MedComm

High-fat diet (HFD) promotes obesity and degenerative diseases. We established a long-term HFD to aging (LHA) mouse model, finding it induces a bone marrow shift from osteogenesis to adipogenesis and abnormal immune cell metabolic adaptations. Signaling axes were identified through single-cell RNA sequencing as potential bone marrow-brain crosstalk pathways, providing insights for treating related diseases.

Crizotinib inhibits CD147-MCT1-mediated lactate transport, suppressing melanoma growth and immune escape, prevents M2 macrophage polarization, and enhances immunotherapy by reducing CXCL13 via histone lactylation.

Targeting ECM dysregulation: therapeutic strategies for disease intervention. Dysregulated ECM composition and biomechanics contribute to disease pathogenesis in cancer and fibrotic disorders. Physical modulation: Nanomedicine-based strategies tune ECM physical properties (e.g., density, stiffness) to enhance drug penetration and therapeutic efficacy in the TME. Molecular targeting: Small-molecule drugs selectively modify ECM components to induce angiogenesis, immune response, and tissue remodeling. Cellular reprogramming: Pharmacological intervention of CAF signaling pathways promotes functional normalization, thereby restoring ECM homeostasis.

This review provides comprehensive overview of astrocytes in neurological disorders. Astrocytes contribute to neurological disorders via A1/A2 polarization, inducing neuroinflammation, synaptic, and BBB dysfunction. Metabolic disturbances in glucose, lipid, and amino acid pathways leading to oxidative stress and mitochondrial damage. Therapeutic targets include inflammation modulation, gene therapy, and nanotechnology. Future directions include multi-omics integration, clinical translation, and resolving astrocyte heterogeneity.

Mechanisms of alleviating resistance to PD-1/PD-L1 blockade by IFN-α and IFN-β. In these mechanisms, the “yin-yang balance” is disrupted, thus preventing T cells from attacking cancer cells. Restoring this balance may improve the efficacy of anti-PD-1/PD-L1 therapy and reinvigorate T cells and other immune cells to target and destroy cancer cells.

In our study, we formulated a protein-based vaccine known as MF59/preF, which contains RSV pre-fusion (preF) protein antigen in combination with an MF59-like oil-in-water adjuvant. Three-dose intramuscular (IM) administration of this vaccine induced robust humoral and cellular immunity against RSV F protein in systemic immune organs rather than at local sites. Intranasal (IN) immunization with MF59/preF demonstrated superior mucosal immunity, characterized by elevated levels of secretory IgA antibodies and an increased frequency of tissue-resident memory T (T_RM) cells locally. We then optimized the MF59/preF vaccine by combining IM and IN immunization, which induced stronger systemic and mucosal immunity.

The deficiency of transient receptor potential melastatin type 2 (TRPM2) channel as a calcium permeable nonselective cation channel, accelerates seizure development in various mouse seizure models including PTZ-, KA-, and kindling-induced models, but does not affect seizure susceptibility in initial acute seizure. Interestingly, the deficiency of TRPM2 in microglia, but not CaMKIIα⁺ or PV⁺ neurons, is mainly responsible for seizure development. Moreover, microglial TRPM2 deficiency increases the excitability of hippocampal pyramidal neurons via enhancing the AMPAR-mediated excitatory synaptic transmission but does not influence the expression of inflammation cytokines.

Synergistic effects of combining bacteriophages and antibiotics in antimicrobial therapy.

The diagram illustrates key advantages of phage-antibiotic synergy, including increased treatment effectiveness, reduced minimum inhibitory concentration (MIC) for drug-resistant strains, enhanced biofilm eradication, and inhibition of resistant bacteria development. Antibiotics can also promote phage production and accelerate bacterial lysis. These interactions suggest promising potential for combined therapies, particularly in overcoming antibiotic resistance. Figure created using Microsoft PowerPoint.