Metallic Cu is a well-known electrocatalyst for nitrate reduction reaction (NO 3 RR), but it suffers from relatively low activity, poor stability, and inducing nitrite accumulation during the long-term operation. Herein, it is found that Cu catalysts minimized at the single-atom level can overcome the limitations of bulk materials in NO 3 RR. A metal-nitrogen-carbon (M-N-C) electrocatalyst composed of carbon nanosheets embedding isolated copper atoms coordinated with N, Cu-N-C-800, is synthesized by pyrolysis of a Cu-based metal-organic framework at 800 °C. In comparison with Cu nanoparticles and Cu plate-800, kinetic measurements show that the Cu-N-C-800 electrocatalyst is more active and stable and distinctly suppresses the release of nitrite intermediate into the solution. The combined results of experimental data and density functional theory calculations indicate that Cu bound with N (particularly Cu-N 2) is the key to favorable adsorption of NO 3 − and NO 2 −. This strong binding is responsible for the enhanced rate of nitrate conversion to the end products of ammonia and nitrogen. These findings highlight the promise of single-atom Cu electrocatalysts for nitrate reduction with desirable performance.

Key Points Antisense oligonucleotides reduce levels of target hepatic mRNA and protein and decrease clotting activity in rabbits. Selective depletion of factors XI and XII in rabbits attenuates catheter thrombosis, whereas factor VII depletion does not.

In patients undergoing percutaneous coronary intervention, catheter thrombosis is more frequent with fondaparinux than heparin. This study was undertaken to identify the responsible mechanism and to develop strategies for its prevention. Percutaneous coronary intervention catheter segments shortened plasma clotting times from 971 ؎ 92 to 352 ؎ 22 seconds. This activity is factor XII (fXII) dependent because it was attenuated with corn trypsin inhibitor and was abolished in fXII-deficient plasma. Heparin and enoxaparin blocked catheter-induced clotting at 0.5 and 2 anti-Xa U/mL, respectively, whereas fondaparinux had no effect. Addition of fondaparinux to bivalirudin or low-dose heparin attenuated catheterinduced clotting more than either agent alone. In a rabbit model of catheter thrombosis, a 70 anti-Xa U/kg intravenous bolus of heparin or enoxaparin prolonged the time to catheter occlusion by 4.6-and 2.5-fold, respectively, compared with saline, whereas the same dose of fondaparinux had no effect. Although 15 antiXa U/kg heparin had no effect on its own, when given in conjunction with 70 antiXa U/kg fondaparinux, the time to catheter occlusion was prolonged 2.9-fold. These findings indicate that (1) catheters are prothrombotic because they trigger fXII activation, and (2) fondaparinux does not prevent catheter-induced clotting unless supplemented with low-dose heparin or bivalirudin. (Blood. 2011;118(25): 6667-6674)