Mechanical overloading effect

Let us consider further reasons of pol5rmer chains breaking at so small stresses, which can be on order lower than ftacture macroscopic stress (i.e., at h5rpothetical k = 0.1). The reasons were pointed for the first time in Refs. [1, 26]. Firstly, anharmonicity intensification in fracture center gives the effect, identical to mechanical overloading effect [26]. Quantitatively this effect is expressed by the ratio of thermal expansion coefficient in fracture center and modal thermal expansion coefficient [5]. The second reason is close inter communication of local yielding and fracture processes [ 1]. This allows to identify fracture center for nonoriented polymers as local plasticity zone [27, 28]. The ratio uJ(X in this case can be reached -100 [5]. This effect compensates completely k reduction lower than one. So, for PC ala 70, K- = 0.44, a. = O.IE. 700 MPa and fiien o = o a /K,a 23 MPa, that by order of magnitude corresponds to experimental value Oj. for PC, which is equal approximately to 50 MPa at T= 293 K [7]. 

This type of test is one of the most versatile methods of see testing because of the flexibility permitted in the type and size of the test specimen, the stressing proc ures, and the range of stress level. It allows the simultaneous exposure of unstressed specimens (no applied load) with stressed specimens and subsequent tension testing to distinguish between the effects of true see and mechanical overload. 

Another way of approaching the problem is to put the lung into overload, which for convenience, can be defined as a situation in which administration of sufficiently high loads of nontoxic insoluble dusts produces marked prolongation or even total failure of macrophage-mediated particle clearance (reviewed in 41,91). The mechanism of the overload effect is not entirely understood (see 91-94 for comments), but it is clear that, under overload conditions, the burden of free particles in the alveoli, the number of particles that are taken up by epithelial cells, and the number of particles translocated to the interstitium, all are greatly increased (41,91). 

In addition to the well-known iron effects on peroxidative processes, there are also other mechanisms of iron-initiated free radical damage, one of them, the effect of iron ions on calcium metabolism. It has been shown that an increase in free cytosolic calcium may affect cellular redox balance. Stoyanovsky and Cederbaum [174] showed that in the presence of NADPH or ascorbic acid iron ions induced calcium release from liver microsomes. Calcium release occurred only under aerobic conditions and was inhibited by antioxidants Trolox C, glutathione, and ascorbate. It was suggested that the activation of calcium releasing channels by the redox cycling of iron ions may be an important factor in the stimulation of various hepatic disorders in humans with iron overload. 

The mechanism of action of ranolazine has not been determined, but it may be related to reduction in calcium overload in ischemic myocytes through inhibition of the late sodium current. Its antianginal effects do not depend on reductions in HR or blood pressure. 

Gritti, F. and Guiochon, G, Effect of the pH, the concentration and the nature of the buffer on the adsorption mechanism of an ionic compound in reversed-phase liquid chromatography, ii. Analytical and overload band profiles on Symmetry-C-18 and Xterra-C-18, J. Chromatogr. A, 1041, 63, 2004. 

Digitalis glycosides enhance the inotropic state by increasing the intracellular calcium concentration. Intracellular calcium overload is also the mechanism for proarrhythmia associated with digitalis intoxication. The direct effect of digitalis on the electrophysiology of the myocytes is to increase the slope of phase 4 depolarization, an effect that enhances automaticity. 

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