New Findings r What is the central question of this study?Clinical studies suggest that obesity 'protects' against osteoporosis. However, these studies used only bone densitometry and assessed only one bone site, which is insufficient to enable conclusions to be drawn about the response of the whole skeleton. Furthermore, the effects of exercise on bone responses in obesity have not been explored previously. r What is the main finding and what is its importance?We show that obesity causes osteopetrosis. Therefore, the classical perspective of 'protective effects of obesity' needs to be reviewed, and exercise is an important tool to avoid these alterations and to maintain the homeostasis of bone.A sedentary lifestyle and obesity induce systemic inflammatory responses. Although the effects of physical inactivity on osseous tissue have been well established, the effects of obesity on bone tissue remain controversial. Furthermore, the effects of physical training on bone tissue responses in the presence of diet-induced obesity are unknown. Our aim was to investigate the effects of obesity and physical training at multiple bone sites in rats. Female Wistar rats were divided into the following four groups: (i) control diet, non-trained (C-NT); (ii) high-refined carbohydrate-containing diet, non-trained (HC-NT); (iii) control diet, trained (C-T); and (iv) high-refined carbohydrate-containing diet, trained (HC-T). At 5 months of age, the rats were submitted to daily exercise for 30 min day −1 . After 13 weeks, blood samples, adipose and skeletal tissues were harvested. Two-way ANOVA was applied to detect differences (significance accepted when P ࣘ 0.05). The HC-NT group exhibited increased body mass, adiposity, serum leptin, serum insulin, insulin resistance index and concentrations of tumour necrosis factor-α and interleukin-6. Obese rats (HC-NT) exhibited thickening of nasal bones, trabecular bones in the lumbar vertebrae and long bones in a site-dependent manner. The HC-T group exhibited similar adiposity and inflammatory results. Morphological analysis of the lumbar vertebrae in rats fed the HC diet revealed characteristics of osteopetrosis that were inhibited by exercise. In conclusion, the HC diet induced obesity and inflammatory/hormonal alterations and increased the trabecular bone in a site-dependent manner. However, obesity caused osteopetrosis in the lumbar vertebrae, which could be inhibited by physical training. Although exercise inhibited the
Acute exercise increases the amount of circulating inflammatory cells and cytokines to maintain physiological homeostasis. However, it remains unclear how physical training regulates exercise-induced inflammation and performance. Here, we demonstrate that acute high intensity exercise promotes an inflammatory profile characterized by increased blood IL-6 levels, neutrophil migratory capacity, and leukocyte recruitment to skeletal muscle vessels. Moreover, we found that physical training amplified leukocyte–endothelial cell interaction induced by acute exercise in skeletal muscle vessels and diminished exercise-induced inflammation in skeletal muscle tissue. Furthermore, we verified that disruption of the gp-91 subunit of NADPH-oxidase inhibited exercise-induced leukocyte recruitment on skeletal muscle after training with enhanced exercise time until fatigue. In conclusion, the training was related to physical improvement and immune adaptations. Moreover, reactive oxygen species (ROS) could be related to mechanisms to limit aerobic performance and its absence decreases the inflammatory response elicited by exercise after training.
The high incidence of wounds by second intention and the high costs associated with their treatment give rise to the need for the development of wound dressings that protect not only the wounds themselves but that are also able to promote cell proliferation and skin regeneration. Moreover, it is also very important that no damage to the new regenerated tissue is generated while removing the dressing. In this work, a novel wound dressing, which would be able to favor tissue repair and be removed at an appropriate scheduled moment by means of an external stimulus without promoting extensive damage to the new tissue, was produced and tested. Polyurethane membranes were modified by grafting polymers based on poly(n-isopropylacrylamide) (P-N-IPAAm). P-N-IPAAm undergoes a phase transition at approximately 32°C, which changes its behavior from hydrophilic (below 32°C) to hydrophobic. It was hypothesized that, by reducing the temperature near the wound dressing to values lower than 32°C, the detachment of the dressing would become more effective. The wound dressings containing P-N-IPAAm grafts were tested in vivo by covering excisional wounds produced in mice. The produced dressings were placed in direct contact with the lesions for 3 days. Results showed that the hypothermia due to anesthesia required to remove the dressings from mice lowered the local temperature to 28°C and favored the detachment of the wound dressings containing P-N-IPAAm grafts. Histological analyses showed that lesions covered by dressings presented less intense inflammatory events and denser connective tissue than did the wounds without dressings. The wounds covered by polyurethane membranes with P-N-IPAAm grafts showed signs of more intense re-epithelization and angiogenesis than did the lesions covered by polyurethane without grafts.
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