Construction and Cost Estimation in Software

Draw Denso QR Bar Code in Software Construction and Cost Estimation

The McGraw Hill Companies, 2010
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secondary feature. The most useful categorization re ects the appearance and location of the malformation by angiography and by surgical examination. These malformations may be divided into three groups: (1) arteriovenous malformations that are strictly intramedullary or also involve the meninges and surrounding structures such as the vertebral bodies to a limited extent; (2) a variety of intradural perimedullary stulas that lie on the subpial surface of the cord (these probably conform most closely to the lesion described by Foix and Alajouanine discussed in the earlier section on necrotic myelopathy); and (3) purely dural stulas. There is not suf cient pathologic material to determine whether these represent distinct pathologic entities or simply differing degrees and con gurations of a common developmental process. Once recognized, treatment may be an urgent matter in cases with rapid clinical deterioration and impending paralysis. Dural Fistula The last of the above listed malformations, spinal dural stula, while not the classic AVM, is addressed rst since it has emerged as the most common type in our practices. Increasingly, it has been recognized that arteriovenous stulas that lie within the dura overlying the spinal cord, are capable of causing a myelopathy, sometimes several segments distant from the vascular nidus. The majority are situated in the region of the low thoracic cord or the conus, with a limited venous draining system. Some appear to be situated in a dural root sleeve and to drain into the normal perimedullary coronal venous plexus. The presenting clinical features in our patients have included slowly progressive bilateral but asymmetric leg weakness with variable sensory loss. According to Jellema and colleagues who studied 80 patients with spinal dural stulas, the most common initial symptoms were gait imbalance, numbness, and paresthesias. As the process progressed, the majority developed urinary problems, leg weakness, and numbness in the legs and buttocks. The degree of leg weakness varied greatly and back pain was infrequent. The myelopathy that results is subacute or saltatory in evolution, presumably from venous congestion within the cord. A claudicatory syndrome has also been reported. Characteristically, activities that increase venous pressure (Valsalva maneuver, exercise) transiently amplify the symptoms or produce irreversible, stepwise worsening. One remarkable such case involved a baritone opera singer whose legs gave way repeatedly while singing (Khurana et al). As mentioned, some cases are painless, although most of our patients have had a moderate spinal ache or sciatica. In contrast to the classic arteriovenous lesions, these bleed only rarely. The spinal uid is normal or shows a slight elevation of protein. Intramedullary AVM The true AVM, previously referred to as angioma racemosum venosum or dorsal extramedullary arteriovenous malformation, is typically located on the dorsal surface of the lower half of the spinal cord and occurs most often in middleaged and elderly men (23 of 25 of Logue s patients were male). However, this lesion may occur at any age and at any location in the cord. In a few cases has there been an overlying dermatomal nevus. The clinical picture has been well described by WyburnMason. Acute cramp-like, lancinating pain, sometimes in a sciatic distribution, is often a prominent early feature. It may occur in a series of episodes over a period of several days or weeks; sometimes it is worse in recumbency. Almost always it is associated with weakness or paralysis of one or both legs and numbness and paresthesias in the same distribution. Wasting and weakness of the legs may introduce the disease in some instances, with uneven progression, sometimes in a series of abrupt episodes. Severe disability
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3. Note the default settings of Daily (Periods) and Fill the Chart (Range), and Candlesticks (Type), which you can change anytime. 4. In the Overlays section, click on the word None. 5. A drop-down menu appears. Guess what This is where other market indicators are hiding. (If you re not using, the indicators are also hidden in a dropdown menu.) 6. Select the exponential moving average (EMA). The default parameter, 20-day moving average, appears. Click on the word Update. Important: Whenever you make changes in, you must click on Update. 7. Scroll back to the middle of the chart. Notice that you have added a third line to the chart, a 20-day EMA. It s the green line. 8. Congratulations! Now that you know how to change the chart settings, you can change the defaults on any other chart.
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The RAC database also uses feedback on the amount of memory used for a single server node in a server pool. If there is too much work for the memory on the node, that node will temporarily stop accepting new connections until the demand for memory is decreased.
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ysis of the cervical sympathetic nerves with a Horner syndrome. Invasion of the lower plexus by tumors is usually painful; postradiation lesions are more likely to cause paresthesias without pain (Lederman and Wilbourn). Infraclavicular Lesions Involving Cords of the Brachial Plexus (See Fig. 46-5) A lesion of the lateral cord causes weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve; it manifests mainly as a weakness of exion and pronation of the forearm. The intrinsic muscles of the hand innervated by the medial root of the median nerve are spared. A lesion of the medial cord of the plexus causes weakness of muscles supplied by the medial root of the median nerve and the ulnar nerve. The effect is that of a combined median and ulnar nerve palsy. A lesion of the posterior cord results in weakness of the deltoid muscle, extensors of the elbow, wrist, and ngers, and sensory loss on the outer surface of the upper arm. One group of infraclavicular injuries, often iatrogenic, results from damage to the subclavian or axillary vessels and the formation of pseudoaneurysms or hematomas. Small puncture wounds as might occur with catheterization of the subclavian vein, anesthetic block of the brachial plexus, or transaxillary arteriography are likely to produce this type of injury. Compression of the plexus usually evolves subacutely, up to 3 weeks, although once started, the deterioration may be rapid. Prompt recognition of the condition and early decompression are essential. Other frequent causes of injury to the cords are dislocation of the head of the humerus, direct axillary trauma (stab wounds), pressure of a cervical rib or band, and supraclavicular compression during anesthesia. All cords of the plexus may be injured, or they may be affected in various combinations. Costoclavicular (Thoracic Outlet) Syndrome This is discussed in Chap. 11 (page 186). Brachial Neuritis, Brachial Plexitis (Neuralgic Amyotrophy, Parsonage-Turner Syndrome) This illness, of obscure nature, may develop abruptly in an otherwise healthy individual; it may also complicate an infection, an injection of vaccine or antibiotic, childbirth, surgical procedures of any type, or the use of heroin. Magee and DeJong in 1960 and Tsairis and coworkers in 1972 reported large series of cases and ampli ed a well-known clinical picture that the clinicians had observed repeatedly and called acute brachial neuritis. The term neuralgic amyotrophy was applied to this symptom complex by Parsonage and Turner, who wrote extensively on the subject. Their term for the condition is not entirely inappropriate, since the clinical and EMG ndings suggest a lesion of the peripheral nerves of the shoulder girdle and upper arm rather than the cords of the plexus. Actually, the exact site of the pathologic changes has not been established. Our patients have nearly all been adults ranging from 20 to 65 years of age. Males may be slightly more susceptible. Beginning as an ache or deep burning in and around the shoulder, centered over the deltoid, at the root of the neck or base of the skull, and suspected at rst of being only a wry neck, or neck muscle strain, the pain rapidly becomes more severe. The onset can be remarkably abrupt and occasionally awakens the patient from sleep. It is made worse by movements that involve the muscles in the region, and the patient searches for a comfortable position. Often, narcotics are required to suppress the pain. After a period of 1 to 10 days there is a rapid development of muscular weakness and,
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Part II:
III. Drawing and Editing
Figure 16-15
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Operating System Fundamentals
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