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WOOTEN GF: Agonists vs levodopa in PD. Neurology 60:360, 2003. WORSTER-DROUGHT C, GREENFIELD JG, MCMENEMEY WH: A form of familial progressive dementia with spastic paralysis. Brain 67:38, 1944. YOUNG AB, SHOULSON I, PENNEY JB, et al: Huntington s disease in Venezuela: Neurologic features and functional decline. Neurology 36: 244, 1986. YOUNG RR: The differential diagnosis of Parkinson s disease. Int J Neurol 12:210, 1977. read barcode-scanner
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Now suppose the two of them play this game repeatedly. If Row always makes the same move, Column will quickly catch on and will always play the countermove, winning every time. Therefore Row should mix things up: we can model this by allowing Row to have a mixed strategy, in which on each turn she plays r with probability x 1 , p with probability x2 , and s with probability x3 . This strategy is speci ed by the vector x = (x 1 , x2 , x3 ), positive numbers that add up to 1. Similarly, Column s mixed strategy is some y = (y 1 , y2 , y3 ).2 On any given round of the game, there is an x i yj chance that Row and Column will play the ith and jth moves, respectively. Therefore the expected (average) payoff is Gij Prob[Row plays i, Column plays j] = Gij xi yj .
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When things go right, developing raw land into a small number of house lots is not too complicated. Let me give you an example of how simple it can be. I bought 18 acres of rural land. If I wanted to cut this acreage into two building lots, say, one 8-acre parcel and one 10-acre piece, I could do it for less than $1,000. The land would have to be perk-tested to be sold as building lots, but this would not be very expensive. In my case, a formal survey would not be needed at the time of development. Using town tax maps, I could draw my own plot plan. Legal expenses would have to be considered. The land has road frontage and available electrical service, so there s no cost in these categories. Filing fees with the town would be minimal If I chose to divide my 18 acres into more than two lots, the game would change. Creating more that two lots falls under different rules and regulations. My engineering costs would escalate, as would most of my other expenses. The amount of time needed to gain approval for a larger subdivision of the land could exceed one year. In theory, I
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In 1950, Adams and Victor observed a rapidly evolving quadriplegia and pseudobulbar palsy in a young alcoholic man who had entered the hospital 10 days earlier with symptoms of alcohol withdrawal. Postmortem examination several weeks later disclosed a large, symmetrical, essentially demyelinative lesion occupying the greater part of the base of the pons. Over the next 5 years, three additional cases (two alcoholic patients and one with scleroderma) were studied clinically and pathologically, and in 1959 these four cases were reported by Adams et al under the heading of central pontine myelinolysis (CPM). This term was chosen because it denotes both the main anatomic localization of the disease and its essential pathologic attribute: the remarkably unsystematic dissolution of the sheaths of myelinated bers and the sparing of neurons. Once attention was focused on this distinctive lesion, many other reports appeared. The exact incidence of this disease is not known, but in a series of 3548 consecutive autopsies in adults, the typical lesion was found in 9 cases, or 0.25 percent (Victor and Laureno). Pathologic Features One is compelled to de ne this disease in terms of its pathologic anatomy, because this stands as its most certain feature. Transverse sectioning of the xed brainstem discloses a grayish discoloration and ne granularity in the center of the basis pontis. The lesion may be only a few millimeters in diameter, or it may occupy almost the entire basis pontis. There is always a rim of intact myelin between the lesion and the surface of the pons. Posteriorly it may reach and involve the medial lemnisci and, in the most advanced cases, other tegmental structures as well. Very rarely, the lesion encroaches on the midbrain, but inferiorly it does not extend as far as the medulla. Exceptionally the extensive pontine lesions may be associated with identical myelinolytic foci symmetrically distributed in the thalamus, subthalamic nucleus, striatum, internal capsule, corpus callosum, amygdaloid nuclei, lateral geniculate body, white matter of the cerebellar folia, and deep layers of the cerebral cortex and subjacent white matter ( extrapontine myelinolysis ; Wright et al). Microscopically, the fundamental abnormality consists of destruction of the myelinated sheaths throughout the lesion, with relative sparing of the axons and intactness of the nerve cells of the pontine nuclei. These changes always begin and are most severe in the geometric center of the pons, where they may proceed to frank necrosis of tissue. Reactive phagocytes and glial cells are in evidence throughout the demyelinative focus, but oligodendrocytes are depleted. Signs of in ammation are conspicuously absent. This constellation of pathologic ndings provides easy differentiation of the lesion from infarction and the in ammatory demyelinations of multiple sclerosis and postinfectious encephalomyelitis. Microscopically, the lesion resembles that of Marchiafava-Bignami disease (Chap. 41), with which it is rarely associated. In the chronic alcoholic, Wernicke disease is not infrequently associated with CPM, but the lesions bear no resemblance to one another in terms of topography and histology. Clinical Features Central pontine myelinosis occurs only sporadically, with no hint of a genetic factor. The two sexes are affected equally, and the patients do not fall into any one age period. Whereas the cases rst reported had occurred in adults, there are now many reports of the disease in children, particularly in those with severe burns (McKee et al).
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This is only a small sampling of the tasks you can perform using objects in the Servers container. We ll look at many of these tasks later in this book.
Create the top, front, right-side, and isometric views of the picnic table. Do research to nd appropriate sizes and dimensions.
Answer the following questions on a separate sheet of paper. 1. What is the purpose of each of the ve items located in the upper right area of the Select File dialog box 2. How do you copy a le in the Select File dialog box 3. In the Select File dialog box, what information can you display by picking Details from the Views drop-down menu 4. How do you create a folder from within AutoCAD 5. What is the primary purpose of the AUDIT command
CHAPTER 4 Negative Numbers
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Another interesting property of the Arabic system is the fact that there is no limit to how large a numeral you can represent. Even if a string of digits is hundreds of miles long, even if it circles the earth, even if it goes from the earth to the moon all you have to do is put a nonzero digit on the left or any digit on the right, and you get the representation for a larger whole number. Mathematicians use the term finite to describe anything that ends somewhere. No matter how large a whole number you want to express, the Arabic system lets you do it in a finite number of digits, and every single one of those digits is from the basic set of 0 through 9. You don t have to keep inventing new symbols when numbers get arbitrarily large, as people did when the Roman system ruled. Every imaginable number can be represented as an Arabic numeral that contains a finite number of digits. But there is no limit to the number of whole numbers you can denote that way. The group, or set, of all whole numbers is said to be infinite (not finite). That means there is no largest whole number.
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