Defect-mediated mechanisms

In Fig. 9.1, Dd for nondissociated dislocations is practically equal to DB, which indicates that the diffusion processes in nondissociated dislocation cores and large-angle grain boundaries are probably quite similar. Evidence for this conclusion also comes from the observation that dislocations can support a net diffusional transport of atoms due to self-diffusion [15]. As with grain boundaries, this supports a defect-mediated mechanism. 

The defect-mediated mechanisms have desorption from the dihydride as a final step. Consequently, they all predict that the transition state for desorption is only a few (3-5) kilocalories per mole above the product state. This is consistent with the observation that product H2 has little excess energy. On the other hand, the low excess energy of the transition state over the desorbed state means that the defect-mediated mechanisms have corresponding low barriers to adsorption. At the time these mechanisms were proposed, there were no measurements of the activation energy to adsorption. If the more recent evidence [41, 73] that adsorption has a high activation barrier is confirmed, these models must be ruled out or at least substantially modified. 

Any explanation of first-order kinetics should be general enough to account for the first-order kinetics (and deviations from first-order kinetics) on Ge (and perhaps C) surfaces. In particular, defect-mediated mechanisms that may appear feasible on Si surfaces would require modification since the defect density and bond energies on the Ge surface are very different. The prepairing model has already been shown to model the kinetics on Ge [44]. 

Carl Wagner in association with Schotlky proposed the point defect-mediated mechanism of mass transport in solids, which Wagner extended to the analysis of electronic defects. For these works and Wagner s subsequent research on local equilibrium, his oxidation rate theory and the concept of counter diffusion of cations, he is considered by some to be the father of solid state chemistry . 

Pathophysiologically, there is little difficulty in recognizing disseminated intravascular coagulation and then treating this on merit. Much more frequent are immunologically mediated mechanisms that may be secondary to underlying collagen-vascular diseases such as systemic lupus erythematosus or where the defect exists in isolation and the process is defined as primary, idiopathic or autoimmune. 

By use of the proper experimental conditions and Ltting the four models described above, it may be possible to arrive at a reasonable mechanistic interpretation of the experimental data. As an example, the crystal growth kinetics of theophylline monohydrate was studied by Rodriguez-Hornedo and Wu (1991). Their conclusion was that the crystal growth of theophylline monohydrate is controlled by a surface reaction mechanism rather than by solute diffusion in the bulk. Further, they found that the data was described by the screw-dislocation model and by the parabolic law, and they concluded that a defect-mediated growth mechanism occurred rather than a surface nucleation mechanism. 

Reaction (6.23) makes no assumptions as to the specific mechanism by which weak bonds are converted into defects. The mechanism determines the entropy of the reaction by defining the sites where the defects can reside. For example, the breaking of one weak Si—Si bond creates two defects, but the equilibrium defect density is different if the two defects are allowed to remain close together as a pair, than it is if they are able to diffuse apart. Alternatively, the defect creation can be mediated by hydrogen diffusion which allows the defects to occupy Si—H sites from which the hydrogen is removed. The different results are illustrated by calculations for two specific models. 

Tunneling in multilayered LB films is defect-mediated via trap sites within the conduction band of the molecules (Poole conduction), or by Schottky emission between widely spaced trap sites (Poole Frenkel conduction) in thicker samples [13]. With good molecular conductors the current from molecular conduction should dominate the small contribution from tunneling. However, the conduction mechanism between adjacent layers is not always obvious, due to the complexity of the interface structure. 

Several cases of hepatotoxicity associated with chaparral use have been described (see Section 16.5). The mechanism of chaparral-associated hepatotoxicity is unknown. It is not known if chaparral is an intrinsic hepatotoxin (i.e., toxic to everyone if the dose is sufficient) or an idiosyncratic hepatotoxin (i.e., toxic only to those who have certain genetically aberrant metabolic pathways or immune system defects). Proposed mechanisms of chaparral-associated hepatotoxicity include (1) inhibition of cyclooxygenase or cytochrome P-450, (2) an immune-mediated reaction, (3) formation of a toxic metabolite, (4) impairment of liver function by phytoestrogens found in chaparral, and (5) cholestatic mechanisms causing impairment of bile formation or excretion. There is likely overlap between the two categories and the various mechanisms. In addition, toxicity may be influenced by age, weight, nutritional status, exposure to other drugs and chemicals, cumulative dose, and preparation (i.e., tea, dried plant parts, etc.) (Sheikh et al., 1997). 

Desorption prefactors provide another test of any mechanism. The measured values are about lO s , at the high end of the typical range. Prefactors for defect-mediated models are likely to be much lower than the measured values. Assuming for illustration that the active defects have a density of 10 and that the monohydride-dihydride conversion is energy neutral, then the equilibrium constant for this isomerization step is = 10. If these two species are in rapid equilibrium, and desorption from the dihydride is rate-limiting with rate constant fesiH2 = the ob-... 

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