A d niobium(V) complex, NbCl(α-diimine) (1a), supported by a dianionic redox-active N,N'-bis(2,6-diisopropylphenyl)-1,4-diaza-2,3-dimethyl-1,3-butadiene (α-diimine) ligand (ene-diamido ligand) served as a catalyst for radical addition reactions of CCl to α-olefins and cyclic alkenes, selectively affording 1:1 radical addition products in a regioselective manner. During the catalytic reaction, the α-diimine ligand smoothly released and stored an electron to control the oxidation state of the niobium center by changing between an η-(σ,π) coordination mode with a folded MNC metallacycle and a κ-(N,N') coordination mode with a planar MNC metallacycle. Kinetic studies of the catalytic reaction elucidated the reaction order in the catalytic cycle: the radical addition reaction rate obeyed first-order kinetics that were dependent on the concentrations of the catalyst, styrene, and CCl, while a saturation effect was observed at a high CCl concentration. In the presence of excess amounts of styrene, styrene coordinated in an η-olefinic manner to the niobium center to decrease the reaction rate. No observation of oligomers or polymers of styrene and high stereoselectivity for the radical addition reaction of CCl to cyclopentene suggested that the C-C bond formation proceeded inside the coordination sphere of niobium, which was in good accordance with the negative entropy value of the radical addition reaction. Furthermore, reaction of 1a with (bromomethyl)cyclopropane confirmed that both the C-Br bond activation and formation proceeded on the α-diimine-coordinated niobium center during transformation of the cyclopropylmethyl radical to a homoallyl radical. With regard to the reaction mechanism, we detected and isolated NbCl(α-diimine) (6a) as a transient one-electron oxidized species of 1a during reductive cleavage of the C-X bonds; in addition, the monoanionic α-diimine ligand of 6a adopted a monoanionic canonical form with selective one-electron oxidation of the dianionic ene-diamido form of the ligand in 1a.

Three-dimensional (3-D) neutron transport benchmark problems proposed from Osaka University to NEACRP in 1988 have been calculated by many participants and the results have been summarized. The results of kef!• control rod worth, and region-averaged group fluxes for proposed four core models calculated by various 3-D transport codes have been compared. There was consistency among the results, when necessary corrections were made. The solutions of the four core models are quite useful as benchmarks for checking the validity of 3-D neutron transport codes.

A dibromobismuthine and a dibromostibine that bear 4-tBu-2,6-[CH­(SiMe3)2]2-C6H2 (Tbb) groups were reduced with 2,3,5,6-tetramethyl-1,4-bis­(trimethylsilyl)-1,4-diaza-2,5-cyclohexadiene to afford the corresponding stable dibismuthene (TbbBiBiTbb) and the distibene (TbbSbSbTbb), respectively. The only byproducts obtained were easily removable tetramethylpyrazine and bromotrimethylsilane. Importantly, inorganic salts were not generated in this reduction: i.e., this is a unique inorganic-salt-free method for the synthesis of compounds with multiple bonds between heavier main-group elements.

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We describe the membrane localization of a new platelet-specific alloantigen, designated Naka, that is involved in refractoriness to HLA- matched platelet transfusions. By indirect immunoprecipitation, anti- Naka antibody precipitated a single, radiolabeled platelet membrane protein with a molecular weight (mol wt) of 91 Kd from Naka-positive platelets. When radiolabeled Naka-negative platelets were used as a source of target antigens, no radiolabeled proteins were precipitated. The analyses using nonreduced-reduced two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and using rabbit antiglycoprotein (GP)IV demonstrated that this protein corresponds to GPIV (alternatively GPIIIb). Furthermore, in dot immunobinding, anti- Naka antibody bound to purified GPIV. Our results provide definitive evidence that the Naka alloantigen is carried on GPIV. These results also demonstrate that, on occasion, antibodies against GPIV may play an important role in refractoriness to platelet transfusions.