MARKET-TIMING RESOURCES in Software

Draw EAN-13 Supplement 5 in Software MARKET-TIMING RESOURCES

2. Pick a couple of objects and press ENTER to copy the objects to the Windows Clipboard. 3. Save your work. 4. Create a new drawing from scratch using Imperial units. 5. On the Clipboard panel, pick the Paste button to enter the PASTECLIP command. 6. Move the crosshairs and notice that the objects are attached to it. 7. Pick an insertion point. 8. Exit AutoCAD without saving the current drawing.

than SIMMs. The technique for installing a DIMM (as shown in Exercise 1-6) is slightly different than for a SIMM.

When the user clicks this button, the browser calls a JavaScript function named getDocumentElement:

Depending on which category you need, you can keep the Properties window focused by toggling between the + and signs next to each category name, so that only the ones you will be using are expanded (have the sign displayed). The Appearance and Behavior

Making sure an item exists before you try to use it. Referring to an application by its formal name rather than its common name. Breaking up a script into subroutines.

and plantar re exes may give little indication of what is happening. Tendon re exes are usually preserved until the late stages of coma due to metabolic disturbances and intoxications. In coma due to a large cerebral infarct or hemorrhage, the tendon re exes may be normal or only slightly reduced on the hemiplegic side and the plantar re exes may be absent or extensor. Plantar exor responses, succeeding extensor responses, signify ether a return to normalcy or, in the context of deepening coma, a transition to brain death. Patterns of Breathing (See pages 437 474) Any massive supratentorial lesions, bilateral deep-seated cerebral lesions, or metabolic disturbances of the brain give rise to a characteristic pattern of breathing, in which a period of waxing and waning hyperpnea regularly alternates with a shorter period of apnea (Cheyne-Stokes respiration, or CSR). This phenomenon has been attributed to isolation of the brainstem respiratory centers from the cerebrum, rendering them more sensitive than usual to carbon dioxide (hyperventilation drive). It is postulated that as a result of overbreathing, the blood carbon dioxide drops below the concentration required to stimulate the centers, and breathing gradually stops. Carbon dioxide then reaccumulates until it exceeds the respiratory threshold, and the cycle then repeats itself. Alternatively, CSR has been attributed to the stimulating effect of a low arterial PO2 on a depressed respiratory center. In either case, the presence of CSR signi es bilateral dysfunction of cerebral structures, usually deep in the hemispheres or diencephalon, and it is seen with states of drowsiness or stupor from a variety of causes. Coma with CSR is usually due to intoxication or to a severe metabolic derangement and occasionally to bilateral lesions, such as subdural hematomas. In itself, CSR is not a grave sign. It may occur during sleep in elderly individuals and can be a manifestation of cardiopulmonary disorders in awake patients. Only when it gives way to more irregular respiratory patterns that implicate structural damage of the brainstem is the patient in imminent danger, as discussed below. A number of other aberrant breathing rhythms occur with brainstem lesions (these are reviewed in Chap. 26), but few are speci cally localizing. The more conspicuous respiratory arrhythmias are associated with brainstem lesions below the level of the reticular activating system and are therefore found in the late stages of brainstem compression or with large brainstem lesions such as infarction, primary hemorrhage, or in ltrating tumor. Lesions of the lower midbrain upper pontine tegmentum, either primary or secondary to a tentorial herniation, may give rise to central neurogenic hyperventilation (CNH). This disorder is characterized by an increase in the rate and depth of respiration to the extent that respiratory alkalosis results. CNH is thought to represent a release of the re ex mechanisms for respiratory control in the lower brainstem. It must be distinguished from hyperventilation caused by medical illnesses, particularly pneumonia and acidosis. Mild degrees of hyperventilation are common after a number of acute neurologic events, notably head injury. The neurologic basis of CNH is uncertain. It has been observed with tumors of the medulla, lower pons, and midbrain. However, North and Jennett, in a study of respiratory abnormalities in neurosurgical patients, found no consistent correlation between tachypnea and the site of the lesion. It is also noteworthy that primary brain lymphoma without brainstem involvement has emerged as a curious cause of CNH (Pauzner et al). Low pontine lesions, usually due to basilar artery occlusion, sometimes cause apneustic breathing (a pause of 2 to 3 s in full inspiration) or so-called short-cycle CSR, in which a few rapid deep breaths alternate with apneic cycles. With lesions of the dorsome-

1. Enter 22 for the width and 17 for the length. Be sure to include the apostrophe for the foot mark. 2. Pick the Finish button. You have completed AutoCAD s Advanced Setup process. 3. Save your work in a le named tmp1.dwg.