A implementação de novos modelos de ensino-aprendizagem vem ocorrendo na Faculdade de Medicina de Marília (Famema) há mais de uma década. O presente estudo analisa as fortalezas e fragilidades dos métodos ativos de aprendizagem na ótica dos estudantes. Para a coleta de dados, realizaram-se entrevistas com estudantes dos cursos de Enfermagem e Medicina. Os dados foram interpretados por meio dos parâmetros da hermenêutica dialética. Os sentidos extraídos das falas dos estudantes indicam que as metodologias ativas estimulam o estudo constante, a independência e a responsabilidade, possibilitam a integração das dimensões biopsicossociais, preparam para o trabalho em equipe e aproximam os alunos dos usuários e da equipe. No entanto, nem todos estão preparados para isso; algumas vezes, sentem-se perdidos em busca de conhecimentos, além de apresentarem dificuldades quanto a sua inserção na equipe de saúde. A construção de novos modelos de aprendizagem requer constante empenho, visando ao seu aperfeiçoamento.

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According to the current clinical practice guidelines for chronic obstructive pulmonary disease (COPD), the addition of inhaled corticosteroids (ICS) to long-acting β2 agonist therapy is recommended in patients with moderate-to-severe disease and an increased risk of exacerbations. However, ICS are largely overprescribed in clinical practice, and most patients are unlikely to benefit from long-term ICS therapy.Evidence from recent randomized-controlled trials supports the hypothesis that ICS can be safely and effectively discontinued in patients with stable COPD and in whom ICS therapy may not be indicated, without detrimental effects on lung function, health status, or risk of exacerbations. This article summarizes the evidence supporting the discontinuation of ICS therapy, and proposes an algorithm for the implementation of ICS withdrawal in patients with COPD in clinical practice.Given the increased risk of potentially serious adverse effects and complications with ICS therapy (including pneumonia), the use of ICS should be limited to the minority of patients in whom the treatment effects outweigh the risks.

Background Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/ CX 3 CL1 upregulation were investigated. Methods and results Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX 3 CL1 expression. Neutralisation of CX 3 CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interfering RNA (siRNA) revealed that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 5 (Nox5) but not Nox2 or Nox4 is the main NADPH isoform involved in CSE-induced CX 3 CL1 upregulation and mononuclear cell arrest. Knock down of HUAEC tumour necrosis factor α expression with siRNA or pharmacological inhibition of p38 mitogen-activated protein kinase and nuclear factor κB also abolished these responses. Interestingly, circulating monocytes and lymphocytes from patients with chronic obstructive pulmonary disease (COPD) (n=29) versus age-matched controls (n=23) showed CX 3 CR1overexpression. Furthermore, CX 3 CL1 neutralisation dramatically diminished their enhanced adhesiveness to CSE-stimulated HUAECs. Finally, when animals were exposed for 3 days to CS, a mild inflammatory response in the lung was observed which was accompanied by enhanced CX 3 CL1 expression in the cremasteric arterioles, an organ distant from the lung. CS exposure resulted in increased leukocyte-arteriolar endothelial cell adhesion which was significantly reduced (51%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Conclusions These results suggest that CS induces functional CX 3 CL1 expression in arterial endothelium and leukocytes from patients with COPD show increased CX 3 CL1-dependent adhesiveness. Therefore, targeting the CX 3 CL1/CX 3 CR1 axis might prevent COPD-associated cardiovascular disorders.