Cerebral ischemia-reperfusion (I-R) is a complex pathological process. Although autophagy can be evoked by ischemia, its involvement in the reperfusion phase after ischemia and its contribution to the fate of neurons remains largely unknown. In the present investigation, we found that autophagy was activated in the reperfusion phase, as revealed in both mice with middle cerebral artery occlusion and oxygen-glucose deprived cortical neurons in culture. Interestingly, in contrast to that in permanent ischemia, inhibition of autophagy (by 3-methyladenine, bafilomycin A 1, Atg7 knockdown or in atg5(-/-) MEF cells) in the reperfusion phase reinforced, rather than reduced, the brain and cell injury induced by I-R. Inhibition of autophagy either with 3-methyladenine or Atg7 knockdown enhanced the I-R-induced release of cytochrome c and the downstream activation of apoptosis. Moreover, MitoTracker Red-labeled neuronal mitochondria increasingly overlapped with GFP-LC3-labeled autophagosomes during reperfusion, suggesting the presence of mitophagy. The mitochondrial clearance in I-R was reversed by 3-methyladenine and Atg7 silencing, further suggesting that mitophagy underlies the neuroprotection by autophagy. In support, administration of the mitophagy inhibitor mdivi-1 in the reperfusion phase aggravated the ischemia-induced neuronal injury both in vivo and in vitro. PARK2 translocated to mitochondria during reperfusion and Park2 knockdown aggravated ischemia-induced neuronal cell death. In conclusion, the results indicated that autophagy plays different roles in cerebral ischemia and subsequent reperfusion. The protective role of autophagy during reperfusion may be attributable to mitophagy-related mitochondrial clearance and inhibition of downstream apoptosis. PARK2 may be involved in the mitophagy process.

Simultaneous highly efficient production of hydrogen and conversion of biomass into value‐added products is meaningful but challenging. Herein, a porous nanospindle composed of carbon‐encapsulated MoO2‐FeP heterojunction (MoO2‐FeP@C) is proposed as a robust bifunctional electrocatalyst for hydrogen evolution reaction (HER) and biomass electrooxidation reaction (BEOR). X‐ray photoelectron spectroscopy analysis and theoretical calculations confirm the electron transfer from MoO2 to FeP at the interfaces, where electron accumulation on FeP favors the optimization of H2O and H* absorption energies for HER, whereas hole accumulation on MoO2 is responsible for improving the BEOR activity. Thanks to its interfacial electronic structure, MoO2‐FeP@C exhibits excellent HER activity with an overpotential of 103 mV at 10 mA cm−2 and a Tafel slope of 48 mV dec−1. Meanwhile, when 5‐hydroxymethylfurfural is chosen as the biomass for BEOR, the conversion is almost 100%, and 2,5‐furandicarboxylic acid (FDCA) is obtained with the selectivity of 98.6%. The electrolyzer employing MoO2‐FeP@C for cathodic H2 and anodic FDCA production requires only a low voltage of 1.486 V at 10 mA cm−2 and can be powered by a solar cell (output voltage: 1.45 V). Additionally, other BEORs coupled with HER catalyzed by MoO2‐FeP@C also have excellent catalytic performance, implying their good versatility.

An in situ catalytic etching strategy is developed to fabricate holey reduced graphene oxide along with simultaneous coupling with a small-sized Mo N-Mo C heterojunction (Mo N-Mo C/HGr). The method includes the first immobilization of H PMo O (PMo ) clusters on graphite oxide (GO), followed by calcination in air and NH to form Mo N-Mo C/HGr. PMo not only acts as the Mo heterojunction source, but also provides the Mo species that can in situ catalyze the decomposition of adjacent reduced GO to form HGr, while the released gas (CO) and introduced NH simultaneously react with the Mo species to form an Mo N-Mo C heterojunction on HGr. The hybrid exhibits superior activity towards the hydrogen evolution reaction with low onset potentials of 11 mV (0.5 m H SO ) and 18 mV (1 m KOH) as well as remarkable stability. The activity in alkaline media is also superior to Pt/C at large current densities (>88 mA cm ). The good activity of Mo N-Mo C/HGr is ascribed to its small size, the heterojunction of Mo N-Mo C, and the good charge/mass-transfer ability of HGr, as supported by a series of experiments and theoretical calculations.

