Synthesis of Tetrahexahedral Platinum Nanocrystals with High-Index Facets andHigh Electro-Oxidation Activity. -Pt nanocrystals of unusual tetrahexahedral shape are electrochemically prepared with high yield from Pt nanospheres electrodeposited on a glassy carbon electrode in a H2SO4 solution of K2PtCl6, followed by a square-wave treatment in a H2SO4/ascorbic acid solution for 10 to 60 min. The samples are characterized by SEM and TEM. The nanocrystals are enclosed by 24 high-index facets such as {730}, {210}, and/or {520} surfaces that have a large density of atomic steps and dangling bonds. The synthesized nanocrystals exhibit up to 400% enhanced catalytic activity for electro-oxidation of small organic fuels such as formic acid and EtOH, demonstrating their potential use in the traditional applications of Pt group metal nanoparticles, including catalysts, automotive catalytic converters, fuel cells, and sensors. -(TIAN, N.; ZHOU, Z.-Y.; SUN*, S.-G.; DING, Y.; WANG, Z. L.; Sci. (Washington, D. C., USA) 316 (2007) 5825, 732-735; State Key Lab. Phys. Chem. Solid Surf., Dep. Chem., Xiamen Univ.,

Background: Receptor interacting protein 3 (RIP3)-mixed lineage kinase domain-like (MLKL) interaction is essential for necroptosis. Results: Murine RIP3 does not interact with human MLKL and vice versa due to sequence differences in and around the RIP3 phosphorylation sites. Conclusion: Different sequences in human and mouse RIP3 control the functionally conserved RIP3-MLKL interaction. Significance: This study provided new insights into the function of RIP3-MLKL interaction in necroptosis.

The electrocatalytic urea oxidation reaction (UOR) provides more economic electrons than water oxidation for various renewable energy‐related systems owing to its lower thermodynamic barriers. However, it is limited by sluggish reaction kinetics, especially by CO2 desorption steps, masking its energetic advantage compared with water oxidation. Now, a lattice‐oxygen‐involved UOR mechanism on Ni4+ active sites is reported that has significantly faster reaction kinetics than the conventional UOR mechanisms. Combined DFT, 18O isotope‐labeling mass spectrometry, and in situ IR spectroscopy show that lattice oxygen is directly involved in transforming *CO to CO2 and accelerating the UOR rate. The resultant Ni4+ catalyst on a glassy carbon electrode exhibits a high current density (264 mA cm−2 at 1.6 V versus RHE), outperforming the state‐of‐the‐art catalysts, and the turnover frequency of Ni4+ active sites towards UOR is 5 times higher than that of Ni3+ active sites.

The auto-phosphorylation of murine receptor-interacting protein 3 (Rip3) on Thr 231 and Ser 232 in the necrosome is required to trigger necroptosis. However, how Rip3 phosphorylation is regulated is still largely unknown. Here we identified protein phosphatase 1B (Ppm1b) as a Rip3 phosphatase and found that Ppm1b restricts necroptosis in two settings: spontaneous necroptosis caused by Rip3 auto-phosphorylation in resting cells, and tumour necrosis factor-α (TNF)-induced necroptosis in cultured cells. We revealed that Ppm1b selectively suppresses necroptosis through the dephosphorylation of Rip3, which then prevents the recruitment of mixed lineage kinase domain-like protein (Mlkl) to the necrosome. We further showed that Ppm1b deficiency (Ppm1bd/d) in mice enhanced TNF-induced death in a Rip3-dependent manner, and the role of Ppm1b in inhibiting necroptosis was evidenced by elevated Rip3 phosphorylation and tissue damage in the caecum of TNF-treated Ppm1bd/d mice. These data indicate that Ppm1b negatively regulates necroptosis through dephosphorylating Rip3 in vitro and in vivo.