BackgroundMedical education can affect medical students’ physical and mental health as well as their quality of life. The aim of this study was to assess medical students’ perceptions of their quality of life and its relationship with medical education.MethodsFirst- to sixth-year students from six Brazilian medical schools were interviewed using focus groups to explore what medical student’s lives are like, factors related to increases and decreases of their quality of life during medical school, and how they deal with the difficulties in their training.ResultsStudents reported a variety of difficulties and crises during medical school. Factors that were reported to decrease their quality of life included competition, unprepared teachers, excessive activities, and medical school schedules that demanded exclusive dedication. Contact with pain, death and suffering and harsh social realities influence their quality of life, as well as frustrations with the program and insecurity regarding their professional future. The scarcity of time for studying, leisure activities, relationships, and rest was considered the main factor of influence. Among factors that increase quality of life are good teachers, classes with good didactic approaches, active learning methodologies, contact with patients, and efficient time management. Students also reported that meaningful relationships with family members, friends, or teachers increase their quality of life.ConclusionQuality of teachers, curricula, healthy lifestyles related to eating habits, sleep, and physical activity modify medical students’ quality of life. Lack of time due to medical school obligations was a major impact factor. Students affirm their quality of life is influenced by their medical school experiences, but they also reframe their difficulties, herein represented by their poor quality of life, understood as necessary and inherent to the process of becoming doctors.

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Inflammation plays a central role in the development of asthma, which is considered an allergic disease with a classic Th2 inflammatory profile. However, cytokine IL-17 has been examined to better understand the pathophysiology of this disease. Severe asthmatic patients experience frequent exacerbations, leading to infection, and subsequently show altered levels of inflammation that are unlikely to be due to the Th2 immune response alone. This study estimates the effects of anti-IL-17 therapy in the pulmonary parenchyma in a murine asthma model exacerbated by LPS. BALB/c mice were sensitized with intraperitoneal ovalbumin and repeatedly exposed to inhalation with ovalbumin, followed by treatment with or without anti-IL-17. Twenty-four hours prior to the end of the 29-day experimental protocol, the two groups received LPS (0.1 mg/ml intratracheal OVA-LPS and OVA-LPS IL-17). We subsequently evaluated bronchoalveolar lavage fluid, performed a lung tissue morphometric analysis, and measured IL-6 gene expression. OVA-LPS-treated animals treated with anti-IL-17 showed decreased pulmonary inflammation, edema, oxidative stress, and extracellular matrix remodeling compared to the non-treated OVA and OVA-LPS groups (p < 0.05). The anti-IL-17 treatment also decreased the numbers of dendritic cells, FOXP3, NF-κB, and Rho kinase 1- and 2-positive cells compared to the non-treated OVA and OVA-LPS groups (p < 0.05). In conclusion, these data suggest that inhibition of IL-17 is a promising therapeutic avenue, even in exacerbated asthmatic patients, and significantly contributes to the control of Th1/Th2/Th17 inflammation, chemokine expression, extracellular matrix remodeling, and oxidative stress in a murine experimental asthma model exacerbated by LPS.

Eosinophils present a widespread distribution within the respiratory tract in FA, from the nasal mucosa to the distal lung. The outer wall of small membranous bronchioles is the main site of inflammatory changes in FA. There is a localized distribution of alveolar inflammation at the peribronchiolar region for mast cells and neutrophils. Our findings provide further evidence of the importance of the lung periphery in the pathophysiology of FA.

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