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Herein, we present an electrochemophysiological microarray (ECPM) for real‐time mapping and simultaneous quantification of chemical signals for multiple ions in the deep brain of a freely moving rat, in which microelectrode arrays were developed for direct determination of multiple ions using open‐circuit potentiometry. Specific recognition ionophores were synthesized and optimized for determination of K+, Ca2+, Na+ and pH. A reference electrode was also developed to avoid interferences in the brain. The microarrays were successfully applied in real‐time monitoring and quantification of ions in a live brain. The extra current‐free potentiometry allowed mapping and biosensing of chemical signals, together with recording of electrical signals in the whole brain without cross‐talk, for the first time. Furthermore, the ECPM provided a platform for real‐time monitoring of the dynamic changes of multiple ions in the deep brain of freely moving rat during a seizure. [ABSTRACT FROM AUTHOR]

Herein, we present an electrochemophysiological microarray (ECPM) for real‐time mapping and simultaneous quantification of chemical signals for multiple ions in the deep brain of a freely moving rat, in which microelectrode arrays were developed for direct determination of multiple ions using open‐circuit potentiometry. Specific recognition ionophores were synthesized and optimized for determination of K+, Ca2+, Na+ and pH. A reference electrode was also developed to avoid interferences in the brain. The microarrays were successfully applied in real‐time monitoring and quantification of ions in a live brain. The extra current‐free potentiometry allowed mapping and biosensing of chemical signals, together with recording of electrical signals in the whole brain without cross‐talk, for the first time. Furthermore, the ECPM provided a platform for real‐time monitoring of the dynamic changes of multiple ions in the deep brain of freely moving rat during a seizure. [ABSTRACT FROM AUTHOR]

Current wound scaffold dressing constructs can facilitate wound healing but do not exhibit antibacterial activity, resulting in high infection rates. We aimed to endow wound scaffold dressing with anti‐infective ability by polyhexamethylenebiguanide (PHMB). We prepared PHMB hydrogel at varying concentrations (0.25%, 0.5%, 1%, 2%) and assessed release and cytotoxicity. PHMB hydrogel was added to the wound scaffold dressing to generate a PHMB hydrogel‐modified wound scaffold dressing. Wound healing and infection prevention were evaluated using a full‐thickness skin defect model in rats. In vitro, the hydrogel PHMB release time positively correlated with PHMB concentration, with 1% allowing sufficiently long release time to encompass the high‐incidence period (3‐5 days) of infection following wound scaffold dressing implantation. Implantation of 1% PHMB hydrogel into the skin did not cause adverse responses. in vitro cytotoxicity assays showed the PHMB hydrogel‐modified wound scaffold dressing did not significantly affect proliferation of fibroblasts or vascular endothelial cells, 99.90% vs 99.84% for fibroblasts and 100.21% vs 99.28% for vascular endothelial cells at 21 days. Transplantation of PHMB hydrogel‐modified wound scaffold dressing/unmodified wound scaffold dressing on the non‐infected wounds of rats yielded no significant difference in relative vascularization rate, 47.40 vs 50.87 per view at 21 days, whereas bacterial content of the wound tissue in the PHMB hydrogel‐modified wound scaffold dressing group was significantly lower than the unmodified wound scaffold dressing group, (1.80 ± 0.35) × 103 vs (9.34 ± 0.45) × 103 at 14 days. Prevalence of persistent wound infection in the rats receiving PHMB hydrogel‐modified wound scaffold dressing transplantation onto infected wounds was significantly lower than the unmodified wound scaffold dressing group, 30% vs 100%. PHMB hydrogel‐modified wound scaffold dressing exhibited suitable antibacterial ability, and its biological activity did not significantly differ from that of the unmodified wound scaffold dressing, thereby allowing it to effectively prevent infection following wound scaffold dressing implantation. [ABSTRACT FROM AUTHOR]

This study aimed to elucidate the effect of depression on the healing of acute wounds in rats. We hypothesized that depression would have negative effects on inflammation and wound healing and that antidepressant therapy would reverse these effects. This study included 100 rats randomly allocated into five groups: control group (CG), depression group (DG), pre‐depression group (PDG), antidepressant group (AG), and pre‐antidepressant group (PAG). Acute wounds were created on the rats' backs. The groups were subjected to no interventions (CG), aversive stimuli before (PDG) and after (DG) wound creation, and antidepressant treatment before (PAG) and after (AG) wound creation. On the day of wound creation and on days 3, 6, 9, and 12 after wound creation, observations of the wound area and degree of depression (evaluated using the sucrose preference test, open‐field test, and weight change) were recorded. On days 6 and 12 after wound creation, venous serum and wound tissues were collected. Tumor necrosis factor alpha (TNF‐α), interleukin (IL)‐1β, IL‐6, and IL‐10 levels were measured using the enzyme‐linked immunosorbent assay. Results showed an initial increase followed by a decrease in the degree of depression in all groups except DG (continuous decline). The wound‐healing rate was significantly lower in PDG and DG than in CG; it was higher in AG and PAG than in CG. DG and PDG had higher concentrations of inflammatory cytokines than CG, and AG and PAG had lower concentrations than CG. This indicates that the onset of depression delays the healing of acute wounds and aggravates the inflammatory response in rats. Antidepressant treatment counteracts both of these negative effects. [ABSTRACT FROM AUTHOR]