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Effect heredity

A problem with the all subsets approach is that all relationships between predictors are ignored. For example, the best subset of size four, Eq, AlCl, BlHq, BqHq), contains an interaction involving factors A and C, but no corresponding main effects. Indeed, one of the main strengths of the Hamada-Wu approach is the incorporation of the principle of effect heredity an interaction between two effects is not considered active unless at least one of the corresponding main effects is also active. [Pg.238]

Neither all subsets regression nor the Hamada-Wu stepwise algorithm represents a complete solution. All subsets regression provides a complete search but ignores effect heredity. The Hamada-Wu approach identifies models obeying effect heredity but has an incomplete search and may miss the best effect heredity models. [Pg.238]

The use of Bayesian priors, coupled with efficient stochastic search algorithms, provides one approach that solves both problems. The stochastic search significantly improves the chances of finding good models, whereas Bayesian priors focus the search on models obeying effect heredity. [Pg.238]

Table 4 lists the 10 most probable subsets found by the Bayesian procedure. With the exception of the second subset listed (BlHq, BqHq), every term in every subset has at least one lower-order effect also in the subset. For example, in the fifth subset listed in Table 4 (FL, HL, Hq, AlHq, GlHq, BlHq, ELFi), ht active effect GlHq has parent Hq which, in turn, has parent Hl. (The notions of parents and effect heredity are stated precisely in Section 2.2.) This fifth subset contains all the effects in the best subset of size 5 listed in Table 3. The Bayesian procedure has found a subset similar to one of the best subsets but which obeys effect heredity. Table 4 lists the 10 most probable subsets found by the Bayesian procedure. With the exception of the second subset listed (BlHq, BqHq), every term in every subset has at least one lower-order effect also in the subset. For example, in the fifth subset listed in Table 4 (FL, HL, Hq, AlHq, GlHq, BlHq, ELFi), ht active effect GlHq has parent Hq which, in turn, has parent Hl. (The notions of parents and effect heredity are stated precisely in Section 2.2.) This fifth subset contains all the effects in the best subset of size 5 listed in Table 3. The Bayesian procedure has found a subset similar to one of the best subsets but which obeys effect heredity.
The Bayesian approach is more than a tool for adjusting the results of the all subsets regression by adding appropriate effects to achieve effect heredity. Take, for example, the sixth model in Table 4 which consists of Al,Bl, AlDq, BlHl, BlHq, BqHq. The AlDq effect identified as part of this model does not appear in the best subsets of size 1-6 in Table 3. The Bayesian procedure has therefore discovered an additional possible subset of effects that describes the data. [Pg.239]

Bayesian methods for subset selection offer several advantages over other approaches the assignment of posterior probabilities to different subsets of active effects provides a way of characterizing uncertainty about effect activity prior distributions can incorporate principles of effect dependence, such as effect heredity the identification of promising models via Bayesian stochastic search techniques is faster than all subsets searches, and more comprehensive than stepwise methods. [Pg.240]

Effect Heredity Subsets should obey heredity of active effects. For example, a subset with an active AB interaction but no A or B main effects may not be acceptable. Nelder (1998) referred to this as the marginality principle . [Pg.244]

The effect heredity principle motivates two simplifying assumptions. The first assumption is that terms of equal order are active independently of each other, given the activity of the lower-order terms. Then (7) becomes... [Pg.244]

Several medical tests can determine whether you have been exposed to methyl parathion. The first medical test measures methyl parathion in your blood or measures 4-nitrophenol, which is a breakdown product of methyl parathion, in your urine. These tests are only reliable for about 24 hours after you are exposed because methyl parathion breaks down quickly and leaves your body. These tests cannot tell whether you will have harmful health effects or what those effects may be. The next medical test measures the levels of a substance called cholinesterase in your blood. If cholinesterase levels are less than half of what they should be and you have been exposed to methyl parathion, then you may get symptoms of poisoning. However, lower cholinesterase levels may also only indicate exposure and not necessarily harmful effects. The action of methyl parathion may cause lower cholinesterase levels in your red blood cells or your blood plasma. Such lowering, however, can also be caused by factors other than methyl parathion. For example, cholinesterase values may already be low in some people, because of heredity or disease. However, a lowering of cholinesterase levels can often show whether methyl parathion or similar compounds have acted on your nerves. Cholinesterase levels in red blood cells can stay low for more than a month after you have been exposed to methyl parathion or similar chemicals. For more information, see Chapters 3 and 7. [Pg.28]

In short, CNTs own potential nanohazards because we still do not know the concrete metabolism course of CNTs within cells and human body, and possible effects on heredity, gene transcriptional, and post-translational regulations, at present, we still do not have enough proofs to confirm CNTs are no toxic, thereby the key is to find these methods to reduce potential risk of CNTs by series of studies. [Pg.192]

The gravity of effects that may be in store for susceptible persons is only revealed by exposure to certain drugs, dietary constituents, or other environmental toxins without this exposure, their genetic predisposition is invisible. Most people perceive heredity as having an important effect on health and disease, but may be unaware of the relevance of genetics to their own responses or of person-to-person differences in response to environmental toxins. The belief is widely held that unexpected responses to these substances are entirely linked to the toxin, but we know that the drug recipient is not a passive participant in these events. [Pg.19]

Nucleic acids are very important in toxicology for two reasons. The first of these is that heredity as directed by DNA determines susceptibility to the effects of certain kinds of toxicants. This phenomenon makes different species respond differently to the same toxicant for example, the LD50 for dioxin in hamsters is 10,000 times that in guinea pigs. In addition, differences in genotype cause substantial differences in the susceptibilities of individuals within a species to effects of toxicants. [Pg.187]

The number of possible subsets of active effects will be 2h if all possible subsets of active effects are considered. Hence a log base 2 transformation is used on the vertical axis of Figure 3. Strong and weak heredity reduce the number of subsets... [Pg.250]

Sequential bifurcation may give misleading results if, say, two factors have unimportant main effects but the interaction between them is important (see, also, Lewis and Dean, 2001). However, we only consider situations in which the following strong heredity assumption of Wu and Hamada (2000) holds. [Pg.300]


See other pages where Effect heredity is mentioned: [Pg.580]    [Pg.93]    [Pg.273]    [Pg.141]    [Pg.69]    [Pg.36]    [Pg.69]    [Pg.20]    [Pg.382]    [Pg.476]    [Pg.711]    [Pg.129]    [Pg.130]    [Pg.82]    [Pg.2]    [Pg.4]    [Pg.5]    [Pg.7]    [Pg.325]    [Pg.331]    [Pg.3]    [Pg.203]    [Pg.89]    [Pg.245]    [Pg.247]    [Pg.251]    [Pg.251]    [Pg.254]    [Pg.258]    [Pg.259]    [Pg.265]    [Pg.268]    [Pg.652]    [Pg.93]    [Pg.278]   
See also in sourсe #XX -- [ Pg.238 , Pg.244 ]




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