Ga-doped Pt-Ni Octahedral Nanoparticles as a Highly Active and Durable Electrocatalyst for Oxygen Reduction Reaction

Bimetallic PtNi nanoparticles have been considered as a promising electrocatalyst for oxygen reduction reaction (ORR) in polymer electrolyte membrane fuel cells (PEMFCs) owing to their high catalytic activity. However, under typical fuel cell operating conditions, Ni atoms easily dissolve into the electrolyte, resulting in degradation of the catalyst and the membrane-electrode assembly (MEA). Here, we report gallium-doped PtNi octahedral nanoparticles on a carbon support (Ga-PtNi/C). The Ga-PtNi/C shows high ORR activity, marking an 11.7-fold improvement in the mass activity (1.24 A mgPt-1) and a 17.3-fold improvement in the specific activity (2.53 mA cm-2) compare to the commercial Pt/C (0.106 A mgPt-1 and 0.146 mA cm-2). Density functional theory calculations demonstrate that addition of Ga to octahedral PtNi can cause an increase in the oxygen intermediate binding energy, leading to the enhanced catalytic activity toward ORR. In a voltage-cycling test, the Ga-PtNi/C exhibits superior stability to PtNi/C and the commercial Pt/C, maintaining the initial Ni concentration and octahedral shape of the nanoparticles. Single cell using the Ga-PtNi/C exhibits higher initial performance and durability than those using the PtNi/C and the commercial Pt/C. The majority of the Ga-PtNi nanoparticles well maintain the octahedral shape without agglomeration after the single cell durability test (30,000 cycles). This work demonstrates that the octahedral Ga-PtNi/C can be utilized as a highly active and durable ORR catalyst in practical fuel cell applications

Ga-doped Pt-Ni Octahedral Nanoparticles as a Highly Active and Durable Electrocatalyst for Oxygen Reduction Reaction

Bimetallic PtNi nanoparticles have been considered as a promising electrocatalyst for oxygen reduction reaction (ORR) in polymer electrolyte membrane fuel cells (PEMFCs) owing to their high catalytic activity. However, under typical fuel cell operating conditions, Ni atoms easily dissolve into the electrolyte, resulting in degradation of the catalyst and the membrane-electrode assembly (MEA). Here, we report gallium-doped PtNi octahedral nanoparticles on a carbon support (Ga-PtNi/C). The Ga-PtNi/C shows high ORR activity, marking an 11.7-fold improvement in the mass activity (1.24 A mgPt-1) and a 17.3-fold improvement in the specific activity (2.53 mA cm-2) compare to the commercial Pt/C (0.106 A mgPt-1 and 0.146 mA cm-2). Density functional theory calculations demonstrate that addition of Ga to octahedral PtNi can cause an increase in the oxygen intermediate binding energy, leading to the enhanced catalytic activity toward ORR. In a voltage-cycling test, the Ga-PtNi/C exhibits superior stability to PtNi/C and the commercial Pt/C, maintaining the initial Ni concentration and octahedral shape of the nanoparticles. Single cell using the Ga-PtNi/C exhibits higher initial performance and durability than those using the PtNi/C and the commercial Pt/C. The majority of the Ga-PtNi nanoparticles well maintain the octahedral shape without agglomeration after the single cell durability test (30,000 cycles). This work demonstrates that the octahedral Ga-PtNi/C can be utilized as a highly active and durable ORR catalyst in practical fuel cell applications

Boosting the Role of Ir in Mitigating Corrosion of Carbon Support by Alloying with Pt

Corrosion of carbon support is one of the most crucial causes of the degradation of polymer electrolyte membrane fuel cells (PEMFCs) utilizing carbon-supported platinum nanoparticles (Pt/C) as a catalyst. To mitigate carbon corrosion, Pt is alloyed with iridium (Ir), which is catalytically active for the oxygen evolution reaction (OER), with various compositions of PtxIry. The carbon-supported PtxIry alloy catalysts (PtxIry/C) show slightly lower initial activity for the oxygen reduction reaction (ORR) than Pt/C. However, the ORR activities of the PtxIry/C catalysts increase with repeating potential cycles from 1.0 to 1.5 V-RHE, while Pt/C exhibits a rapid decay in the ORR activity and a mixture of Pt/C and Ir/C (Pt/C + Ir/C, Pt-to-Ir ratio of 85:15) maintains its initial activity. After 5k potential cycles, the mass activity of Pt85Ir15 was 0.071 A mg(PGM)(-1), which is significantly higher than that of Pt/C (0.017 A mg(PGM)(-1)) and Pt/C + Ir/C (0.039 A mg(PGM)(-1)). These results can be attributed to the atomically distributed Ir in Pt85Ir15. Clearly, carbon corrosion occurs in Pt/C and in Pt-rich regions of Pt/C + Ir/C, whereas the carbon support in Pt85Ir15/C is effectively protected from corrosion. As a result, the greatest amount of CO2 emission is detected as coming from Pt/C, followed by Pt/C + Ir/C and Pt85Ir15/C. During the potential cycles, high-index Pt facets are formed on the surface of Pt85Ir15/C, leading to an increase in the ORR activity. When employed as cathode catalysts of a PEMFC, Pt85Ir15/C exhibits improved durability compared to Pt/C and Pt/C + Ir/C under high-voltage cycles to 1.5 V (5k cycles). This work demonstrates that the atomic distribution of Ir in Pt is an effective strategy for mitigating corrosion of the carbon support and to enhance the durability of PEMFCs exposed to high potentials.11Nsciescopu

Induction of Fatty Acid Oxidation Underlies DNA Damage‐Induced Cell Death and Ameliorates Obesity‐Driven Chemoresistance

Abstract The DNA damage response is essential for preserving genome integrity and eliminating damaged cells. Although cellular metabolism plays a central role in cell fate decision between proliferation, survival, or death, the metabolic response to DNA damage remains largely obscure. Here, this work shows that DNA damage induces fatty acid oxidation (FAO), which is required for DNA damage‐induced cell death. Mechanistically, FAO induction increases cellular acetyl‐CoA levels and promotes N‐alpha‐acetylation of caspase‐2, leading to cell death. Whereas chemotherapy increases FAO related genes through peroxisome proliferator‐activated receptor α (PPARα), accelerated hypoxia‐inducible factor‐1α stabilization by tumor cells in obese mice impedes the upregulation of FAO, which contributes to its chemoresistance. Finally, this work finds that improving FAO by PPARα activation ameliorates obesity‐driven chemoresistance and enhances the outcomes of chemotherapy in obese mice. These findings reveal the shift toward FAO induction is an important metabolic response to DNA damage and may provide effective therapeutic strategies for cancer patients with obesity