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Various pliers, a wrench, and screwdrivers.
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Abnormal histiocytes in marrow smears: Gaucher cells, foamy histiocytes in Niemann-Pick disease, generalized GM1 gangliosidosis and closely related diseases, Farber disease Colorless, friable hair: Menkes disease
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date infarctions, a syndrome of inattentiveness, abulia, forgetfulness, and sometimes agitation and psychosis was observed. Transitory choreoathetosis and other dyskinesias have also been attributed to ischemia of basal ganglia, occurring sometimes under conditions of prolonged standing and exercise (Caplan and Sergay; Margolin and Marsden).
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power applied to the motor to lift the actuator arm. This wood screw stops the eyelids from dropping below the eyes to create a more natural blinking illusion. If you have trouble tying the elastic to either part of the wire, just do your best, then use a bit of hot glue to secure it in place. Now, your motor should be able to lift the eyelids up and down at levels that look like realistic blinking from a distance in the dark. Avoid dropping the 9-volt battery directly across the motor at this point, or you may bend or loosen the copper arm from the torque. It s best to try the motor on less voltage or through a current limiting resistor of 10 or 20 ohms. The schematic for the eye blinker is shown in Figure 5-7, and it uses a simple 555 timer circuit to drive the motor for about half a second and then repeats the cycle about once a second. This timing cycle can be altered by changing the values of resistors R1 and R2 or by increasing the value of C1 for much longer blink cycles. Resistors R3 and R4 limit the current to both the LEDs and the motor, and should be chosen based on the components you plan to use. If you do not know the current capabilities of the LEDs you have, then start with a higher value for R3 such 1K, and work your way down to increase the
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For a sample period of T = 0.1 seconds, the equivalent discrete-time state space model given by eqn. (3.65) is xk+1 pk = = 0.8187 0.0000 0.0906 1.0000 0.0000 1.0000 xk + xk . 0.0906 0.0047 fk (3.83) (3.84)
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Trees on a piece of land increase the cost of building a home. This cost is usually offset by the desirability of a lot with trees, but you should still be aware that extra
of downward volatility will develop, thereby increasing the risk of premium loss on purchased options. The downturn in the last few days of trading before this option model was captured could be interpreted as a warning that you may be facing a reduction in implied volatility over time. If we remember back to our discussion of the Greeks, vega is the measure of sensitivity to volatility. The vega on this particular option is 2.90 so if volatility continues to fall, we could sustain a loss on the option of $2.90 per point of volatility change as well as the time value loss even if the underlying price remained unchanged. We need to be mindful of the potential for decreasing volatility in analyzing purchased option positions. This is not to say that options cannot be purchased in periods of high implied volatility because the increased volatility may be a result of a long-term or permanent fundamental shift in volatility for the particular asset. However, the increased risk of buying in high volatility means that your analysis must be accurate for the sustainability of the volatility during the term of the option. Volatility is relative to a particular point of view. If you look at the volatility chart again in Figure 4.4 and forget what you know beyond January 2008, you would be seeing a market in high volatility for the historical average. At this point, buying a call option would have been deemed to be high risk and may have not been recommended when in reality volatility nearly doubled, which would have increased the value of a purchased call option in relation to the underlying. In six months, the market may appear to be at low volatility when it is still signi cantly above the historical average. The loss of time value and the loss of implied volatility are the main features of risk when you are buying options outright, especially at the money options with high premium that are at or out
