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In this paper, 550 h ͑500 h continuous and 50 h intermittent͒ high-temperature proton exchange membrane fuel cell ͑PEMFC, phosphoric acid-doped polybenzimidazole system, H 3 PO 4 /PBI͒ life test was performed without humidification at 150°C; constant current ͑at 640 mA cm −2 ͒ performance and polarization curves were recorded. Electrochemical and physical characterizations were applied to investigate the degradation of the membrane electrode assembly ͑MEA͒. The results showed that the constant current performance started to reduce with a rate of 0.18 mV h −1 after about 90 h activation. Surface area loss of the cathode platinum due to agglomeration was detected by cyclic voltammetry and transmission electron microscopy. A slight increase of internal resistance of the single cell due to H 3 PO 4 leaching was found by electrochemical impedance spectroscopy and energy dispersive X-ray analysis. H 2 permeability of MEA increased during the last 50 h intermittent test because of appearing of cracks, that were detected by linear sweep voltammetry and scanning electron microscopy. These results suggested that catalyst agglomeration and H 3 PO 4 leaching from catalyst layers contributed to the performance degradation of the MEA during the life test, and mechanical properties degradation of H 3 PO 4 /PBI membrane impacted badly the lifetime of the single cell.

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Clinically, inhibition of both bacterial infection and excessive inflammation is a crucial step for improved wound treatments. Herein, the fabrication of near‐infrared‐light (NIR)‐activatable deoxyribonuclease (DNase)–carbon monoxide (CO)@mesoporous polydopamine nanoparticles (MPDA NPs) is demonstrated for efficient elimination of methicillin‐resistant Staphylococcus aureus (MRSA) biofilms and the following anti‐inflammatory activity. Specifically, thermosensitive CO‐gas‐releasing donors (CO releasing molecules, FeCO) are first encapsulated into MPDA NPs, followed by covalently immobilizing deoxyribonuclease I (DNase I) on the surfaces of MPDA NPs. DNase I can degrade the extracellular DNA in biofilms, which site specifically destroys the compactness of the biofilms. With NIR irradiation, DNase–CO@MPDA NPs display great photothermal ability, and further trigger on‐demand delivery of bactericidal CO gas that can adequately permeate the impaired biofilms. Eventually, they achieve effective MRSA biofilm elimination in virtue of the synergistic effects of both DNase I participation and CO‐gas‐potentiated photothermal therapy. Importantly, the inflammatory responses of DNase–CO@MPDA NPs and NIR‐treated wounds are simultaneously alleviated owing to the anti‐inflammatory features of released CO. Finally, NIR‐activatable DNase–CO@MPDA NPs accelerate the healing process of MRSA‐biofilm‐infected cutaneous wounds. Taken together, this phototherapeutic strategy displays great therapeutic potential in treating the formidable clinical problems caused by MRSA biofilms and the accompanying inflammation.

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