ABSTRACT
Constructing heterostructured electrocatalysts has proven effective in enhancing intrinsic catalytic activity. Herein, under guidance of theoretical calculations, hierarchical porous quasi-hexagonal Co2P nanosheets/Co heterostructures supported on carbon cloth (Co2P/Co/CC) with a high surface area were rationally designed and elaborately constructed through electroless Co plating, electrochemical oxidation, and phosphidation process, which showed significant electrocatalytic performance toward water electrolysis. Specifically, theoretical calculations revealed that the Co2P/Co heterostructure adjusted the electronic structure of Co2P and Co, reducing the energy barrier for target reactions and thereby boosting electrocatalytic activities for the hydrogen evolution reaction (HER). Notably, the typical Co2P/Co/CC catalyst demonstrated impressive HER performance, with low overpotentials of only 52 and 48 mV to achieve a current density of 10 mA/cm2 in 0.5 M H2SO4 and 1.0 M KOH solutions, respectively. The remarkable electrocatalytic performance of the catalyst can be attributed to the improved intrinsic activity resulting from the Co2P/Co heterostructures and the highly exposed active sites provided by the hierarchical porous structures. Furthermore, the Co2P/Co/CC catalyst exhibited excellent oxygen evolution reaction (OER) performance in alkaline electrolyte, requiring a low overpotential of only 306 mV to achieve a current density of 100 mA/cm2. Additionally, a two-electrode electrolyzer assembled with the Co2P/Co/CC electrodes achieved a current density of 10 mA/cm2 at a low cell voltage of 1.54 V and demonstrated excellent long-term stability. This work presents a novel and feasible strategy for constructing hierarchical heterostructured electrocatalysts that enable efficient water electrolysis. By combining rational design and theoretical guidance, our approach offers promising prospects for advancing the field of electrocatalysis and facilitating sustainable energy conversion.
ABSTRACT
OBJECTIVE: To investigate the clinical and genetic features of two families with late-onset glutaric aciduria type II caused by ETFDH mutations. METHODS: Target gene sequence capture and next generation sequencing were used for sequencing of suspected patients and their family members. The patients' clinical features were retrospectively analyzed and literature review was performed. RESULTS: The probands of the two families had a clinical onset at the ages of 10 years and 5.5 years respectively, with the clinical manifestations of muscle weakness and muscle pain. Laboratory examinations revealed significant increases in the serum levels of creatine kinase, creatine kinase-MB, and lactate dehydrogenase. Tandem mass spectrometry showed increases in various types of acylcarnitines. The analysis of urine organic acids showed an increase in glutaric acid. Electromyography showed myogenic damage in both patients. Gene detection showed two novel mutations in the ETFDH gene (c.1331T>C from the mother and c.824C>T from the father) in patient 1, and the patient's younger brother carried the c.1331T>C mutation but had a normal phenotype. In patient 2, there was a novel mutation (c.177insT from the father) and a known mutation (c.1474T>C from the mother) in the ETFDH gene. Several family members carried such mutations. Both patients were diagnosed with glutaric aciduria type II. Their symptoms were improved after high-dose vitamin B2 treatment. CONCLUSIONS: For patients with unexplained muscle weakness and pain, serum creatine kinase, acylcarnitines, and urinary organic acids should be measured, and the possibility of glutaric aciduria type II should be considered. Genetic detection is helpful to make a confirmed diagnosis.
