This report outlines the determination of a reaction mechanism that can be manipulated to develop directed syntheses of gold monolayer-protected clusters (MPCs) prepared by reduction of solutions containing 1,3-bis(diphenylphosphino)propane (L(3)) ligand and Au(PPh(3))Cl. Nanocluster synthesis was initiated by reduction of two-coordinate phosphine-ligated [Au(I)LL'](+) complexes (L, L' = PPh(3), L(3)), resulting in free radical complexes. The [Au(0)LL'](•) free radicals nucleated, forming a broad size distribution of ligated clusters. Timed UV-vis spectroscopy and electrospray ionization mass spectrometry monitored the ligated Au(x), 6 ≤ x ≤ 13, clusters, which comprise reaction intermediates and final products. By employing different solvents and reducing agents, reaction conditions were varied to highlight the largest portion of the reaction mechanism. We identified several solution-phase reaction classes, including dissolution of the gold precursor, reduction, continuous nucleation/core growth, ligand exchange, ion-molecule reactions, and etching of colloids and larger clusters. Simple theories can account for the reaction intermediates and final products. The initial distribution of the nucleation products contains mainly neutral clusters. However, the rate of reduction controls the amount of reaction overlap occurring in the system, allowing a clear distinction between reduction/nucleation and subsequent solution-phase processing. During solution-phase processing, the complexes undergo core etching and core growth reactions, including reactions that convert neutral clusters to cations, in a cyclic process that promotes formation of stable clusters of specific metal nuclearity. These processes comprise "size-selective" processing that can narrow a broad distribution into specific nuclearities, enabling development of tunable syntheses.

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This report documents work performed supporting the Department of Energy (DOE) Office of Nuclear Energy (NE) Fuel Cycle Technologies Used Fuel Disposition Campaign (UFDC) under work breakdown structure element 1.02.08.10, ST Analysis. In particular, this report fulfills the M4 milestone M4FT-15OR0810036, Quantify effects of power uncertainty on fuel assembly characteristics, within work package FT-15OR081003-ST Analysis-ORNL. This research was also supported by the Consortium for Advanced Simulation of Light Water Reactors (http://www.casl.gov), an Energy Innovation Hub (http://www.energy.gov/hubs) for Modeling and Simulation of Nuclear Reactors under U.S. Department of Energy Contract No. DE-AC05-00OR22725.

Ring substituted derivatives of 2-(4-aminophenyl)benzothiazole, 1a, 1b–1g, are under development as anti-tumor agents. One derivative, 1f, has reached Phase 1 clinical trials as the pro-drug, 2f, Phortress (NSC 710305). These amines are activated by CYP450 1A1, apparently into hydroxylamines, 8a–8g, that are likely metabolized into esters that ionize into nitrenium ions responsible for cellular damage. Previously we showed that 9a, the acetic acid ester of 8a, generates the long-lived (530 ns) nitrenium ion 11a by hydrolysis or photolysis in water. In this study, azide trapping shows that 9b–9g generate 11b–11g via rate-limiting N-O heterolysis. Ion lifetimes, estimated from azide/solvent selectivities, range from 250–1150 ns with identical lifetimes for 11a and 11f. Differences in biological activity of the amines are likely not due to differences in the chemistry of the cations, but to differences in metabolic activation/deactivation of individual amines. Unlike the nitrenium ions, lifetimes of the esters are strongly dependent on the 3′-Me substituent. Esters containing 3′-Me (9b, 9f, 9g) have lifetimes of 5–10 s compared to 400–800 s for esters without 3′-Me (9a, 9c, 9d, 9e). This restricts 3′-Me esters to cells/tissues in which activation occurs, concentrating their effects in tumor cells if metabolism is restricted to those cells.

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