Although various single-atom catalysts have been designed, atomically engineering their coordination environment remains a great challenge. Herein, a one-pot template-sacrificing pyrolysis approach is developed to synthesize well-defined Ni−N 4 −O catalytic sites on highly porous graphitic carbon for electrocatalytic CO 2 reduction to CO with high Faradaic efficiency (maximum of 97.2%) in a wide potential window (−0.56 to −1.06 V vs RHE) and with high stability. In-depth experimental and theoretical studies reveal that the axial Ni−O coordination introduces asymmetry to the catalytic center, leading to lower Gibbs free energy for the rate-limiting step, strengthened binding with *COOH, and a weaker association with *CO. The present results demonstrate the successful atomic-level coordination environment engineering of high-surface-area porous graphitic carbon-supported Ni single-atom catalysts (SACs), and the demonstrated method can be applied to synthesize an array of SACs (metal−N 4 −O) for various catalysis applications.

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Borides have been recently identified to be a class of earth-abundant and low-cost materials that are surprisingly active towards oxidative dehydrogenation, and hydrogen evolution reaction (HER) catalysis. Here we explain from first principle calculations the HER activity of WB, an industrial material known for its superior physical properties and chemical inertness. We find that, compared to bulk termination, a major surface reconstruction takes place, leading to the offstoichiometric B-rich surface termination that contains the active sites. The hydrogen adsorbate configurations are further investigated under various adsorbate coverages. Many competing configurations appear to be accessible in reaction conditions, and thus, a grand canonical ensemble is established to describe the catalytic system. A phase diagram of adsorbate coverages is constructed as a function of pH and applied potential. A complex reaction network is presented based on the ensemble-averaged reaction rates, and the electrocatalytic activities are evaluated under different overpotentials. The major contributors to the activity are found to be a few metastable surface states with distinct electronic structure that are only accessible at high adsorbate coverages in reaction conditions. In addition, while the activity of the dominant active site is nearly the same as on the unreconstructed WB, the B-rich formations play an important role of isolating the active sites, and preventing the passivation of the surface with bubble of forming H 2 .

Among numerous gene therapeutic strategies for cancer treatment, gene transfer by conditionally replicative adenovirus (CRAd) of interferon-gamma (IFN-gamma) may be useful because of the possibility that it will yield IFN-gamma-mediated antiangiogenesis, immune responses, and CRAd-mediated oncolysis. In this study, we constructed a human TERT promoter-mediated oncolytic adenovirus targeting telomerase-positive cancers and armed with a mouse or human IFN-gamma gene to generate novel immune gene-viral therapeutic systems, CNHK300-mIFN-gamma and CNHK300-hIFN-gamma, respectively. The systems can specifically target, replicate in, and lyse cancer cells, while sparing normal cells. The advantage of these systems is that the number of transgene copies and their expression increase markedly via viral replication within infected cancer cells, and replicated viral progeny can then infect additional cancer cells within the tumor mass. CNHK300-mIFN-gamma induced regression of xenografts in liver cancer models in both immunodeficient and immunocompetent mice by triplex mechanisms including selective oncolysis, antiangiogenesis, and immune responses. We conclude that combining immune gene therapy and oncolytic virotherapy can enhance antitumor efficacy as a result of synergism between CRAd oncolysis and transgene composite antitumor responses.

Gene-viral therapy, which uses replication-selective transgene-expressing viruses to manage tumors, can exploit the virtues of gene therapy and virotherapy and overcome the limitations of conventional gene therapy. Using a human telomerase reverse transcriptase-targeted replicative adenovirus as an antiangiogenic gene transfer vector to target new angiogenesis and making use of its unrestrained proliferation are completely new concepts in tumor management. CNHK300-mE is a selective replication transgene-expressing adenovirus constructed to carry mouse endostatin gene therapeutically. Infection with CNHK300-mE was associated with selective replication of the adenovirus and production of mouse endostatin in telomerase-positive cancer cells. Endostatin secreted from a human gastric cell line, SGC-7901, infected with CNHK300-mE was significantly higher than that infected with nonreplicative adenovirus Ad-mE in vitro (800 ؎ 94.7 ng/ml versus 132.9 ؎ 9.9 ng/ml) and in vivo (610 ؎ 42 ng/ml versus 126 ؎ 13 ng/ml). Embryonic chorioallantoic membrane assay showed that the mouse endostatin secreted by CNHK300-mE inhibited angiogenesis efficiently and also induced distortion of pre-existing vasculature. CNHK300-mE exhibited a superior suppression of xenografts in nude mice compared with CNHK300 and AdmE. In summary, we provided a more efficient gene-viral therapy strategy by combining oncolysis with antiangiogenesis.