Molecular mechanism, demonstration

Before dealing with reinforcement of elastomers we have to introduce the basic molecular features of mbber elasticity. Then, we introduce—step-by-step—additional components into the model which consider the influence of reinforcing disordered solid fillers like carbon black or silica within a rabbery matrix. At this point, we will pay special attention to the incorporation of several additional kinds of complex interactions which then come into play polymer-filler and filler-filler interactions. We demonstrate how a model of reinforced elastomers in its present state allows a thorough description of the large-strain materials behavior of reinforced mbbers in several fields of technical applications. In this way we present a thoroughgoing line from molecular mechanisms to industrial applications of reinforced elastomers. 

Examples representing the very wide range of self-assembled protein structures obtained as just described are presented in Figure 1. These examples demonstrate that the size and shape of self-assembled nanostructures made of proteins primarily depend on the molecular mechanism effecting self-assembly and are not merely an amplified reflection of the shape and size of the starting building block. ... 

Combined quantum mechanics/molecular mechanics studies have demonstrated that 7r-7r stacking interactions are important in determining the structural features of polyarene transition metal compounds such as the two ds Pd complexes.96... 

Recent advances in PAH carcinogenesis research over the past decade have led to identification of diol epoxide metabolites as the principal active forms of the PAH investigated to date Q,2). Benzo-(a)pyrene (BP) has been most intensively investigated, and it has been demonstrated that a diol epoxide metabolite anti-BPDE is the active intermediate which binds covalently to DNA in human and other mammalian tissues 0,4). Anti-BPDE was also demonstrated to be a powerful mutagen in both bacterial and mammalian cells (15) These findings stimulated an outpouring of research directed towards elucidation of the molecular mechanism of PAH carcinogenesis. 

The authors demonstrated that this ion-molecular mechanism explains the experimental results from the viewpoints of the process energetics and the reaction kinetics. 

Additional molecular mechanisms must also mediate IFN-y effects, as it promotes a marked clinical improvement in some CGD patients without enhancing phagocyte activity. IFN-y s demonstrated ability to stimulate aspects of cellular and humoral immunity (e.g. via T- and B-lymphocytes), as well as NK cell activity, is most likely responsible for these observed improvements. 

A variety of biochemical and molecular mechanisms have been described to explain how PUFAs can modulate immune cell fate and function. The primary mechanism of action of dietary n-3 PUFAs involves the replacement of AA in the lipid membrane of the cells with either EPA or DHA. This, in effect, competitively inhibits the oxygenation of AA by the COX enzymes. For example, the EPA-induced suppression in the production of AA-derived eicosanoids is followed by a subsequent increase in the production of those from EPA. Generally, the EPA-derived eicosanoids are considered to be much less potent than those from AA, thus explaining, at least partially, the anti-inflammatory effects of PUFAs. A similar mechanism of action can be demonstrated for DHA, either directly or by retroconversion to EPA. 

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