A UNIVERSIDADE CORPORATIVA E O TREINAMENTO INDUSTRIAL A DISTÂNCIA PARA PROFISSIONAIS DE MANUTENÇÃO

Este trabalho trata dos principais aspectos envolvidos na avaliação e características conceituais acerca dos fundamentos e práticas do ensino a distância enfocando o treinamento industrial a distância para profissionais de manutenção, utilizando a internet como principal ferramenta e o desafio de relacionar a tecnologia com a metodologia voltada para o profissional técnico operacional. A internet é uma ferramenta que pode ser utilizada para o ensino em geral, ela permite acesso fácil a uma infinidade de material informativo autêntico e atualizado, além de exemplos concretos e interativos na perspectiva de transformar a informação recebida por meios eletrônicos em conhecimento sólido adquirido. Diante disso, a análise do trabalho recai, num primeiro momento, sobre os pressupostos que criaram o treinamento industrial, o treinamento na área de manutenção industrial e, os aspectos da estrutura que cria o treinamento industrial a distância, em seguida, aprofundamos-nos no conhecimento acerca das técnicas que envolvem o treinamento para profissionais da área de manutenção industrial a distância. Também é apresentada a experiência dos cursos profissionalizantes a distância através de vários meios e a experiências dos portais de educação a distância voltados para área de manutenção industrial.

A UNIVERSIDADE CORPORATIVA E O TREINAMENTO INDUSTRIAL A DISTÂNCIA PARA PROFISSIONAIS DE MANUTENÇÃO

Este trabalho trata dos principais aspectos envolvidos na avaliação e características conceituais acerca dos fundamentos e práticas do ensino a distância enfocando o treinamento industrial a distância para profissionais de manutenção, utilizando a internet como principal ferramenta e o desafio de relacionar a tecnologia com a metodologia voltada para o profissional técnico operacional. A internet é uma ferramenta que pode ser utilizada para o ensino em geral, ela permite acesso fácil a uma infinidade de material informativo autêntico e atualizado, além de exemplos concretos e interativos na perspectiva de transformar a informação recebida por meios eletrônicos em conhecimento sólido adquirido. Diante disso, a análise do trabalho recai, num primeiro momento, sobre os pressupostos que criaram o treinamento industrial, o treinamento na área de manutenção industrial e, os aspectos da estrutura que cria o treinamento industrial a distância, em seguida, aprofundamos-nos no conhecimento acerca das técnicas que envolvem o treinamento para profissionais da área de manutenção industrial a distância. Também é apresentada a experiência dos cursos profissionalizantes a distância através de vários meios e a experiências dos portais de educação a distância voltados para área de manutenção industrial.

Physiological response to long-term peripheral and central leptin infusion in lean and obese mice

Recent data have identified leptin as an afferent signal in a negative-feedback loop regulating the mass of the adipose tissue. High leptin levels are observed in obese humans and rodents, suggesting that, in some cases, obesity is the result of leptin insensitivity. This hypothesis was tested by comparing the response to peripherally and centrally administered leptin among lean and three obese strains of mice: diet-induced obese AKR/J, New Zealand Obese (NZO), and Ay. Subcutaneous leptin infusion to lean mice resulted in a dose-dependent loss of body weight at physiologic plasma levels. Chronic infusions of leptin intracerebroventricularly (i.c.v.) at doses of 3 ng/hr or greater resulted in complete depletion of visible adipose tissue, which was maintained throughout 30 days of continuous i.c.v. infusion. Direct measurement of energy balance indicated that leptin treatment did not increase total energy expenditure but prevented the decrease that follows reduced food intake. Diet-induced obese mice lost weight in response to peripheral leptin but were less sensitive than lean mice. NZO mice were unresponsive to peripheral leptin but were responsive to i.c.v. leptin. Ay mice did not respond to subcutaneous leptin and were 1/100 as sensitive to i.c.v. leptin. The decreased response to leptin in diet-induced obese, NZO, and Ay mice suggests that obesity in these strains is the result of leptin resistance. In NZO mice, leptin resistance may be the result of decreased transport of leptin into the cerebrospinal fluid, whereas in Ay mice, leptin resistance probably results from defects downstream of the leptin receptor in the hypothalamus.

Synergistic interaction between leptin and cholecystokinin to reduce short-term food intake in lean mice

Leptin is a circulating protein involved in the long-term regulation of food intake and body weight. Cholecystokinin (CCK) is released postprandially and elicits satiety signals. We investigated the interaction between leptin and CCK-8 in the short-term regulation of food intake induced by 24-hr fasting in lean mice. Leptin, injected intraperitoneally (i.p.) at low doses (4–120 μg/kg), which did not influence feeding behavior for the first 3 hr postinjection, decreased food intake dose dependently by 47–83% during the first hour when coinjected with a subthreshold dose of CCK. Such an interaction was not observed between leptin and bombesin. The food-reducing effect of leptin injected with CCK was not associated with alterations in gastric emptying or locomotor behavior. Leptin–CCK action was blocked by systemic capsaicin at a dose inducing functional ablation of sensory afferent fibers and by devazepide, a CCK-A receptor antagonist but not by the CCK-B receptor antagonist, L-365,260. The decrease in food intake which occurs 5 hr after i.p. injection of leptin alone was also blunted by devazepide. Coinjection of leptin and CCK enhanced the number of Fos-positive cells in the hypothalamic paraventricular nucleus by 60%, whereas leptin or CCK alone did not modify Fos expression. These results indicate the existence of a functional synergistic interaction between leptin and CCK leading to early suppression of food intake which involves CCK-A receptors and capsaicin-sensitive afferent fibers.

Insulin depletion leads to adipose-specific cell death in obese but not lean mice

Mutation of the obese gene produces obesity, hyperinsulinemia, and compensatory “overexpression” of the defective gene. As insulin activates obese gene expression, it seemed possible that hyperinsulinemia might be responsible for overexpression of the gene. To address this question we rapidly neutralized circulating insulin by injection of an insulin antibody. Unexpectedly, insulin depletion in obese (ob/ob or db/db) mice caused massive adipose RNA degradation confirmed by histological analysis to result from adipocyte cell death by a largely necrotic mechanism. This effect was not observed in lean littermates and was completely corrected by coadministration of insulin. Comparison of multiple tissues demonstrated that the effect was restricted to adipose tissue. Insulin depletion in obese mice by administration of streptozotocin also led to cell death, but this death was less extensive and appeared to be apoptotic in mechanism. Thus insulin may promote the survival side of the physiological balance between adipocyte survival and death.

Contratos reajustados com base na variação cambial : um fator de manutenção do equilíbrio dos negócios / Marcos Juruena Villela Souto. --

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