High glucose concentration in the airway surface liquid (ASL) is an important feature of diabetes that predisposes to respiratory infections. We investigated the role of alveolar epithelial SGLT1 activity on ASL glucose concentration and bacterial proliferation. Non-diabetic and diabetic rats were intranasally treated with saline, isoproterenol (to increase SGLT1 activity) or phlorizin (to decrease SGLT1 activity); 2 hours later, glucose concentration and bacterial proliferation (methicillin-resistant Sthaphylococcus aureus, MRSA and Pseudomonas aeruginosa, P. aeruginosa) were analyzed in bronchoalveolar lavage (BAL); and alveolar SGLT1 was analyzed by immunohistochemistry. BAL glucose concentration and bacterial proliferation increased in diabetic animals: isoproterenol stimulated SGLT1 migration to luminal membrane, and reduced (50%) the BAL glucose concentration; whereas phlorizin increased the BAL glucose concentration (100%). These regulations were accompanied by parallel changes of in vitro MRSA and P. aeruginosa proliferation in BAL (r = 0.9651 and r = 0.9613, respectively, Pearson correlation). The same regulations were observed in in vivo P. aeruginosa proliferation. In summary, the results indicate a relationship among SGLT1 activity, ASL glucose concentration and pulmonary bacterial proliferation. Besides, the study highlights that, in situations of pulmonary infection risk, such as in diabetic subjects, increased SGLT1 activity may prevent bacterial proliferation whereas decreased SGLT1 activity can exacerbate it.

Our results indicate that laser therapy improves bone repair in rats as depicted by differential histopathological and osteogenic genes expression, mainly at the late stages of recovery.

The aim of this study was to investigate and to compare the effects of low intensity ultra-sound (LIPUS) and low-level laser therapy (LLLT) during the process of bone healing by means of histopathological and morphometric analysis. The animals were randomly distributed into three groups of 30 animals each: the control group (bone defect without treatment); the laser-treated group: (bone defect treated with laser), and the LIPUS-treated (bone defect treated with ultrasound). Each group was further divided into three different subgroups (n = 10) and on days 7, 13, and 25 post-injury, rats were killed with an intra-peritoneal injection of general anesthetic. The rats were treated with a 30-mW/cm(2) low-intensity pulsed ultrasound and a 830-nm laser at 50 J/cm(2). The results showed intense new bone formation surrounded by highly vascularized connective tissue presenting a slight osteogenic activity, with primary bone deposition being observed in the group exposed to laser in the intermediary (13 days) and late stages of repair (25 days). This was confirmed by morphometric analysis in which significant statistical differences (p < 0.05) were noticed when compared to the control. No remarkable differences were noticed in the specimens treated with ultrasound with regard to the amount of newly formed bone in comparison to the control group. Taken together, our results indicate that laser therapy improves bone repair in rats as depicted by histopathological and morphometric analysis, mainly at the late stages of recovery. Moreover, it seems that this therapy was more effective than US to accelerate bone healing.

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