The present work reports a general approach to improve the electrocatalytic property of noble metal through regulating its electron status by introducing the electronic metal–support interaction (EMSI). As a case study, the catalytic activity of metallic Pd toward oxygen evolution reaction (OER) in alkaline solution has been significantly promoted by stabilizing Pdδ+ oxidic species at the interface of the Pd–metal oxide support with the help of EMSI effect, suggesting an intrinsic advantage of Pdδ+ in driving OER. We further demonstrate that the chemical state of Pdδ+ can be easily modulated in the range of 2+ to 3+ by changing the metal oxide support, interestingly, accompanied by a clear dependence of the OER activity on the oxidation state of Pdδ+. The high Pd3+ species-containing Fe2O3/Pd catalyst has fed an impressively enhanced OER property, showing an overpotential of 383 mV at 10 mA cm–2 compared to those of >600 mV on metallic Pd and 540 mV on Fe2O3/glassy carbon. The greatly enhanced OER performance is believed to primarily derive from the distinctive improvement in the adsorption of oxygenated intermediates (e.g., *OH and *OOH) on metal-oxide/Pd catalysts. Moreover, similar EMSI induced improvements in OER activity in alkaline solution are also achieved on both of the Fe2O3/Au and Fe2O3/Pt, which possess the oxidic species of Au3+, and Pt2+ and Pt4+, respectively.

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Hypokalemic periodic paralysis (HypoPP) is an autosomal dominant disorder which is characterized by periodic attacks of muscle weakness associated with a decrease in the serum potassium level. The skeletal muscle calcium channel α-subunit gene CACNA1S is a major disease-causing gene for HypoPP, however, only three specific HypoPP-causing mutations, Arg528His, Arg1,239His and Arg1,239Gly, have been identified in CACNA1S to date. In this study, we studied a four-generation Chinese family with HypoPP with 43 living members and 19 affected individuals. Linkage analysis showed that the causative mutation in the family is linked to the CACNA1S gene with a LOD score of 6.7. DNA sequence analysis revealed a heterozygous C to G transition at nucleotide 1,582, resulting in a novel 1,582C→G (Arg528Gly) mutation. The Arg528Gly mutation co-segregated with all affected individuals in the family, and was not present in 200 matched normal controls. The penetrance of the Arg528Gly mutation was complete in male mutation carriers, however, a reduced penetrance of 83% (10/12) was observed in female carriers. No differences were detected for age-at-onset and severity of the disease (frequency of symptomatic attacks per year) between male and female patients. Oral intake of KCl is effective in blocking the symptomatic attacks. This study identifies a novel Arg528Gly mutation in the CACNA1S gene that causes HypoPP in a Chinese family, expands the spectrum of mutations causing HypoPP, and demonstrates a gender difference in the penetrance of the disease.

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