ABSTRACT
Osteomyelitis, a grave deep tissue infection primarily caused by Staphylococcus aureus, results in serious complications such as abscesses and sepsis. With the incidence from open fractures exceeding 30 % and prevalent antibiotic resistance due to extensive treatment regimens, there's an urgent need for innovative, antibiotic-free strategies. Photothermal therapy (PTT) and photodynamic therapy (PDT) renowned for generating localized reactive oxygen species (ROS), face limitations in penetration depth. To overcome this, our method combines the deep penetration attributes of medical microwaves (MW) with the synergistic effects of the ZnO/ZrO2 solid solution. Comprehensive in vitro and in vivo evaluations showcased the solid-solution's potent antibacterial efficacy and biocompatibility. The ZnO/ZrO2 solid solution, especially in a 7:3 M ratio, manifests superior microstructural characteristics, optimizing MW-assisted therapy. Our findings highlight the potential of this integrated strategy as a promising avenue in osteomyelitis management.
Subject(s)
Microwaves , Osteomyelitis , Staphylococcus aureus , Zirconium , Osteomyelitis/drug therapy , Osteomyelitis/microbiology , Osteomyelitis/pathology , Osteomyelitis/therapy , Animals , Staphylococcus aureus/drug effects , Zirconium/chemistry , Mice , Humans , Catalysis , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/chemistry , Photochemotherapy/methods , Zinc/chemistry , Staphylococcal Infections/drug therapy , Staphylococcal Infections/microbiology , Staphylococcal Infections/pathology , Oxygen/chemistry , Oxygen/metabolism , Reactive Oxygen Species/metabolism , Photothermal Therapy/methods , Microbial Sensitivity TestsABSTRACT
Metallic atoms within metal-organic framework (MOF) materials exhibit a distinctive and adaptable coordination structure. The three-dimensional (3D) pore configuration of MOFs enables the complete exposure of metal active sites, rendering them prevalent in various catalytic reactions. In this study, zinc (Zn) atoms within Zn-based MOF materials, characterized by an abundance of valence electrons, are utilized for the transesterification of dimethyl carbonate (DMC). Additionally, the introduction of zirconium (Zr) effectively addresses the susceptibility of the MOFs' crystal structure to dissolution in organic solvents. The formulated catalyst, Zn-10%Zr-MOF(300), demonstrates remarkable catalytic performance with 91.5% DMC selectivity, 61.9% propylene carbonate (PC) conversion, and 56.6% DMC yield. Impressively, the catalyst maintains its high performance over five cycles. Results indicate that Zr interacts with Zn, forming new coordination bonds and enhancing the catalyst crystal structure stability. Moreover, electron transfer intensifies the alkalinity of the active Zn atoms, enhancing the overall catalyst performance. This research informs the development of transesterification heterogeneous catalysts and broadens the application scope of MOF catalysts.
ABSTRACT
Recent clinical studies have highlighted mutations in the voltage-gated potassium channel Kv10.2 encoded by the KCNH5 gene among individuals with autism spectrum disorder (ASD). Our preliminary study found that Kv10.2 was decreased in the hippocampus of valproic acid (VPA) - induced ASD rats. Nevertheless, it is currently unclear how KCNH5 regulates autism-like features, or becomes a new target for autism treatment. We employed KCNH5 knockout (KCNH5-/-) rats and VPA - induced ASD rats in this study. Then, we used behavioral assessments, combined with electrophysiological recordings and hippocampal brain slice, to elucidate the impact of KCNH5 deletion and environmental factors on neural development and function in rats. We found that KCNH5-/- rats showed early developmental delay, neuronal overdevelopment, and abnormal electroencephalogram (EEG) signals, but did not exhibit autism-like behavior. KCNH5-/- rats exposed to VPA (KCNH5-/--VPA) exhibit even more severe autism-like behaviors and abnormal neuronal development. The absence of KCNH5 excessively enhances the activity of the Protein Kinase B (Akt)/Mechanistic Target of Rapamycin (mTOR) signaling pathway in the hippocampus of rats after exposure to VPA. Overall, our findings underscore the deficiency of KCNH5 increases the susceptibility to autism under environmental exposures, suggesting its potential utility as a target for screening and diagnosis in ASD.