Strategies to Improve the Oxygen Reduction Reaction Activity on Pt-Bi Bimetallic Catalysts: A Density Functional Theory Study.

Decreasing the level of use of Pt in proton exchange membrane fuel cells is of great research interest both academically and industrially. In this work, we systematically studied the oxygen reduction reaction (ORR) following the four-electron association mechanism at various Pt-Bi surfaces with density functional theory calculations. The results showed that the introduction of Bi changes the potential-determining step of ORR. Moreover, the hydroxy adsorption free energy (GOH*) can be used as a descriptor of ORR activity, and 0.74 eV is the ideal GOH* for it to reach its maximum. Notably, we also found that the tensile strain introduced by Bi and electron transfer between Pt and Bi synergize to modulate the d-band of Pt to contract, shift downward, and break the 5d96s1 valence electron configuration of Pt, and accordingly, PtBi(100), with the lowest d-band center, gives the best ORR activity, which is even slightly higher than that of Pt(111).

An amorphous ultrathin iridium/carbon catalyst realizing efficient electrochemical hydrogen evolution.

An amorphous 1.1 nm Ir/C catalyst exhibits ultralow overpotentials of 10 and 64 mV for the hydrogen evolution reaction at current densities of 10 and 100 mA cm-2, together with 117 A mg-1 mass activity and outstanding long-term durability, superior to those of the commercial Pt/C catalyst.

GSK-3ß Contributes to Parkinsonian Dopaminergic Neuron Death: Evidence From Conditional Knockout Mice and Tideglusib.

Glycogen synthase kinase-3 (GSK-3) dysregulation has been implicated in nigral dopaminergic neurodegeneration, one of the main pathological features of Parkinson's disease (PD). The two isoforms, GSK-3α and GSK-3ß, have both been suggested to play a detrimental role in neuronal death. To date, several studies have focused on the role of GSK-3ß on PD pathogenesis, while the role of GSK-3α has been largely overlooked. Here, we report in situ observations that both GSK-3α and GSK-3ß are dephosphorylated at a negatively acting regulatory serine, indicating kinase activation, selectively in nigral dopaminergic neurons following exposure of mice to 1-methyl-4-pheny-1,2,3,6-tetrahydropyridine (MPTP). To identify whether GSK-3α and GSK-3ß display functional redundancy in regulating parkinsonian dopaminergic cell death, we analysed dopaminergic neuron-specific Gsk3a null (Gsk3a ΔDat ) and Gsk3b null (Gsk3b ΔDat ) mice, respectively. We found that Gsk3b ΔDat , but not Gsk3a ΔDat , showed significant resistance to MPTP insult, revealing non-redundancy of GSK-3α and GSK-3ß in PD pathogenesis. In addition, we tested the neuroprotective effect of tideglusib, the most clinically advanced inhibitor of GSK-3, in the MPTP model of PD. Administration of higher doses (200 mg/kg and 500 mg/kg) of tideglusib exhibited significant neuroprotection, whereas 50 mg/kg tideglusib failed to prevent dopaminergic neurodegeneration from MPTP toxicity. Administration of 200 mg/kg tideglusib improved motor symptoms of MPTP-treated mice. Together, these data demonstrate GSK-3ß and not GSK-3α is critical for parkinsonian neurodegeneration. Our data support the view that GSK-3ß acts as a potential therapeutic target in PD and tideglusib would be a candidate drug for PD neuroprotective therapy.