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• Ni(OOH) catalysts decorated by iron oxide atomic layer deposition are demonstrated. • Surface iron on pm on Ni(OOH) catalystsis responsible for high OER OER activity. • Thick, high surface area Ni-Fe(OOH) catalysts require bulk iron for highest activity. • Ni-FeO x films deposited by ALD exhibit high OER activity and good corrosion resistance. Atomic layer deposition (ALD) has become a versatile tool in catalysis, allowing for precise synthesis of catalysts useful for gaining fundamental understanding of complex systems. In this work, ALD was used to perform surface-directed modification of Ni(OH) 2 /Ni(OOH) electrocatalysts for the oxygen evolution reaction (OER) to elucidate the different roles of iron as a surface dopant and of iron distributed throughout the NiOOH structure. Electrochemical and material characterization of FeO x ALD-modified Ni(OH) 2 indicates that iron is deposited on the surface of Ni(OH) 2 sheets without modifying its bulk properties. Sub-monolayer amounts of iron were deposited on the surface of Ni(OH) 2 using low cycle numbers of ALD. This surface iron results in high OER activity, characteristic of Ni-Fe(OOH) catalysts. Ni(OH) 2 /Ni(OOH) catalysts modified to incorporate iron throughout the structure were prepared by depositing large cycle numbers of FeO x ALD, which results in the deposition of a Fe 2 O 3 overlayer. Corrosion of this Fe 2 O 3 overlayer during electrochemical cycling in alkaline electrolyte leads to the incorporation of iron throughout the structure of Ni(OH) 2 /Ni(OOH) while leaving some iron at the surface. Incorporation of iron throughout the Ni(OH) 2 /Ni(OOH) structure was found to increase OER geometric activity for thick, high surface area Ni(OH) 2 /Ni(OOH) catalysts. Lastly, Ni-FeO x electrocatalysts synthesized fully by ALD were investigated for the OER; these catalysts demonstrated high OER activity and potential for photocatalysis applications. [ABSTRACT FROM AUTHOR]

Structure-based iterative design was used to prepare a disulfide-containing nonapeptide as a fluorimetric probe for chemical and biochemical disulfide forming and breaking reactions. The peptide is composed entirely of natural amino acids and exhibits a marked (42%) change in fluorescence between its oxidized and its reduced states. The probe is easily synthesized and highly water soluble and exhibits well-behaved kinetics on reduction with the reductant tris–carboxyethylphosphine. The reduced peptide is an excellent substrate of the enzyme quiescin–sulfhydryl oxidase and may find utility in the characterization of other disulfide oxidoreductases. [Copyright &y& Elsevier]

Abstract: The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium–endothelium–epicardium). We previously described that Id1Id3 double knockout (dKO) mouse embryos die at mid-gestation from multiple cardiac defects, but early lethality precluded the studies of the roles of Id in the postnatal heart. To elucidate postnatal roles of Id genes, we ablated the Id3 gene and conditionally ablated the Id1 gene in the endothelium to generate conditional KO (cKO) embryos. We observed cardiac phenotypes at birth and at 6months of age. Half of the Id cKO mice died at birth. Postnatal demise was associated with cardiac enlargement and defects in the ventricular septum, trabeculation and vasculature. Surviving Id cKO mice exhibited fibrotic vasculature, cardiac enlargement and decreased cardiac function. An abnormal vascular response was also observed in the healing of excisional skin wounds of Id cKO mice. Expression patterns of vascular, fibrotic and hypertrophic markers were altered in the Id cKO hearts, but addition of Insulin-Like Growth Factor binding protein-3 (IGFbp3) reversed gene expression profiles of vascular and fibrotic, but not hypertrophic markers. Thus, ablation of Id genes in the vasculature leads to distinct postnatal cardiac phenotypes. These findings provide important insights into the role/s of the endocardial network of the endothelial lineage in the development of cardiac disease, and highlight IGFbp3 as a potential link between Id and its vascular effectors. [ABSTRACT FROM AUTHOR]