselines, and cross-domain generalization experiments confirm that its accuracy advantage holds when training and test distributions differ, enabling medical professionals to verify automated assessments before clinical deployment.
This study presents a tannic acid (TA)-mediated strategy to engineer the structure and functionality of chitosan/polyvinyl alcohol (CS/PVA) packaging films by simultaneously crosslinking polymers and integrating nanoparticles. TA served as a multifunctional structuring agent, forming extensive hydrogen-bonding networks within the CS/PVA matrix and coordinating with MgO–TiO2 nanoparticles to generate stable metal–phenolic interfaces. This dual interaction produced a more compact, integrated film network with enhanced interfacial compatibility and reduced polymer chain mobility. Consequently, the composite film showed a 79% increase in tensile strength (29.3 MPa), along with significant reductions in water vapor permeability (21%) and oxygen permeability (36.4%), indicating improved barrier performance through increased network density and tortuous diffusion pathways. TA-mediated coordination further modified the optical properties of MgO–TiO2, enabling visible-light responsiveness and promoting reactive oxygen species generation, which contributed to strong antibacterial activity, with bacterial reduction exceeding 5 log CFU mL−1 against Escherichia coli and Staphylococcus aureus within 24 h. In addition, the films exhibited enhanced antioxidant activity and complete UV shielding. When applied to banana preservation, the optimized film effectively delayed ripening, extending shelf life by approximately four days while maintaining acceptable quality. Overall, this work highlights a synergistic approach to tailoring hybrid film networks via polyphenol-mediated crosslinking and metal–phenolic coordination, providing insights into structure–property relationships for the design of advanced active packaging materials.
Implant-related inflammation and insufficient alveolar bone regeneration remain significant challenges for calcium-based biomaterials. In this study, single-cell RNA sequencing combined with metabolomic analysis revealed that hydroxyapatite (HA) implantation is associated with inflammatory metabolic dysfunction in macrophages, characterized by disruption of arginine-ornithine metabolism, oxidative phosphorylation, and efferocytosis, thereby identifying a potential metabolic target for biomaterial design. Based on these findings, an ornithine-loaded mesoporous calcium silicate nanoplatform (CS-O) was developed and incorporated into collagen scaffolds (COL-CS-O) for post-extraction alveolar bone repair. The CS-O platform achieved an ornithine loading capacity of 16.1wt.% and enabled sustained release over 25 days. Compared with HA, CS-O restored arginine-ornithine metabolic balance and redox homeostasis, re-established mitochondrial bioenergetics in macrophages, increased adenosine triphosphate production by 2.05-fold, and enhanced efferocytosis by 2.17-fold. These effects promoted macrophage reprogramming toward a reparative phenotype and further enhanced osteogenic differentiation of MC3T3-E1 cells. In a rat model of maxillary first molar extraction defects, COL-CS-O significantly enhanced alveolar bone regeneration, achieving a bone volume/total volume of 30.51%, which was 1.49-fold higher than that of the COL-C group. Trabecular thickness reached 88.2 & micro;m, representing an increase of 17.2 & micro;m compared with the COL-HA group. This study highlights the potential of COL-CS-O as an immunometabolic inorganic composite scaffold for alveolar bone regeneration. (c) 2026 Published by Elsevier Ltd on behalf of The editorial office of Journal of Materials Science & Technology.
The interface around a dental implant behaves as a dynamic ecosystem. The metal surface, the colonizing microbiota, and the host immune network continually interact rather than remaining inert neighbors. Once this equilibrium breaks, a destructive cascade can feed on itself. This challenges the older view that peri-implantitis stems only from plaque infection or from mechanical overload. We integrate evidence from the peri-implantitis microenvironment to build a framework organized around an immune–microbe–metal triad, which we use to explain how biomaterials corrode in this disease. Three pillars carry intrinsic weaknesses: the titanium passive film, the biofilm's ecological balance, and host immune tolerance. When these fail together, they set off an autocatalytic corrosion cycle. Key molecular mediators—lipopolysaccharide (LPS), intracellular metal nanoparticles, and neutrophil extracellular traps (NETs)—amplify the damage. The cycle then lowers the threshold for inflammatory cell-induced corrosion (ICIC), and tissue destruction advances toward irreversibility. Against this framework we assess current therapies and where they fall short. In their place we propose multi-targeted, ecosystem-level strategies that hit the cycle at several points, aiming to restore interfacial homeostasis. Treating peri-implantitis as a nonlinear, self-reinforcing system reframes how we understand its pathogenesis, offering a roadmap toward next-generation biomaterials and combination therapies suited to the complexity of the implant–host interface.
Hepatic osteodystrophy (HOD) is a debilitating metabolic bone disorder inextricably linked to chronic liver disease, with its prevalence surging alongside the global rise of metabolic dysfunction-associated steatohepatitis (MASH). Current clinical interventions remain fragmented, failing to concurrently address the upstream hepatic lipotoxicity and the downstream skeletal deterioration. Herein, we engineer copper-doped bioactive glasses (CuBGs) as a multifunctional ion-therapy nanoplatform that exploits natural hepatic tropism to synchronously rescue MASH-HOD pathology via targeted reprogramming of the liver-bone axis. By delivering localized therapeutic ions, CuBGs orchestrate robust hepatic metabolic recovery: they enhance glucose tolerance and restore mitochondrial oxidative phosphorylation (OXPHOS), thereby effectively halting intrahepatic triglyceride accumulation and quenching ROS-driven inflammation. Crucially, this hepatic rescue reactivates the liver-bone endocrine crosstalk by robustly upregulating the secretion of the hepatokine lecithin-cholesterol acyltransferase (LCAT). Systemic LCAT restoration directly stimulates profound osteoblastogenesis and new bone formation, decisively reversing MASH-induced trabecular bone loss without acting as a conventional anti-resorptive agent. This dual-organ modulation comprehensively ameliorates the interconnected multi-organ microenvironment in MASH-HOD without inducing systemic toxicity. Ultimately, this bioactive glass-mediated copper delivery system establishes a novel, highly scalable strategy for ion-based nanotherapeutics, offering a promising and integrated strategy for complex liver-bone comorbidities.
