Excavating and developing highly efficient and cost‐effective nonnoble metal single‐atom catalysts for electrocatalytic reactions is of paramount significance but still in its infancy. Herein, reported is a general NaCl template‐assisted strategy for rationally designing and preparing a series of isolated transition metal single atoms (Fe/Co/Ni) anchored on honeycomb‐like nitrogen‐doped carbon matrix (M1‐HNC‐T1‐T2, M = Fe/Co/Ni, T1 = 500 °C, T2 = 850 °C). The resulting M1‐HNC‐500‐850 with M‐N4 active sites exhibits superior capability for oxygen reduction reaction (ORR) with the half‐wave potential order of Fe1‐HNC‐500‐850 > Co1‐HNC‐500‐850 > Ni1‐HNC‐500‐850, in which Fe1‐HNC‐500‐850 shows better performance than commercial Pt/C. Density functional theory calculations reveal a choice strategy that the strong p–d‐coupled spatial charge separation results the Fe‐N4 effectively merges active electrons for elevating d‐band activity in a van‐Hove singularity like character. This essentially generalizes an optimal electronic exchange‐and‐transfer (ExT) capability for boosting sluggish alkaline ORR activity. This work not only presents a universal strategy for preparing single‐atom electrocatalyst to accelerate the kinetics of cathodic ORR but also provides an insight into the relationship between the electronic structure and the electrocatalytical activity.

In the CNS, myelination and remyelination depend on the successful progression and maturation of oligodendroglial lineage cells, including proliferation and differentiation of oligodendroglial progenitor cells (OPCs). Previous studies have reported that Sox2 transiently regulates oligodendrocyte (OL) differentiation in the embryonic and perinatal spinal cord and appears dispensable for myelination in the postnatal spinal cord. However, the role of Sox2 in OL development in the brain has yet to be defined. We now report that Sox2 is an essential positive regulator of developmental myelination in the postnatal murine brain of both sexes. Stage-specific paradigms of genetic disruption demonstrated that Sox2 regulated brain myelination by coordinating upstream OPC population supply and downstream OL differentiation. Transcriptomic analyses further supported a crucial role of Sox2 in brain developmental myelination. Consistently, oligodendroglial Sox2-deficient mice developed severe tremors and ataxia, typical phenotypes indicative of hypomyelination, and displayed severe impairment of motor function and prominent deficits of brain OL differentiation and myelination persisting into the later CNS developmental stages. We also found that Sox2 was required for efficient OPC proliferation and expansion and OL regeneration during remyelination in the adult brain and spinal cord. Together, our genetic evidence reveals an essential role of Sox2 in brain myelination and CNS remyelination, and suggests that manipulation of Sox2 and/or Sox2-mediated downstream pathways may be therapeutic in promoting CNS myelin repair. Promoting myelin formation and repair has translational significance in treating myelin-related neurological disorders, such as periventricular leukomalacia and multiple sclerosis in which brain developmental myelin formation and myelin repair are severely affected, respectively. In this report, analyses of a series of genetic conditional knock-out systems targeting different oligodendrocyte stages reveal a previously unappreciated role of Sox2 in coordinating upstream proliferation and downstream differentiation of oligodendroglial lineage cells in the mouse brain during developmental myelination and CNS remyelination. Our study points to the potential of manipulating Sox2 and its downstream pathways to promote oligodendrocyte regeneration and CNS myelin repair.

Designing well‐defined nanointerfaces is of prime importance to enhance the activity of nanoelectrocatalysts for different catalytic reactions. However, studies on non‐noble‐metal‐interface electrocatalysts with extremely high activity and superior stability at high current density still remains a great challenge. Herein, a class of Co3O4/Fe0.33Co0.66P interface nanowires is rationally designed for boosting oxygen evolution reaction (OER) catalysis at high current density by partial chemical etching of Co(CO3)0.5(OH)·0.11H2O (Co‐CHH) nanowires with Fe(CN)63−, followed by low‐temperature phosphorization treatment. The resulting Co3O4/Fe0.33Co0.66P interface nanowires exhibit very high OER catalytic performance with an overpotential of only 215 mV at a current density of 50 mA cm−2 and a Tafel slope of 59.8 mV dec−1 in 1.0 m KOH. In particular, Co3O4/Fe0.33Co0.66P exhibits an obvious advantage in enhancing oxygen evolution at high current density by showing an overpotential of merely 291 mV at 800 mA cm−2, much lower than that of RuO2 (446 mV). Co3O4/Fe0.33Co0.66P is remarkably stable for the OER with negligible current loss under overpotentials of 200 and 240 mV for 150 h. Theoretical calculations reveal that Co3O4/Fe0.33Co0.66P is more favorable for the OER since the electrochemical catalytic oxygen evolution barrier is optimally lowered by the active Co‐ and O‐sites from the Co3O4/Fe0.33Co0.66P interface.

The mechanisms by which oligodendroglia modulate CNS angiogenesis remain elusive. Previous in vitro data suggest that oligodendroglia regulate CNS endothelial cell proliferation and blood vessel formation through hypoxia inducible factor alpha (HIFα)-activated Wnt (but not VEGF) signaling. Using in vivo genetic models, we show that HIFα in oligodendroglia is necessary and sufficient for angiogenesis independent of CNS regions. At the molecular level, HIFα stabilization in oligodendroglia does not perturb Wnt signaling but rather activates VEGF. At the functional level, genetically blocking oligodendroglia-derived VEGF but not Wnt significantly decreases oligodendroglial HIFα-regulated CNS angiogenesis. Blocking astrogliaderived Wnt signaling reduces astroglial HIFα-regulated CNS angiogenesis. Together, our in vivo data demonstrate that oligodendroglial HIFα regulates CNS angiogenesis through Wnt-independent and VEGF-dependent signaling. These findings suggest an alternative mechanistic understanding of CNS angiogenesis by postnatal glial cells and unveil a glial cell type-dependent HIFα-Wnt axis in regulating CNS vessel formation.