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A diamond-like amorphous Fe-Co-PO x catalyst is created through a controllable amorphization engineering. It showcases wonderful OER activity, reaching a potential of 270 mV at 10 mA cm−2, and can operate as an anode stably at 200 mA cm−2 for 300 h with little degradation in overall water splitting. Studies observe that the unique amorphous structure, abundant oxygen vacancies, and the synergistic effect of Fe and Co species are the keys to gain excellent water splitting performance. [Display omitted] • An amorphous FeCo-PO x is constructed by hydrothermal and phosphating treatments. • The catalyst owns a diamond-like morphology and abundant oxygen vacancies. • The catalyst exhibits excellent OER and overall water splitting activity and stability. • The synergy of rich oxygen vacancy and amorphous structure are the key to improve performance. Strategically tuning the composition and structure of transition metal phosphates (TMPs) holds immense promise in the development of efficient oxygen evolution reaction (OER) electrocatalysts. However, the effect of crystalline phase transformation for TMPs on the catalytic OER activity remains relatively uncharted. In this study, we have deftly orchestrated the reaction process of anion-etched precursor to induce the amorphization process of FeCo-PO x from crystalline to amorphous states. The as-obtained amorphous FeCo-PO x (A-FeCo-PO x) exhibited an optimized OER performance with a low overpotential of 270 mV at a current density of 10 mA cm−2, which could be attributed to the flexibility of its amorphous structure and the synergistic effect of oxygen vacancies. Moreover, when incorporated into an overall water splitting (OWS) device configured as A-FeCo-POx(+)||Pt/C(–), it displayed long-term solid stability, sustaining operation for 300 h at a current density of 200 mA cm−2. This work not only provides valuable insights into understanding the transformation from crystalline to amorphous states, but also establishes the groundwork for the practical utilization of amorphous nanomaterials in the field of water splitting. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) is a progressive genetic neurodegenerative disease caused by an abnormal expansion of a cytosine-adenine-guanine trinucleotide repeat in the huntingtin gene. One pathological feature of HD is neuronal loss in the striatum. Despite many efforts, mechanisms underlying neuronal loss in HD striatum remain elusive. It was suggested that the mutant huntingtin protein interacts mitochondrial proteins and causes mitochondrial dysfunction in striatal neurons. However, whether axonal transport of mitochondria is altered in HD striatal neurons remains controversial. Here, we examined axonal transport of single mitochondria labelled with Mito-DsRed2 in cultured striatal neurons of zQ175 knock-in mice (a knock-in mouse model of HD). We observed decreased anterograde axonal transport of proximal mitochondria in HD striatal neurons compared with wild-type (WT) striatal neurons. Decreased anterograde transport in HD striatal neurons was prevented by overexpressing mitochondrial Rho GTPase 1 (Miro1). Our results offer a new insight into mechanisms underlying neuronal loss in the striatum in HD. • Cultured striatal neurons were mainly MSNs that are the most vulnerable neurons in HD. • Anterograde axonal transport of proximal mitochondria was altered in HD striatal neurons. • Overexpressing Miro1 prevented altered mitochondrial transport in HD striatal neurons. [ABSTRACT FROM AUTHOR]