MXene-based hydrogel disrupt bacterial biofilms and reprogram immune cell metabolism to reverse bone resorption in periodontitis
Peer-Reviewed Publication
Updates every hour. Last Updated: 24-Oct-2026 14:17 ET (24-Oct-2026 18:17 GMT/UTC)
Researchers in Lin Quan's research group at Jilin University have developed an injectable MXene-based hydrogel specifically for treating periodontitis. This hydrogel, named GQM, consists of oxidized gellan gum, quaternized chitosan, and magnesium-tannic acid-modified MXene nanosheets. It can be injected into periodontal pockets, overcoming the problem of traditional drugs' inability to remain within these pockets. Under near-infrared light irradiation, it can gently disrupt bacterial biofilms through photothermal activity, while the electrostatic effect of the QCS (quaternary cytosolic crystals) helps kill periodontal pathogens. Furthermore, the nanosheets promote electron transport, restore mitochondrial NAD+/NADH balance, and induce macrophages to transform into the M2 type. In a rat model of periodontitis, GQM combined with near-infrared light therapy reduced bacterial count, inflammatory response, and alveolar bone resorption. The MXene-based hydrogels treat periodontitis by disrupting bacterial biofilms and reprogramming immune metabolism, offering a novel strategy for its management.
To overcome the fragility of soft sensing materials under long-term cyclic loading, researchers have developed a highly durable "eutectogel" utilizing a novel nanoscale cavitation mechanism. By integrating this fatigue-resistant material into a smart glove with deep learning algorithms, the team achieved a 99.9% accuracy rate in real-time sign language recognition. This innovation paves the way for seamless communication and advances the durability of next-generation human-machine interfaces.
A revised species inventory updates Hainan’s terrestrial mammal fauna, highlights island‑specific conservation risks and provides baseline data for regional wildlife management.
Patients with severe β-thalassemia face not only lifelong dependence on blood transfusions but also the management of serious and potentially life-threatening complications. The pathophysiology of this disorder is largely attributed to a defective transition from γ-globin to β-globin gene expression, a process essential for normal hemoglobin production after birth. This developmental transition involves the silencing of fetal γ-globin and coordinated activation of adult β-globin gene transcription. Central to this regulation are transcription factors that directly bind to the γ-globin promoter. This review synthesized recent advances in understanding the γ-to-β-globin switch, focusing on four principal transcription factors – GATA1, BCL11A, ZBTB7A, and NFY – and partner proteins including GATA2 and KLF1. In addition, we proposed a competitive binding model in which the GATA1/NFY and ZBTB7A/BCL11A protein complexes compete for promoter occupancy. This model provides a useful framework that may inform future strategies for the prevention, diagnosis, and treatment of β-thalassemia.
This study explored the link between cuproptosis, a type of cell death, and unexplained infertility (UI) using gene expression data. Researchers analyzed 27 cuproptosis-related genes in endometrial samples from UI patients, identifying two molecular clusters linked to immune cell infiltration. They tested seven machine learning models to predict UI, finding the support vector machine (SVM) model most effective, with high accuracy (AUC 0.918). The study suggests five cuproptosis-related genes could be potential biomarkers for UI, offering insights into the disease's molecular basis and aiding in future diagnostic and treatment strategies.
Parkinson’s disease is expected to cause a substantial economic burden from 2020 to 2040, amounting to 473 billion CNY in constant 2024 prices, which represents 0.017% of projected GDP in China. Utilizing a health-augmented macroeconomic model across 31 provinces, researchers found that disease-induced reductions in physical capital accumulation outweigh labor supply declines in most regions. The findings support tailored prevention and long-term care strategies.
The cutting-edge advances in multivalent mRNA–exosome vaccines provides a mechanistic blueprint showing how these customized mRNA payloads can systematically reprogram the immunosuppressive architecture of “cold” tumor microenvironments and mobilize potent, antigen-specific cytotoxic T-lymphocyte responses to overcome cancer immunotherapy resistance.A primary challenge in oncology vaccinology is delivering payloads to lymphoid-resident antigen-presenting cells (APCs) without triggering systemic toxicities or rapid hepatic clearance. While synthetic lipid nanoparticles (LNPs) are standard for systemic delivery, they face hepatocyte sequestration driven by blood-borne apolipoprotein E (ApoE) binding, which limits extrahepatic bioavailability. To bypass this constraint, engineered exosomes offer a biological alternative. These cell-derived vesicles feature a native lipid bilayer enriched with cholesterol and sphingomyelin that shields mRNA from ribonuclease degradation. By presenting surface markers like CD47—a “don’t eat me” signal blocking macrophage phagocytosis via SIRPα—exosomes achieve extended circulation half-lives (Figure 1).