Oxidation-induced ambiphilicity triggers N-N bond formation and dinitrogen release in octahedral terminal molybdenum(v) nitrido complexes.

Coupling of octahedral, terminal d1 molybdenum(v) nitrido complexes supported by a dianionic pentadentate ligand via N-N bond formation to give µ-dinitrogen complexes was found to be thermodynamically feasible but faces significant kinetic barriers. However, upon oxidation, a kinetically favored nucleophilic/electrophilic N-N bond forming mechanism was enabled to give monocationic µ-dinitrogen dimers. Computational and experimental evidence for this "oxidation-induced ambiphilic nitrido coupling" mechanism is presented. The factors influencing release of dinitrogen from the resulting µ-dinitrogen dimers were also probed and it was found that further oxidation to a dicationic species is required to induce (very rapid) loss of dinitrogen. The mechanistic path discovered for N-N bond formation and dinitrogen release follows an ECECC sequence (E = "electrochemical step"; C = "chemical step"). Experimental evidence for the intermediacy of a highly electrophilic, cationic d0 molybdenum(vi) nitrido in the N-N bond forming mechanism via trapping with an isonitrile reagent is also discussed. Together these results are relevant to the development of molecular catalysts capable of mediating ammonia oxidation to dihydrogen and dinitrogen.

Spontaneous Ammonia Activation Through Coordination-Induced Bond Weakening in Molybdenum Complexes of a Dianionic Pentadentate Ligand Platform.

Ammonia oxidation catalyzed by molecular compounds is of current interest as a carbon-free source of dihydrogen. Activation of N-H bonds through coordination to transition metal centers is a key reaction in this process. We report the substantial activation of ammonia via reaction with low-valent molybdenum complexes of a diborate pentadentate ligand system. Spontaneous loss of dihydrogen from (B2 Pz4 Py)MoII -NH3 at room temperature to produce the dinuclear µ-nitrido compound (B2 Pz4 Py)Mo-N-Mo(B2 Pz4 Py) is observed due to substantial N-H bond weakening upon coordination to Mo. Mechanistic details are supported through the experimental observation/characterization of terminal amido, imido and nitrido complexes and density functional theory computations. The generally under-appreciated role of bridging nitrido intermediates is revealed and discussed, providing guidance for further catalyst development for this process.

Preferential survival of mice expressing the Qa-2 antigen.

The Ped gene, a gene that influences the rate of embryonic cleavage division, birth weight, litter size and weaning weight, is at least partially encoded by gene(s) that specify the Qa-2 antigen. Two congenic strains of mice, B6.K1 (Qa-2 negative) and B6.K2 (Qa-2 positive), which differ only at the Q region of the mouse major histocompatibility complex (MHC), were tested for the effect of the presence or absence of Qa-2 antigen on litter size, duration of gestation and embryo survival. It was confirmed that B6.K1 (Qa-2 negative) mice have smaller litters than do B6.K2 (Qa-2 positive) mice. In addition, the duration of gestation for the B6.K1 mice was found to be longer than the duration of gestation for the B6.K2 mice. Finally, a comparison of the relative survival of Qa-2-positive and Qa-2-negative mice in a single uterine environment showed the preferential survival of mice expressing the Qa-2 antigen. Thus, the presence of Qa-2 antigen appears to be advantageous for reproductive success.

Induction of embryonic major histocompatibility complex antigen expression by gamma-IFN.

Preimplantation mouse embryos were incubated in vitro with mouse recombinant gamma-interferon (IFN). The effect of the gamma-IFN on major histocompatibility complex (MHC) class I antigen expression was tested using an ELISA procedure. It was found that there is a doubling of Db antigens and a tripling of Qa-2 antigens on C57BL/6 mouse embryos cultured from the 8-cell stage for 24 h in the presence of 10(5) units/ml gamma-IFN. The effect of gamma-IFN on the rate of preimplantation embryonic development was tested by culturing 2-cell embryos for 48 h and 8-cell embryos for 24 h in the presence of varying concentrations of gamma-IFN up to 10(6) units/ml. Two methods were used to assess the cell number per embryo after the culture period: incorporation of [3H]thymidine into DNA, and direct counting of nuclei in fixed and stained embryos. Both methods showed that treatment with gamma-IFN increases the rate of development of preimplantation mouse embryos. Since rate of preimplantation embryonic development is genetically controlled by the Ped gene, it is suggested that gamma-IFN has a direct effect on the Ped gene phenotype of preimplantation mouse embryos.

Temporal stability of sequential pulse defibrillation threshold.

We have shown that sequential pulse defibrillation threshold voltage and total delivered energy do not change with maturation of the electrode tissue interface for up to 12 weeks after implantation of two different electrode configurations. This result is important to predict the future performance of an implantable defibrillator that is tested only at implant.