Cleavage stresses

Fig. 3.14. Performance of emery cloth abraded adherends, and the influence of a silane primer, in stressed cleavage tests (Ref. 4). (a) Aromatic amine cured epoxy, (b) Aliphatic amine cured epoxy, (c) Epoxy polysulphide.

Fig. 3.16. Effect of time lapse between gritblasting and bonding in stressed cleavage specimens constructed with an aromatic amine cold-cured epoxide (Ref. 4).

There are four types of stresses which are commonly referred to when considering adhesive bonded joints. These are normal (or direct) stresses, shear stresses, cleavage stresses and peel stresses and they are illustrated in Fig. 6.1. As the name suggests, normal or direct stresses are normal to the plane on which they act and may be tensile or compressive whilst shear stresses are parallel to the plane on which they act. These two types of stresses represent the two sorts of components into which the total stress on any arbitrary plane can be divided. However, it is convenient to identify two further types of stress cleavage stresses which typically arise as the result of an offset tensile force or bending moment and peel stresses which arise if one or both of the substrates are flexible. (These last two terms are frequently used interchangeably by authors.)... 

The value of alkyl halides as starting materials for the preparation of a variety of organic functional groups has been stressed many times In our earlier discussions we noted that aryl halides are normally much less reactive than alkyl halides m reactions that involve carbon-halogen bond cleavage In the present chapter you will see that aryl halides can exhibit their own patterns of chemical reactivity and that these reac tions are novel useful and mechanistically interesting... 

Initiation. Free-radical initiators are produced by several processes. The high temperatures and shearing stresses required for compounding, extmsion, and molding of polymeric materials can produce alkyl radicals by homolytic chain cleavage. Oxidatively sensitive substrates can react directly with oxygen, particularly at elevated temperatures, to yield radicals. 

The anthrax toxin is a tripartite toxin and consists ofthe binding component protective antigen (PA), the lethal factor (LF), which is a metalloprotease, and the edema factor (EF), which is a calmodulin-dependent adenylyl-cyclase. Both enzyme components are translocated via PA into target cells. PA is activated by furin-induced cleavage and forms heptamers, which are similar to the binding components of C2 toxin and iota toxin. In the low pH compartment of endosomes, the heptamers form pores to allow translocation of LF and EF. LF cleaves six of the seven MEKs (MAPK-kinases) thereby inhibiting these enzymes. The functional consequence is the blockade of the MAPK pathways that control cell proliferation, differentiation, inflammation, stress response, and survival. Whether this is the reason for the LT-induced cell death of macrophages is not clear [1]. 

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