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Objective To investigate the changes of motor function in children with cerebral palsy undergoing ankle-foot strengthening therapy. Methods A total of 80 children with cerebral palsy were enrolled in this study，and divided into the control group（n = 40）and observation group（n = 40）. In the control group，children received regular trunk training based on motor control theory combined with neurodevelopmental therapy，and those in the observation group received ankle-foot strengthening therapy in addition to those interventions in the control group. Pre-and post-treatment assessments including the Gross Motor Function Measure（GMFM-88）scores for Sections D and E，the 6-minute walk test（6-MWT），the Timed Up and Go Test（TUGT），and the Pediatric Balance Scale（PBS）were recorded to compare clinical efficacy between two groups. Results Following corresponding interventions，significant improvement was observed in all observed indexes in two groups（all P < 0.05）. Notably，children in the observation group exhibited better post-treatment scores in GMFM Section E，6-MWT，TUGT，and PBS compared to their counterparts in the control group，with statistically significant differences（all P < 0.05）. Conclusion Ankle-foot strengthening therapy effectively promotes the recovery of motor function in children with cerebral palsy.

Designing catalysts with desirable oxygen evolution reaction (OER) performance under pH-universal conditions is of great significance to promote the development of hydrogen production. Herein, we successfully synthesized a crystalline-amorphous IrO x supported on perovskite oxide nanotubes to obtain IrO x @La 0.6 Ca 0.4 Fe 0.8 Ni 0.2 O 3 with superior OER performance in whole pH media. The overpotential of the IrO x @La 0.6 Ca 0.4 Fe 0.8 Ni 0.2 O 3 catalyst in media of pH 14, 7.2, and 1 has been demonstrated to be 120, 400, and 143 mV, respectively, with no significant element dissolution as well as double-layer capacitance decay after the durability test. Through comparative experiments with IrO x @CNT and the physical mixture of IrO x and La 0.6 Ca 0.4 Fe 0.8 Ni 0.2 O 3 , it is found that the strong metal-support interaction (SMSI) in IrO x @La 0.6 Ca 0.4 Fe 0.8 Ni 0.2 O 3 makes IrO x exist in an amorphous state rich in Ir 3+ , which is closely associated with the surface-active species Ir-OH. Through the regulation of Ir by a perovskite oxide support at the heterointerface, the reaction breaks through the limitation of the adsorbate evolution mechanism (AEM) and converts to a lattice-oxygen-mediated mechanism (LOM), which was fully demonstrated by the addition of the probe tetramethylammonium cation (TMA + ), a LOM reaction intermediate, to the electrolyte. This work fills the research gap of perovskite oxide supported Ir-based catalysts with heterogeneous structures, providing an excellent strategy for the structural design of efficient pH-universal OER catalysts for hydrogen production systems.

As a basic member of the Class III histone deacetylases, SIRT1 has been implicated in the occurrence and progression of diabetic retinopathy (DR). The current study aimed to investigate the roles of SIRT1/miR-20a/Yse-associated protein (YAP)/hypoxia-inducible factor 1 α (HIF1α)/vascular endothelial growth factor A (VEGFA) in DR. The expression of SIRT1 was initially determined through quantitative RT-PCR and Western blot analysis following the successful establishment of a DR mouse model, followed by detection of SIRT1 catalytic activity. Retinal microvascular endothelial cells (RMECs) were cultured in media supplemented with normal glucose (NG) or high glucose (HG). Thereafter, SIRT1 was either silenced or overexpressed in RMECs, after which EdU staining and Matrigel-based tube formation assay were performed to assess cell proliferation and tube formation. The binding relationship between YAP, HIF1α, and VEGFA was further illustrated using dual-luciferase reporter assay. Preretinal neovascular cell number was tallied with the IB4-positive vascular endothelial cells, as determined by immunofluorescence. SIRT1 was poorly expressed in mice with DR and HG-treated RMECs with low catalytic activity. The proliferation and tube formation capabilities of RMECs were elevated under HG conditions, which could be reversed following overexpression of SIRT1. SIRT1 was identified as positively regulating the expression of miR-20a with YAP detected as the key target gene of miR-20a. Our data suggested that YAP could upregulate VEGFA via induction of HIF1α. Moreover, SIRT1 overexpression strongly repressed RMEC proliferation and angiogenesis, which could be reversed via restoration of YAP/HIF1α/VEGFA expression. Taken together, the key findings of our study suggest that upregulation of SIRT1 inhibits the development of DR via miR-20a-induced downregulation of YAP/HIF1α/VEGFA.