What we know about the world and its opportunities limits what we do. If we do not know that there is a pot of gold at the end of the rainbow, we will not follow it. If we do not know that a desert cactus contains water, we will not cut into it for sustenance. Often, however, we do know things about the world and yet the knowledge does not seem to be reflected in behavior. Explaining this fact simply in terms of inadequate motivation for expression or incomplete memory for the important in formation does not really add much to our understanding. The ex pression of knowledge can be interrupted in very special ways by a variety of more specific conditions-fatigue, sources of forgetting that may include failure of memory retrieval, emotion, and various dysfunc tions of brain and body systems-that are not satisfactorily incorporated by any current theories of motivation or memory. Also, a dissociation between knowledge and its expression can take the form of applying knowledge without apparent awareness of this action, a phenomenon that requires complicated assumptions for explanation in terms of either motivation or memory. Dissociations between knowledge and action may be striking. After driving home on a familiar route we may not be able to report whether the last three traffic lights were red or green; yet we must have re sponded appropriately to them.
The field of microfluidics has in the last decade permeated many disciplines, from physics to biology and chemistry, and from bioengineering to medical research. One of the most important applications of lab-on-a-chip devices in medicine and related disciplines is disease diagnostics, which involves steps from biological sample/analyte loading to storage, detection, and analysis. The chapters collected in this book detail recent advances in these processes using microfluidic devices and systems. The reviews of portable devices for diagnostic purposes are likely to evoke interest and raise new research questions in interdisciplinary fields (e.g., efficient MEMS/microfluidic engineering driven by biological and medical applications).The variety of the selected topics (general relevance of microfluidics in medical and bioengineering research, fabrication, advances in on-chip sample detection and analysis, and specific disease models) ensures that each of them can be viewed in the larger context of microfluidic-mediated diagnostics.
This book presents an introduction to the problems and strategies for modeling age, period, and cohort (APC) effects for aggregate-level data. These strategies include constrained estimation, the use of age and/or period and/or cohort characteristics, estimable functions, variance decomposition, and a new technique called the s-constraint approach. Emphasizing both the geometry and algebra of several APC approaches, the book develops readers' understanding of the statistical issues of APC analysis and shows how common methods are related to each other.
Ce document est orienté vers la personne ayant une déficience intellectuelle, sa condition de vie, ce qu'elle est, quels sont ses problèmes et comment rendre sa vie enrichissante et significative.
107 with treatments that affect the arousal of the animals is also implied on the basis of the behavioral changes induced in the lesioned animals by amphetamine administration and by changes in the motivational circumstances under which the animals are tested. Studies of the effects of cingulate lesions in the rat have involved the production of midline cortical damage. Unfortunately, as reported in the previous chapter, the midline cortex of the rat is not comparable to the midline cortex of other animals as defined on the basis of the fibers it receives from the thalamus. In addition, lesions of the midline cortex, whether in the rat or in other species, are likely to interfere with fibers of the neural systems in or near it. These include the cingulum bundle and the supracallosal fibers of the fornix. Norepi nephrine-containing fibers also pass through this region in or near the cingulum bundle. These fibers ascend through the anterior dor solateral septal area and turn up and back to pass through the midline regions and innervate the entire medial cortex (Morrison, Molliver, & Grzanna, 1979). Lesions in this area reduce the norepinephrine distribution throughout the rostrocaudal extent of the medial cortex. A similar problem results from destruction to the anterior cortical regions. Lesions in that region could reduce the norepinephrine sup plies of the entire dorsolateral cortex.
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