Geometrically Controlled Nanoporous PdAu Bimetallic Catalysts with Tunable Pd/Au Ratio for Direct Ethanol Fuel Cells

We report nanoporous Pd_{100–<i>x</i>}Au_<i>x</i> (<i>x</i> = 0, 25, 50, 75, 100; np-PdAu) bimetallic catalysts fabricated by electrochemically dealloying isomorphous Pd_{20–<i>y</i>}Au_<i>y</i>Ni₈₀ (<i>y</i> = 0, 5, 15, 20) precursors. The chemical composition of the nanoporous bimetallic catalysts can be precisely controlled by predesigning Pd/Au ratios in the ternary alloys. Dealloying at an appropriate potential for each alloy can selectively leach Ni away while the Pd and Au remain intact to form a geometrically controllable nanoporous structure. The electrocatalysis of the np-PdAu shows evident dependence on the Au/Pd atomic ratio, and the np-Pd₇₅Au₂₅ bimetallic catalyst shows superior electrocatalytic performance toward ethanol electrooxidation in comparison with commercial Pt/C, np-Pd, and other np-PdAu alloys. Since there are no obvious geometric shape and pore size disparities among the np-PdAu samples, the dealloyed catalysts also provide an ideal system to explore the chemical origins of the excellent catalytic properties of bimetallic catalysts

52 Genetic Loci Influencing Myocardial Mass.

BACKGROUND: Myocardial mass is a key determinant of cardiac muscle function and hypertrophy. Myocardial depolarization leading to cardiac muscle contraction is reflected by the amplitude and duration of the QRS complex on the electrocardiogram (ECG). Abnormal QRS amplitude or duration reflect changes in myocardial mass and conduction, and are associated with increased risk of heart failure and death. OBJECTIVES: This meta-analysis sought to gain insights into the genetic determinants of myocardial mass. METHODS: We carried out a genome-wide association meta-analysis of 4 QRS traits in up to 73,518 individuals of European ancestry, followed by extensive biological and functional assessment. RESULTS: We identified 52 genomic loci, of which 32 are novel, that are reliably associated with 1 or more QRS phenotypes at p < 1 × 10(-8). These loci are enriched in regions of open chromatin, histone modifications, and transcription factor binding, suggesting that they represent regions of the genome that are actively transcribed in the human heart. Pathway analyses provided evidence that these loci play a role in cardiac hypertrophy. We further highlighted 67 candidate genes at the identified loci that are preferentially expressed in cardiac tissue and associated with cardiac abnormalities in Drosophila melanogaster and Mus musculus. We validated the regulatory function of a novel variant in the SCN5A/SCN10A locus in vitro and in vivo. CONCLUSIONS: Taken together, our findings provide new insights into genes and biological pathways controlling myocardial mass and may help identify novel therapeutic targets