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Salaried claims adjusters can earn in the mid $20,000 range a year to start. Salaries rise to near $60,000 after twenty-five to thirty years, and recent statistics show that the median annual earnings income is $41,080. Mike says that the field is still open to anyone with a college degree who can pass a proficiency exam after several weeks of training. About one-third of the states require independent, or public, adjusters to be licensed, but the requirements vary by state. Claims adjusters working for companies can usually work under the company license and do not need to become licensed. Basic computer skills are a job necessity, and many adjusters are now equipped with laptop computers so they can have instant access to the necessary forms and files they need. Past automotive experience is not needed, and only about 20 percent of adjusters come from the auto repair industry. Local or regional travel is usually required, and since most information can be retrieved from a laptop, many adjusters work from their homes. For additional information, go to the Independent Automotive Damage Appraiser Association website at www.iada.org.
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spinal damage become detectable. The severity of paralysis and its permanence vary with the dosage of TOCP. Whether a polyneuropathy can arise without the preceding symptoms of cholinergic toxicity is debated; however, based on a review of the subject and a study of 11 patients exposed to these agents, 3 of whom later acquired sensory neuropathy, Moretto and Lotti express the view that such an occurrence must be rare. In addition to the acute and delayed neurotoxic effects of organophosphorus, an intermediate syndrome has been described (Senanayake and Karalliedde). Symptoms come on 24 to 96 h after the acute cholinergic phase and consist of weakness or paralysis of proximal limb muscles, neck exors, motor cranial nerves, and respiratory muscles. Respiratory paralysis may prove fatal. In patients who survive, the paralytic symptoms last for 2 to 3 weeks and then subside. The intermediate and delayed symptoms do not respond to atropine or other drugs. Several striking outbreaks of TOCP poisoning have been reported. During the latter part of the prohibition era and to a lesser extent thereafter, outbreaks of so-called jake paralysis were traced to drinking an extract of Jamaica ginger that had been contaminated with TOCP. Adams had examined several ginger jake patients many years later and related to us that he found only signs of corticospinal disease. Presumably in the early stage of this disease they were obscured by the neuropathy. Another outbreak occurred in Morocco, in 1959, when lubricating oil containing TOCP was used deliberately to dilute olive oil. Several other outbreaks have been caused by the ingestion of grain and cooking oil that had been stored in inadequately cleaned containers previously used for storing TOCP. The effect of TOCP on the peripheral nervous system has been studied extensively in experimental animals. In cats, there occurs a dying back from the terminal ends of the largest and longest medullated motor nerve bers, including those from the annulospiral endings of the muscle spindles (Cavanagh and Patangia). The long ber tracts of the spinal cord show a similar dying-back phenomenon. Abnormal membrane-bound vesicles and tubules were observed by Prineas to accumulate in axoplasm before degeneration. These effects have been traced to the inhibitory action of TOCP on esterases. There is still uncertainty as to the details of these reactions, and no treatment for the prevention or control of the neurotoxic effects has been devised.
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Relativistic speeds that is, speeds high enough to cause significant time dilation cause objects to appear foreshortened in the direction of their motion. As with time dilation, relativistic spatial distortion occurs only from the point of view of an observer watching an object speed by at a sizable fraction of the speed of light.
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where f lies somewhere the interval from in a to b. Thus, Simpson's1/3 ruleismore accuratethan the trapezoidal rule' However,comparisonwith Eq. (17.] that )indicates it is nore accuratethan expected'Rather than being proportionalto the third denvative, the etror is proportional to the fourth derivative. consequently,Simpson,sl/3 rule is thirdorder accurate even though it is basedon only threepoints. In other words,it yields exact resultsfor cubic porynomialseven thoughit is derivedfrom a parabora! EXAMPLE 7.3 1 S i n g l eA p p l i c o r i o no f S i m p s o n , s / 3 R u l e l ProblemSiotement. Use Eq. (17.23) ro inregrate f ( . x ' ) : 0 . 2 * 2 5 " u - 2 0 0 1 2* 6 i 5 x 3 _ 9 0 0 x a *400rs frorn.l 0 b : 0'8' Employ Es. o7.24) to esrimare rhe enor. Recall that theexacr !9 inregratis 1.640-533. S o l u t i o n .n : 2 l h : J'(0) : 0.2 0.4); f ( 0 . 4 ): 2 . 4 5 6 /(0.8) : 0.232
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Binswanger disease has been mentioned brie y in the discussion of the course and prognosis of atherothrombotic infarction and as a cause of dementia in Chaps. 21 and 39. The term has come to denote a widespread degeneration of cerebral white matter having a vascular causation and observed in the context of hypertension, atherosclerosis of the small blood vessels, and multiple strokes (see page 909). Hemiparesis, dysarthria, TIAs, and typical lacunar or cortical strokes are admixed in many cases. The process has been associated with a particular radiologic appearance that re ects the con uence of areas of white matter changes. The term leukoareosis, meant to describe the less intense appearance of periventricular tissues in imaging studies, complicates the matter, since this condition is also assumed to have a vascular basis, and the term has been used indiscriminately, particularly by some radiologists, as equivalent to Binswanger disease. Whether multiple discrete lacunes in the deep white matter constitutes Binswanger disease may be a semantic issue, but we adhere to the notion that the former is characterized by a more con uent and widespread ischemic and gliotic change in the deep white matter. Dementia, a pseudobulbar state, and a gait disorder, alone or in combination, are the main features of Binswanger cases. They have been attributed to the cumulative effects of the ischemic changes and speci cally to the white matter degeneration. The pathologic basis of such a clinical entity has not been well delineated. More importantly, the gliosis that is found in white matter has been assumed to represent a special type of ischemic change,
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In the rst three chapters of this book, we were getting ourselves ready for biology. We painted with a wide brush, making broad strokes through several key areas of the subject matter that we will now examine in greater depth. First among these will be the chemicals the tiniest blocks (or levels) in the Great Pyramid of Life.
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Figure 15-2 Induction loop transmitter I
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