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tion that impairs ATP synthase can closely mimic the MarinescoSjogren syndrome. Doubtless, many of the progressive forms of cerebellar ataxia now classi ed as degenerative and described in Chap. 39 will be proved to have an underlying biochemical or similar subcellular pathogenesis and will logically fall in place here, with the metabolic diseases. At present, when faced with a progressive ataxia of cerebellar type even in a young adult, the reader should consult both this chapter and Chap. 39. The acute forms of cerebellar ataxia that occur in late childhood and adolescence are essentially nonmetabolic, being traceable to postinfectious encephalomyelitis (page 641) or to postanoxic, postmeningitic, or posthyperthermic states and certain drug intoxications. With relatively pure cerebellar ataxias of this age period, postinfectious cerebellitis, cerebellar tumors (medulloblastomas, astrocytomas, hemangioblastomas, and ganglioneuromas of Lhermitte-Duclos) should be considered in the differential diagnosis. MRI establishes the correct diagnosis. Bassen-Kornzweig Acanthocytosis (Abetalipoproteinemia) This disease, rst described by Bassen and Kornzweig in 1950, excited great interest, for it gave promise of a breakthrough into a hitherto obscure group of degenerative disorders. In the 15-year period that followed the original report, less than a dozen cases were recorded, and several of the reports were based on the study of the same case. In our experience, it is a rare disease; we have seen only four cases. The resemblance to Friedreich ataxia is not so close that an experienced clinician would be likely to confuse the two. The inheritance of this disease is autosomal recessive. The initial symptoms, occurring between 6 and 12 years (range, 2 to 20 years), are weakness of the limbs with are exia and an ataxia of sensory (tabetic) type, to which a cerebellar component is added later (see also page 1158). Steatorrhea, raising the suspicion of celiac disease (sprue), often precedes the weak, unsteady gait. Later, in more than half the patients, vision may fail because of retinal degeneration (similar to retinitis pigmentosa). Kyphoscoliosis, pes cavus, and Babinski signs are other elements in the clinical picture. The neurologic disorder is relatively slowly progressive by the second to third decade, the patient is usually bedridden. The diagnostic laboratory ndings are spiky or thorny red blood cells (acanthocytes), low sedimentation rate, and a marked reduction in the serum of low-density lipoproteins (cholesterol, phospholipid, and -lipoprotein levels are all subnormal). Pathologic study has revealed the presence of foamy, vacuolated epithelial cells in the intestinal mucosa (causing absorption block); diminished numbers of myelinated nerve bers in sural nerve biopsies, depletion of Purkinje and granule cells in all parts of the cerebellum; loss of bers in the posterior columns and spinocerebellar tracts; loss of anterior horn and retinal ganglion cells and of muscle bers and brosis of the myocardium. It has been proposed that the basic defect is an inability of the body to synthesize the proteins of cell membranes because of the impaired absorption of fat through the mucosa of the small intestine. Vitamin E de ciency may be a pathogenic factor, since the administration of a low-fat diet and high doses of vitamins A and E may prevent progression of the neurologic disorder, according to Illingworth and colleagues. Often mentioned in the context of acanthocytosis is another rare condition, the McLeod syndrome, in which are combined heterogeneous combinations of progressive muscular atrophy, seizures, involuntary movements, and elevated serum CK. The acan-
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First, we must get the equation into polynomial standard form. We can do that by adding x to both sides and then switching the right and left sides, getting 3x 2 + x + 4 = 0 In the general polynomial standard equation ax 2 + bx + c = 0 we have a = 3, b = 1, and c = 4. Plugging these into the quadratic formula, we get x = [ b (b2 4ac)1/2] / (2a) = [ 1 (12 4 3 4)1/2] / (2 3) = [ 1 (1 48)1/2] / 6 = [ 1 ( 47)1/2] / 6 The quantity ( 47)1/2 is the imaginary number j(471/2). Therefore x = [ 1 j(471/2)] / 6 If we want to express these roots individually, we can write x = [ 1 + j(471/2)] / 6 or x = [ 1 j(471/2)] / 6 We can reduce these to standard complex-number form using the right-hand distributive law for division over addition or subtraction, getting x = 1/6 + j(471/2/6) or x = 1/6 j(471/2/6)
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Draw hidden lines to show the holes in the front view. (Hidden lines are the short dashed lines in the multiview drawing that are used to indicate features that are hidden from view.) For now, create them using two short line segments. 5. Save your work. 6. Create the right-side view by projecting lines from the top and front views. Consider the following suggestions: Create temporary lines as shown in Fig. 12-4. The vertical line is at an arbitrary distance from the top view. Draw the angled line at a 45 angle. (Use the Angle option of the XLINE command.) Use it to project the dimensions from the top view to the right-side view. Project lines from the top view to the 45 line. Then project vertical lines down from the intersections of the horizontally projected lines and the 45 lines to locate the right-side view. Use the height dimensions from the front view to nish the rightside view. In practice, the views in a multiview drawing are laid out carefully to ensure that the distance between the front and top views is approximately equal to the space between the front and side views. Keep this in mind as you create the construction lines in Step 6. 7. Erase all temporary construction lines. Your multiview drawing should now look similar to the multiview drawing shown in Fig. 12-2 on page 153, except that your drawing will not include construction lines. You will learn more about multiview drawings in 26. 8. Close any open toolbars, save your work, and exit AutoCAD.
