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Moreover, even convinced geneticists make reference to the notion of phenocopies, a concept signifying that characteristics usually traceable to genetic action can be simulated by environmental factors; thus, overtly identical forms of pathology may arise from either genetic or environmental sources As a consequence, the clinical picture of a disorder may give no clue to its origins since similar appearances do not necessarily signify similar etiologies To complicate matters further, different genes vary in their responsiveness to environmental influences; some produce uniform effects under all environmental conditions, whereas others can be entirely suppressed in certain environments (Plomin, DeFries, & McClearn, 1990) Moreover, it appears that genes have their effects at particular times of maturation and their interaction with environmental conditions is minimal both before and after these periods.

7.6 FINITE PATCH ARRAY It is instructive to examine the impedance match of patch elements in a real finite array. We compute the active reflection coefficients of the individual patch elements using the procedure developed in Section 4.7. To compute the active reflection coefficients we first obtain the scattering parameters of the finite array 4 (see Section 4.3). We assume that the scattering parameters of a real finite array are

I 2 = I 2(1) + I 2( 2)

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Despite these ambiguities and complications, there can be little question that genetic factors do play some dispositional role in shaping the morphological and biochemical substrate of certain traits However, these factors are by no means necessary to the development of personality pathology, nor are they likely to be sufficient in themselves to elicit pathological behaviors They may serve, however, as a physiological base that makes the person susceptible to dysfunction under stress or inclined to learn behaviors that prove socially troublesome..

(9.3.7)

While our knowledge of how to assess and treat ADHD symptoms improves with advances in the research literature, practitioners have at their disposal a collection of well-established interventions, such as behavioral parent training programs, behavioral classroom management, classroom modi cations, and stimulant medications. Future research may focus on re ning these identi ed intervention approaches in order to maximize their effectiveness and improve implementation. Additional research also is needed on the effectiveness of interventions designed to improve academic outcomes (as opposed to behavioral and social outcomes) among children and adolescents with ADHD.

In a provocative article, Professor Sonia Suter raised the issue of whether genetic discrimination is largely a concern of the middle and upper classes.

Behavioral functioning. See Emotional/ Behavioral functioning Benzodiazepine syndrome, 365 366 Biofeedback, 131, 136, 247, 250 Birth to 3 Program, 384 Blood disorders, 274 Brain injuries. See Traumatic brain injury (TBI) Brain tumors. See Tumors Broca s aphasia, 64

NAV period for neighboring STAs. NAV protects the current transmission, thus solving the hidden terminal problem.

Figure 230: A simple business process view with organizational units Another technique used in Figure 230 is stereotyping Stereotypes enable you to create new building blocks in UML based on existing blocks but specific to the problem at hand All model elements in UML (classes, objects, states, etc) can have stereotypes For example, if it is important to denote that an object is an information object holding only information, we can stereotype the object as information object ; if it is a physical item, then we can stereotype it as physical item There are no predefined building blocks for information objects and physical objects in UML, but by defining stereotypes for them based on the standard class concept we can adapt and extend UML to support these concepts In Figure 230, the information and physical stereotypes are used.

It is believed that, in some cases, autism is due to a disruption (e.g., prenatal viral infection, mid-trimester bleeding) of normal brain development. For example, during the 1964 rubella outbreak, 8% to 13% of children born developed autism along with other problems associated with congenital rubella syndrome (Hertz-Picciotto et al., 2006; Muhle et al., 2004). Additional nongenetic causes may include exposure to teratogens (e.g., fetal alcohol syndrome, fetal valproate syndrome; see 14). Some questions have been raised in relation to thimerosal in vaccines as well as exposure to pollutants and heavy metals (see 13); the relation between vaccination and autism has not been supported by research (K. Madsen et al., 2002). In general, children with nongenetic forms of ASDs tend to have experienced complications prenatally or perinatally and show a high rate of soft neurological signs (Lannetti, Mastrangelo, & Di Netta, 2005). Further, in many instances, ASD co-occurs with mental retardation, epilepsy (Ciaranello & Ciaranello, 1995), chromosomal abnormalities, neurocutaneous disorders, or metabolic disorders (A. Bailey, Phillips, & Rutter, 1996; M. Barton & Volkmar, 1998). In these cases, the same factor that results in the co-occurring disorder may be the cause of the ASD.

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