Photothermal therapy( PTT) has been extensively developed as an effective approach against cancer.H owever, PTT can trigger inflammatory responses,i nt urn simulating tumor regeneration and hindering subsequent therapy. A therapeutic strategy was developed to deliver enhanced PTT and simultaneously inhibit PTT-induced inflammatory response.1 -Pyrene methanol was utilizet os ynthesize the anti-inflammatory prodrug pyrene-aspirin (P-aspirin) with ac leavable ester bond and also facilitate loading the prodrug on gold nanorod (AuNR)-encapsulated graphitic nanocapsule (AuNR@G), ap hotothermal agent, through p-p interactions. Such AuNR@G-P-aspirin complexes were used for nearinfrared laser-triggered photothermal ablation of solid tumor and simultaneous inhibition of PTT-induced inflammation through the release of aspirin in tumor milieu. This strategy showed excellent effects in vitro and in vivo.

We have fabricated gold nanorod graphitic nanocapsule (AuNR@G) doped poly(vinyl alcohol) (PVA)/chitosan (CS) hydrogels, which possessed highly efficient and stable photothermal antibacterial properties under the irradiation of a near-infrared laser.

Photothermal therapy( PTT) has been extensively developed as an effective approach against cancer.H owever, PTT can trigger inflammatory responses,i nt urn simulating tumor regeneration and hindering subsequent therapy. A therapeutic strategy was developed to deliver enhanced PTT and simultaneously inhibit PTT-induced inflammatory response.1 -Pyrene methanol was utilizet os ynthesize the anti-inflammatory prodrug pyrene-aspirin (P-aspirin) with ac leavable ester bond and also facilitate loading the prodrug on gold nanorod (AuNR)-encapsulated graphitic nanocapsule (AuNR@G), ap hotothermal agent, through p-p interactions. Such AuNR@G-P-aspirin complexes were used for nearinfrared laser-triggered photothermal ablation of solid tumor and simultaneous inhibition of PTT-induced inflammation through the release of aspirin in tumor milieu. This strategy showed excellent effects in vitro and in vivo.

Type 2 diabetes (T2D) is characterized by the malfunction of pancreatic β cells. Susceptibility and pathogenesis of T2D can be affected by multiple factors, including sex differences. However, the mechanisms underlying sex differences in T2D susceptibility and pathogenesis remain unclear. Using single-cell RNA sequencing (scRNA-seq), we demonstrate the presence of sexually dimorphic transcriptomes in mouse β cells. Using a high-fat diet-induced T2D mouse model, we identified sex-dependent T2D altered genes, suggesting sex-based differences in the pathological mechanisms of T2D. Furthermore, based on islet transplantation experiments, we found that compared to mice with sex-matched islet transplants, sex-mismatched islet transplants in healthy mice showed down-regulation of genes involved in the longevity regulating pathway of β cells. Moreover, the diabetic mice with sex-mismatched islet transplants showed impaired glucose tolerance. These data suggest sexual dimorphism in T2D pathogenicity, indicating that sex should be considered when treating T2D. We hope that our findings could provide new insights for the development of precision medicine in T2D.