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wherethe two vectors,x &od-r,. hold the independent dependent and variables, respectively. Here is a simple MATLAB sessionthat uses this function to integratethe data from T a b l e1 7 . 3 : >> x = t0 .I2 .22 .32 .3,h .4 .44 .54 .64 .7 .81; > > y = 0 . 2 + 2 5 * x - 2 0 0 " x . " ' 2 + 6 1 * x . ^ 3 - 9 0 0 * x . ^ 4 + 4 0 0 * x .^ 5 ; 5
Our testbed deployment currently includes two Exchange servers located in Vancouver, but we have a branch office in Seattle and want to install a third server there. Before installing our third server, we should create a second administrative group, called Seattle, to which this new server will belong (we want to follow a distributed administration model for our Exchange organization). To create the Seattle administrative group, right-click on the Administrative Groups container shown in Figure 12.2 and select New Administrative Group. Specify Seattle as the name of the new group and click OK. At this point, our new administrative group is simply an empty container with no configurable properties other than its name (Figure 12.3).
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But the optimum scenario is to be 100 percent in stocks in bull markets to capture the highest returns for your portfolio. And to be 100 percent in cash or cash equivalents (or to be short the market) during bear markets. By watering down your portfolio with bonds, you are denying yourself the incremental profits from stocks. If bear markets are inevitable, then prepare for them, and sell your stocks and mutual funds before the bear takes hold. Consider using market timing to help you achieve that goal. That is what the heart of this book is all about providing simple strategies to keep you on the right side of the market. I want to emphasize here that this book and market timing are not about stock selection. The key to market timing is knowing when to enter the market and when to exit. All stocks are bad unless they go up in prices. The best stocks lose money in bear markets. At least 80 percent of stocks decline in a bear market. The art of the game is to be in the market at the right times, and to be out of the market at the right times. Picking the right stock is only secondary to this overriding principle, because a rising tide will lift all stocks and a falling tide will lower all stocks regardless of the stock you may happen to own at the time. What leads to people s downfall in following a timing approach is, like most other things with the stock market, execution. When it is time to exit you may rationalize to yourself that this time will be different. This year the decline in the market will not happen because of certain factors, etc. Therefore, I will stay put despite the historical record and the readings of the indicators. Or, you may say that even if the market should fall, the story behind the stock is so compelling that it cannot possibly decline. This is a gambler s approach, not an investor s approach. The odds are heavily against you and you are bucking the odds. Far better to forego the profits you anticipate from that stock than for it to disappoint you and fall under the weight of the bear market. Preservation of capital is the ultimate consideration, and well worth the cost of foregone profits. Look at Table 2-1, which provides a comparison of specific percentage allocations of stocks and bonds with their resultant risk and returns. Being 100 percent invested over the 76-year period from 1926 through 2002, each rolling 12-month period produced an average return of 13 percent with a risk of 22 percent (risk is the variability in return over the 76-year 12-month rolling periods. In this example with a return of 13 percent, the risk of 22 percent
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