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Preformation factor

Some investigators have suggested that this expression should be multiplied by an additional factor to describe the probability of preformation of an a particle inside the parent nucleus. Unfortunately, there is no clear way to calculate such a factor, but empirical estimates have been made. As we will see below, the theoretical estimates of the emission rates are higher than the observed rates, and the preformation factor can be estimated for each measured case. However, there are other uncertainties in the theoretical estimates that contribute to the differences. [Pg.186]

Note that the observed half-life of 433 y is again significantly longer than the predicted half-life of 3 y. This difference is attributed to the combined effects of the preformation factor and the hindrance effect of the odd proton in the americium parent (Z = 95) see below. [Pg.192]

Proton decay should be a simple extension of a decay with the same ideas of barrier penetration being involved. A simplification with proton decay relative to a decay is that there should be no preformation factor for the proton. The situation is shown in Figure 7.12 for the case of the known proton emitter 151Lu. One notes certain important features/complications from this case. The proton energies, even for the heavier nuclei, are low (Ep 1 —2 MeV). As a consequence, the barriers to be penetrated are quite thick (Rom = 80 fm), and one is more sensitive to the proton energy, angular momentum changes, and so forth. [Pg.195]

Use the one-body theory of a decay to estimate the half-life of 224Ra for decay by emission of a 14C ion or a 4He ion. The measured half-life for the 14C decay mode is 10-9 relative to the 4He decay mode. Estimate the relative preformation factors for the a particle and 14C nucleus in the parent nuclide. [Pg.197]

The most commonly used oral anticoagulant drug in the U.S. is warfarin. It acts by altering vitamin K so that it is unavailable to participate in synthesis of vitamin K-dependent coagulation factors in the liver (coagulation factors II, VII, IX, and X). Because of the presence of preformed clotting factors in the blood, the full antithrombotic effect of warfarin therapy may require 36 to 72 h. [Pg.238]

Whereas studies have been carried out on the factors (surface coverage, residence time, pH) which influence the desorption of arsenate previously sorbed onto oxides, phyllosilicates and soils (O Reilly et al. 2001 Liu et al. 2001 Arai and Sparks 2002 Violante and Pigna 2002 Pigna et al. 2006), scant information are available on the possible desorption of arsenate coprecipitated with iron or aluminum. In natural environments arsenic may form precipitates or coprecipitates with Al, Fe, Mn and Ca. Coprecipitation of arsenic with iron and aluminum are practical and effective treatment processes for removing arsenic from drinking waters and might be as important as sorption to preformed solids. [Pg.60]

Figure 4.8. Hypothesis for the local generation of mast-cell-stimulating peptides by the action of neutrophil-derived enzymes on albumin. Initial stimulation of the mast cell by any of a variety of agents causes the release of preformed histamine (H) neutrophil and eosinophil chemotactic factors (NCF, ECF) and enzymes and the de novo synthesis of prostaglandins (PG) and leukotrienes (LT). These agents increase vascular permeability and vessel diameter. As a result, albumin and later neutrophils (PMN) enter the tissue space where the latter undergo phagocytosis and the secretion of proteolytic enzymes to the extracellular space where they act on albumin to generate NRP (neurotensin-related peptide) and HRP (histamine-releasing peptide). These newly formed peptides then act as a second stimulus to the mast cell. In addition NRP and HRP may affect other immunocompetent celt such as monocytes, macrophages or eosinophils. Figure 4.8. Hypothesis for the local generation of mast-cell-stimulating peptides by the action of neutrophil-derived enzymes on albumin. Initial stimulation of the mast cell by any of a variety of agents causes the release of preformed histamine (H) neutrophil and eosinophil chemotactic factors (NCF, ECF) and enzymes and the de novo synthesis of prostaglandins (PG) and leukotrienes (LT). These agents increase vascular permeability and vessel diameter. As a result, albumin and later neutrophils (PMN) enter the tissue space where the latter undergo phagocytosis and the secretion of proteolytic enzymes to the extracellular space where they act on albumin to generate NRP (neurotensin-related peptide) and HRP (histamine-releasing peptide). These newly formed peptides then act as a second stimulus to the mast cell. In addition NRP and HRP may affect other immunocompetent celt such as monocytes, macrophages or eosinophils.
In addition to its role as a preformed resistance factor, Hijwegen (5) has also proposed active induction of lignification as a defense mechanism of cucumber against Cladosporium. Subsequently, in a number of host-pathogen interactions, induced lignification has been proposed as the active... [Pg.370]


See other pages where Preformation factor is mentioned: [Pg.188]    [Pg.194]    [Pg.136]    [Pg.188]    [Pg.194]    [Pg.136]    [Pg.353]    [Pg.1103]    [Pg.48]    [Pg.182]    [Pg.133]    [Pg.286]    [Pg.1237]    [Pg.34]    [Pg.134]    [Pg.35]    [Pg.46]    [Pg.23]    [Pg.169]    [Pg.46]    [Pg.104]    [Pg.116]    [Pg.224]    [Pg.167]    [Pg.1493]    [Pg.263]    [Pg.144]    [Pg.145]    [Pg.102]    [Pg.239]    [Pg.13]    [Pg.81]    [Pg.408]    [Pg.179]    [Pg.182]    [Pg.19]    [Pg.251]    [Pg.77]    [Pg.28]    [Pg.659]    [Pg.380]    [Pg.479]    [Pg.101]   
See also in sourсe #XX -- [ Pg.186 , Pg.188 ]




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