MOHR JP, MAST H: Binswanger s disease, in Barnett HJM et al (eds): Stroke: Pathophysiology, Diagnosis, and Management, 3rd ed. New York, Churchill Livingstone, 1998, pp 921 931. MOHR JP, THOMPSON JL, LAZAR RM, et al: A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. N Engl J Med 345:1444, 2001. MOKRI B, HOUSER W, SANDOK BA, PIEPGRAS DG: Spontaneous dissections of the vertebral arteries. Neurology 38:880, 1988. MOKRI B, SUNDT TM JR, HOUSER W, PIEPGRAS DG: Spontaneous dissection of the cervical internal carotid artery. Ann Neurol 19:126, 1986. MOORE PM: Diagnosis and management of isolated angiitis of the central nervous system. Neurology 39:167, 1989. MOORE PM (ed): Vasculitis. Semin Neurol 14:291, 1994. MOORE WS, BARNETT HJ, BEEBE HG, et al: Guidelines for carotid endarterectomy: A multidisciplinary consensus statement from the ad hoc committee, American Heart Association. Stroke 25:188, 1995. MRC ASYMPTOMATIC CAROTID SURGERY TRIAL (ACST) COLLABORATIVE GROUP: Prevention of disabling and fatal strokes by succesful carotid endarterctomy in patients without recent neurological symptoms: randomized controlled trial. Lancet 363:1491, 2004. MULGES W, BABIN-EBEL J, REENTS W, TOYKA KV: Cognitive performance after coronary bypass grafting: a follow-up study. Neurology 59: 741, 2002. MULTICENTER ACUTE STROKE TRIAL EUROPE STUDY GROUP: Thrombolytic therapy with streptokinase in acute stroke. N Engl J Med 335:145, 1996. MULTICENTRE ACUTE STROKE TRIAL ITALY (MAST-I) GROUP: Randomised controlled trial of streptokinase, aspirin, and combination of both in treatment of acute ischaemic stroke. Lancet 346:1509, 1995. MYERS RE, YAMAGUCHI S: Nervous system effects of cardiac arrest in monkeys. Arch Neurol 34:65, 1977. NAKAJIMA K: Clinicopathological study of pontine hemorrhage. Stroke 14: 485, 1983. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE RTPA STROKE STUDY GROUP: Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 333:1581, 1995. NELSON J, BARRON MM, RIGGS JE, et al: Cerebral vasculitis and ulcerative colitis. Neurology 36:719, 1986. NICHOLLS ES, JOHANSEN HL: Implications of changing trends in cerebrovascular and ischemic heart disease mortality. Stroke 14:153, 1983. NISHIMOTO A, TAKEUCHI S: Moyamoya disease, in Vinken PJ, Bruyn GW (eds): Handbook of Clinical Neurology: Vol 12. Vascular Diseases of the Nervous System. Part 2. Amsterdam, North-Holland, 1972, pp 352 383. NISHINO H, RUBINO FA, DEREMEE RA, et al: Neurological involvement in Wegener s granulomatosis: An analysis of 324 consecutive patients at the Mayo Clinic. Ann Neurol 33:4, 1993. NISHIOKA H, TORNER JC, GRAF CJ, et al: Cooperative study of intracranial aneurysms and subarachnoid hemorrhage: A long-term prognostic study: II. Ruptured intracranial aneurysms managed conservatively. Arch Neurol 41:1142, 1984. NORTH AMERICAN SYMPTOMATIC CAROTID ENDARTERECTOMY TRIAL COLLABORATORS: Bene cial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 325:445, 1991. NORVING B, CRONQVIST S: Lateral medullary infarction: Prognosis in an unselected series. Neurology 41:244, 1991. NUBIOLA AR, MASANA L, MASDEU S, et al: High-density lipoprotein cholesterol in cerebrovascular disease. Arch Neurol 38:468, 1981. OJEMANN RG, FISHER CM, RICH JC: Spontaneous dissecting aneurysms of the internal carotid artery. Stroke 3:434, 1972. OJEMANN RG, OGILVY CS, CROWELL RM, HEROS RC: Surgical Management of Neurovascular Disease, 3rd ed. Baltimore, Williams & Wilkins, 1995. OLSEN TS, LARSEN B, HERNING M, et al: Blood ow and vascular reactivity in collaterally perfused brain tissue. Stroke 14:332, 1983. ONDRA SL, TROUPP H, GEORGE ED, SCHWAB K: The natural history of
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