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Phosphorus-modified tungsten nitride/reduced graphene oxide (P-WN/rGO) is designed as a high-efficient, low-cost electrocatalyst for the hydrogen evolution reaction (HER). WN (ca. 3 nm in size) on rGO is first synthesized by using the H3[PO4(W3O9)4] cluster as a W source. Followed by phosphorization, the particle size increase slightly to about 4 nm with a P content of 2.52 at %. The interaction of P with rGO and WN results in an obvious increase of work function, being close to Pt metal. The P-WN/rGO exhibits low onset overpotential of 46 mV, Tafel slope of 54 mV dec(-1), and a large exchange current density of 0.35 mA cm(-2) in acid media. It requires overpotential of only 85 mV at current density of 10 mA cm(-2), while remaining good stability in accelerated durability testing. This work shows that the modification with a second anion is powerful way to design new catalysts for HER.

Overall water splitting driven by a low voltage is crucial for practical H2 evolution, but it is challenging. Herein, anion‐modulation of 3D Ni–V‐based transition metal interstitial compound (TMIC) heterojunctions supported on nickel foam (Ni3N‐VN/NF and Ni2P‐VP2/NF) as coupled hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) catalysts for efficient overall water splitting is demonstrated. The heterointerface in Ni3N‐VN has a suitable H* absorption energy, being favorable for enhancing HER activity with onset overpotential (ηonset) of zero and Tafel slope of 37 mV dec−1 in 1 m KOH (close to that of Pt/C/NF). For the OER, the synergy of Ni2P‐VP2 with oxide species can give enhanced activity with ηonset of 220 mV and Tafel slope of 49 mV dec−1. The good activity is ascribed to heterointerface for activating the intermediates, good conductivity of TMICs for electron‐transfer, and porous structure facilitation of mass‐transport. Additionally, the minimal mutual influence of Ni3N‐VN/NF and Ni2P‐VP2/NF allows easy coupling for efficient overall water splitting with a low driving voltage (≥1.43 V), a voltage of 1.51 V at 10 mA cm−2, and remarkable durability for 100 h. It can be driven by a solar cell (1.5 V), indicating its potential to store intermittent energy.

Transient cerebral ischemia leads to endoplasmic reticulum (ER) stress. However, the contributions of ER stress to cerebral ischemia are not clear. To address this issue, the ER stress activators tunicamycin (TM) and thapsigargin (TG) were administered to transient middle cerebral artery occluded (tMCAO) mice and oxygen-glucose deprivation-reperfusion (OGD-Rep.)-treated neurons. Both TM and TG showed significant protection against ischemia-induced brain injury, as revealed by reduced brain infarct volume and increased glucose uptake rate in ischemic tissue. In OGD-Rep.-treated neurons, 4-PBA, the ER stress releasing mechanism, counteracted the neuronal protection of TM and TG, which also supports a protective role of ER stress in transient brain ischemia. Knocking down the ER stress sensor Eif2s1, which is further activated by TM and TG, reduced the OGD-Rep.-induced neuronal cell death. In addition, both TM and TG prevented PARK2 loss, promoted its recruitment to mitochondria, and activated mitophagy during reperfusion after ischemia. The neuroprotection of TM and TG was reversed by autophagy inhibition (3-methyladenine and Atg7 knockdown) as well as Park2 silencing. The neuroprotection was also diminished in Park2(+/-) mice. Moreover, Eif2s1 and downstream Atf4 silencing reduced PARK2 expression, impaired mitophagy induction, and counteracted the neuroprotection. Taken together, the present investigation demonstrates that the ER stress induced by TM and TG protects against the transient ischemic brain injury. The PARK2-mediated mitophagy may be underlying the protection of ER stress. These findings may provide a new strategy to rescue ischemic brains by inducing mitophagy through ER stress activation.

A new trapping route has been used to synthesize MoxCoxC confined in carbon polyhedrons, through trapping PMo12 clusters into pre-synthesized ZIF-67 polyhedrons. The catalysts showed excellent performance for water splitting.