Nickel proximal

Nickel(O) reacts with the olefin to form a nickel(0)-olefin complex, which can also coordinate the alkyl aluminum compound via a multicenter bond between the nickel, the aluminum and the a carbon atom of the trialkylaluminum. In a concerted reaction the aluminum and the hydride are transferred to the olefin. In this mechanistic hypothesis the nickel thus mostly serves as a template to bring the olefin and the aluminum compound into close proximity. No free Al-H or Ni-H species is ever formed in the course of the reaction. The adduct of an amine-stabihzed dimethylaluminum hydride and (cyclododecatriene)nickel, whose structure was determined by X-ray crystallography, was considered to serve as a model for this type of mechanism since it shows the hydride bridging the aluminum and alkene-coordinated nickel center [31]. 

Smith-Sivertsen, T., V. Tchachtchine, E. Lund, V. Bykov, Y. Thomassen, and T. Norseth. 1998. Urinary nickel excretion in populations living in the proximity of two Russian nickel refineries a Norwegian-Russian population-based study. Environ. Health Perspec. 106 503-511. 

The proximal cluster donates an electron to the external acceptor. Two electrons are transferred from the hydride, at first reducing the nickel from Ni(III) to Ni(I). An electron is transferred from the nickel to the proximal cluster. 

As indicated in Figure 3.2, this is probably just the binding of hydrogen (presumably as -1- H ) to the active site at some distance from nickel. This binding induces the oxidation of the nickel center (Ni Ni ), whereby the electron initially enters the proximal Fe-S cluster. CO can bind to the divalent nickel in the Nia-S state and thereby fixes the active site in the Nia-S-CO state ... 

This might alter the electric field of the metal or that experienced by the incoming hydrocarbon, leading to enhanced dehydrogenation on the metal site, and cyclization on the nearby acid sites. Neither of the first two routes would be expected to increase the activity associated with vanadium, since vanadium is much more mobile than nickel, and appears to remain as V + in these systems (Schubert, P. F. Altomare, C. A. Koermer, G. S., Engelhard Corporation Willis, W. S. Suib, S. L., University of Connecticut, manuscript in preparation). While vanadium might be expected to be affected by proximity to the zeolite, this effect could be masked by the destruction of the zeolite. 

Our third hypothesis, i.e., that the activity enhancement involves the proximity of the zeolite s acid sites, appears to be consistent with the hydrocarbon adsorption experiments, but may also be due to differences in the nickel dispersion arising from surface area differences between the two types of particles. Clearly, the adsorption of hexane at lower temperature on the nickel contaminated zeolitic particles suggests a significantly altered environment from both the uncontaminated and the non-zeolitic materials. 

Biophysical studies of the urease metal centre in the presence and absence of inhibitors, in conjunction with kinetic data provide the model of the bi-Ni site shown in 1. Certain inhibitors are thought to bridge the two nickel atoms consistent with a bridged transition state during urea hydrolysis. The ligands for nickel are believed not to contain sulphur, however, an essential cysteine is proximal to the active site. Comparisons of diethylpyrocarbonate reactivity for apo- and halo-enzyme are consistent with His as a ligand to nickel (Lee et al., 1990). 

In this system, the catalyst G3-I9 showed a similar reaction rate and turnover number as observed with the parent unsupported NCN-pincer nickel complex under the same conditions. This result is in contrast to the earlier observations for periphery-functionalized Ni-containing carbosilane dendrimers (Fig. 4), which suffer from a negative dendritic effect during catalysis due to the proximity of the peripheral catalytic sites. In G3-I9, the catalytic active center is ensconced in the core of the dendrimer, thus preventing catalyst deactivation by the previous described radical homocoupling formation (Scheme 4). 

Silyl(pinacol)borane added to terminal alkenes in the presence of Pt(GH2=CH2)(PPh3)2 to give l-boryl-2-silylalk-anes 247 Platinum-catalyzed silylboration of methylene cyclopropanes provided alkenylboron derivatives via a proximal G-G bond cleavage (Equation (41))250 Nickel(0)-catalyzed silylboration of vinyl cyclopropanes and cyclobutanes provided allylsilane derivatives via analogous G-G bond cleavage (Equation (42)).251... 

One group of NADH oxidants, which does not fit the proposed reaction scheme in Fig. 2.4 are the metal complexes. Examples of this type include nickel hexacyanoferrate deposited on porous nickel electrodes [29], gold electrodes modified with cobalt hexacyanoferrate films [30] and adsorbed l,10-phenanthroline-5,6-dione complexes of ruthenium and osmium [31]. It is unclear how these systems work and no mechanism has been proposed to date. It may be worth noting that dihydronicotinamide groups have been shown to reduce aldehydes in a non-enzymatic reaction when the reaction is catalysed by zinc, a metal ion [15]. In a reaction between 1,10-phenanthroline-2-carboxaldehyde and N-propyl-l,4-dihydronicotinamide, no reaction was seen in the absence of zinc but when added to the system, the aldehyde was reduced and the nicotinamide was oxidised. This implies that either coordination to, or close proximity of, the metal ion activates... 

Rote et al. (1993, 1994) used a carotid thrombosis model in dogs. A calibrated electromagnetic flow meter was placed on each common carotid artery proximal to both the point of insertion of an intravascular electrode and a mechanical constrictor. The external constrictor was adjusted with a screw until the pulsatile flow pattern decreased by 25 % without altering the mean blood flow. Electrolytic injury to the intimal surface was accomplished with the use of an intravascular electrode composed of a Teflon-insulated silver-coated copper wire connected to the positive pole of a 9-V nickel-cadmium battery in series with a 250000 ohm variable resistor. The cathode was connected to a subcutaneous site. Injury was initiated in the right carotid artery by application of a 150 xA continuous pulse anodal direct current to the intimal surface of the vessel for a maximum duration of 3 h or for 30 min beyond the time of complete vessel occlusion as determined by the blood flow recording. Upon completion of the study on the right carotid, the procedure for induction of vessel wall injury was repeated on the left carotid artery after administration of the test drug. 

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