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sale on the CAT underlying stock at $32.15, and this time we will sell the at-the-money put option with the assumption that CAT remains range bound. If we sell the May $32.00 put option for a premium of 3.0, then we have a maximum pro t of $3.15 minus the costs of trading with a result of $315.00 per 100 shares. The risk on this position is unlimited, unlike the covered call in which the stock can only go to zero, the covered put is truly an unlimited risk. The breakeven can be calculated by: Strike price $32.00 $3.15 premium captured breakeven
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Fig. 43-19 Problem 4 courtesy of Gary J. Hordemann, Gonzaga University
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1. Pick the List button from the expanded Properties panel. 2. Pick any point on the shaft and press ENTER. The AutoCAD Text window displays the object type, layer, space, center point, radius, circumference, and area. 3. Close the window. 4. Select the shaft. 5. Right-click and pick Properties from the shortcut menu. AutoCAD displays most of the same information, but does not give the space. The bene t of this list is that you can make changes to the object, such as changing its circumference and area. 6. Pick the text eld to the right of Area. Notice the calculator button that appears on the right side of the Area line. This provides you with another way to open QuickCalc. 7. Pick the calculator button to open the QuickCalc palette, then close it. 8. In the Properties palette, change the area of the shaft to 3. AutoCAD redraws the shaft with an area of 3 units. 9. Close the Properties palette and undo Step 8.
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for discussion of control of cerebral hemodynamics and effects of medications in the neonatal period). Acetazolamide and furosemide, which reduce the formation of spinal uid, have been widely used in the treatment of posthemorrhagic hydrocephalus. However, in a large-scale controlled study, the effects were negligible and shunt placement was required to control worsening hydrocephalus (see International PHVD Drug Trial Group in the References). Periventricular Leukomalacia These are zones of necrosis of white matter in the deep watershed territories of cortical and central arteries. They lie lateral and posterolateral to the lateral ventricles, in a position to involve the occipital radiations and the sensorimotor bers in the corona radiata ( rst described by Banker and Larroche; see also Shuman and Selednik). The white matter lesions occur in about one-third of cases of subependymal hemorrhage (see above), but they may develop independently in both premature and fullterm infants who have suffered hypotension and apnea. In a study of 753 preterm infants, those born at 28 weeks gestation were at highest risk of this complication; the combination of intrauterine infection and premature rupture of membranes carried a 22 percent risk (Zupan et al). Survivors often manifest cerebral hemiplegia or diplegia and variable degrees of mental impairment. The motor disorder is usually more severe than the cognitive and language impairment. Increasingly, small lesions of this nature are being identi ed in term infants. The mechanism of this type of periventricular infarction has been debated and the terminology and clinical features, insofar as they overlap with germinal matrix hemorrhage, have been confusing. In recent years, most theories and experimental evidence converge on the notion that these represent venous infarctions. By ultrasonographic examination, the lesions appear as an echodensity in the periventricular white matter. They are also visible by MRI. Hypoxic-Ischemic Damage and Neonatal Encephalopathy Little s conception of the hypoxic-ischemic form of birth injury, enunciated in 1862, has been scrutinized over the years. While it is evident that many newborns suffer some degree of perinatal asphyxia, relatively few seem to manifest brain damage. Moreover, many infants with a variety of cerebral motor syndromes appear to have passed the parturitional (perinatal) period without mishap, indicating the greater importance of other prenatal and postnatal causative factors. Nonetheless, severe neonatal asphyxia of term or preterm babies can be an important cause of spastic-dystonicataxic syndromes, often accompanied by seizures and mental subnormality. One has the impression that the CNS tolerates hypoxia and reduced blood ow in the immediate postnatal period better than at any other time in life. Indeed, animal experimentation supports this view. Not until the arterial oxygen tension is reduced dramatically to 10 to 15 percent of normal does brain damage occur, and even then the impaired function of other organs contributes to the damage. Nearly always there are irregularities of the heart and hypotension from myocardial damage as well as hepatic and renal failure. Thus it is more correct to think of the encephalopathy in terms of both hypoxia and ischemia, which usually occur in utero and are expressed postnatally by recognizable clinical syndromes. Fenichel, following the original work of Sarnat and Sarnat in 1976 and of Levene and colleagues, nds it helpful to divide the cerebral syndromes that follow a dif cult birth into three groups, according to their severity, each having a greater prognostic value than the Apgar score: (1) In newborns with mild hypoxic-ischemic
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