994 resultados para Medicine, Industrial


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McArdle disease is arguably the paradigm of exercise intolerance in humans. This disorder is caused by inherited deficiency of myophosphorylase, the enzyme isoform that initiates glycogen breakdown in skeletal muscles. Because patients are unable to obtain energy from their muscle glycogen stores, this disease provides an interesting model of study for exercise physiologists, allowing insight to be gained into the understanding of glycogen-dependent muscle functions. Of special interest in the field of muscle physiology and sports medicine are also some specific (if not unique) characteristics of this disorder, such as the so-called 'second wind' phenomenon, the frequent exercise-induced rhabdomyolysis and myoglobinuria episodes suffered by patients (with muscle damage also occurring under basal conditions), or the early appearance of fatigue and contractures, among others. In this article we review the main pathophysiological features of this disorder leading to exercise intolerance as well as the currently available therapeutic possibilities.

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N.W. Hardy and M.H. Lee. The effect of the product cost factor on error handling in industrial robots. In Maria Gini, editor, Detecting and Resolving Errors in Manufacturing Systems. Papers from the 1994 AAAI Spring Symposium Series, pages 59-64, Menlo Park, CA, March 1994. The AAAI Press. Technical Report SS-94-04, ISBN 0-929280-60-1.

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V. Robinson, N. W. Hardy, D. P. Barnes, C. J. Price, M. H. Lee. Experiences with a knowledge engineering toolkit: an assessment in industrial robotics. Knowledge Engineering Review, 2 (1):43-54, 1987.

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M. H. Lee, D. P. Barnes, and N. W. Hardy. Knowledge based error recovery in industrial robots. In Proc. 8th. Int. Joint Conf. Artificial Intelligence, pages 824-826, Karlsruhe, FDR., 1983.

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Barnes, D. P., Lee, M. H., Hardy, N. W. (1983). A control and monitoring system for multiple-sensor industrial robots. In Proc. 3rd. Int. Conf. Robot Vision and Sensory Controls, Cambridge, MA. USA., 471-479.

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Lee M.H., Many-Valued Logic and Qualitative Modelling of Electrical Circuits, in Proc. QR?2000, 14th Int. Workshop on Qualitative Reasoning, Morelia, Mexico June 3rd - 7th 2000.

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Lee M.H., ?Tactile Sensing: new directions, new challenges?, Int J. Robotics Research 19: 7, 636-643. July 2000.

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Editorial for Bioethics 2016. 30:(2)

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Dissertação de Mestrado apresentada à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências da Comunicação, com especialização em Marketing e Comunicação Estratégica.

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27 hojas : ilustraciones, planos.

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A worker developed angiosarcoma, porphyria cutanea tarda, and skin lesions characteristic of mild chloracne. About 10 years earlier he had been employed at a truck terminal in Saint Louis, Missouri, at a time when it was sprayed with waste oil contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The occurrence of these three rare conditions in a single exposed worker supports the aetiological relation between environmental exposure to TCDD and the subsequent development of soft tissue sarcoma and porphyria cutanea tarda.

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To evaluate the effects of chronic lead exposure on the nervous system in adults, a set of neurobehavioural and electrophysiological tests was administered to 99 lead exposed foundry employees and 61 unexposed workers. Current and past blood lead concentrations were used to estimate the degree of lead absorption; all previous blood lead concentrations had been less than or equal to 90 micrograms/100 ml. Characteristic signs (such as wrist extensor weakness) or symptoms (such as colic) of lead poisoning were not seen. Sensory conduction in the sural nerve was not affected. By contrast, various neurobehavioural functions deteriorated with increasing lead burden. Workers with blood lead concentrations between 40 and 60 micrograms/100 ml showed impaired performance on tests of verbal concept formation, visual/motor performance, memory, and mood. Thus impairment in central nervous system function in lead exposed adults occurred in the absence of peripheral nervous system derangement and increased in severity with increasing lead dose.

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To evaluate critical exposure levels and the reversibility of lead neurotoxicity a group of lead exposed foundry workers and an unexposed reference population were followed up for three years. During this period, tests designed to monitor neurobehavioural function and lead dose were administered. Evaluations of 160 workers during the first year showed dose dependent decrements in mood, visual/motor performance, memory, and verbal concept formation. Subsequently, an improvement in the hygienic conditions at the plant resulted in striking reductions in blood lead concentrations over the following two years. Attendant improvement in indices of tension (20% reduction), anger (18%), depression (26%), fatigue (27%), and confusion (13%) was observed. Performance on neurobehavioural testing generally correlated best with integrated dose estimates derived from blood lead concentrations measured periodically over the study period; zinc protoporphyrin levels were less well correlated with function. This investigation confirms the importance of compliance with workplace standards designed to lower exposures to ensure that individual blood lead concentrations remain below 50 micrograms/dl.