Our results suggest that the anti-inflammatory therapy with low-power LED (880 nm) enhanced the tissue response in all groups. We can conclude that the LED was able to reduce signs of inflammation in collagenase-induced tendinitis in rats by reducing the number of inflammatory cells and decrease mRNA expression of cytokines.

Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions, even when inflammation is a secondary consequence, such as in myocardial infarction (MI). However, the mechanism by which LLLT is able to protect the remaining myocardium remains unclear. The present study tested the hypothesis that LLLT reduces inflammation after acute MI in female rats and ameliorates cardiac function. The potential participation of the Renin-Angiotensin System (RAS) and Kallikrein-Kinin System (KKS) vasoactive peptides was also evaluated. LLLT treatment effectively reduced MI size, attenuated the systolic dysfunction after MI, and decreased the myocardial mRNA expression of interleukin-1 beta and interleukin-6 in comparison to the non-irradiated rat tissue. In addition, LLLT treatment increased protein and mRNA levels of the Mas receptor, the mRNA expression of kinin B2 receptors and the circulating levels of plasma kallikrein compared to non-treated post-MI rats. On the other hand, the kinin B1 receptor mRNA expression decreased after LLLT. No significant changes were found in the expression of vascular endothelial growth factor (VEGF) in the myocardial remote area between laser-irradiated and non-irradiated post-MI rats. Capillaries density also remained similar between these two experimental groups. The mRNA expression of the inducible nitric oxide synthase (iNOS) was increased three days after MI, however, this effect was blunted by LLLT. Moreover, endothelial NOS mRNA content increased after LLLT. Plasma nitric oxide metabolites (NOx) concentration was increased three days after MI in non-treated rats and increased even further by LLLT treatment. Our data suggest that LLLT diminishes the acute inflammation in the myocardium, reduces infarct size and attenuates left ventricle dysfunction post-MI and increases vasoactive peptides expression and nitric oxide (NO) generation.

Osteoarthritis (OA) resulting from injury or disease is associated with increased levels of several matrix metalloproteinases (MMPs), which degrade all components of the complex extracellular matrix in the cartilage. The objective of this study is to investigate the effect of low-level laser therapy (LLLT) on papain-induced joint damage in rats by histopathology and analysis of metalloproteinase 2 and 9 production. Sixty male Wistar rats were randomly distributed into four groups of 15 animals: (1) non-injury negative control, (2) injury positive control, (3) treated with LLLT at 50 mW, and (4) treated with LLLT at 100 mW. OA was induced in animals using papain (4 % solution) followed by treatment with LLLT. After 7, 14, and 21 days, the animals were euthanized. The articular lavage was collected and centrifuged; then, the supernatant was stored prior to protein analysis by western blot. The material was stained with hematoxylin and eosin for histopathological analysis, and Picrosirius Red was used to estimate the percentage of collagen fibers. To determine normal distribution, ANOVA and Tukey's post hoc test were used for comparison between and within each group at each time period. All data are expressed as mean and standard deviation values, with the null hypothesis considered as p < 0.05. Both laser groups (50 and 100 mW) were effective in tissue repair, decreasing collagen type III expression and increasing type I expression in all experimental periods; however, LLLT at 50 mW reduced metalloproteinase 9 more than at 100 mW in 21 days. LLLT at 50 mW was more efficient in the modulation of matrix MMPs and tissue repair.

The aim of the study was to correlate several studies dating from 1997 to 2015 to identify the most effective treatments for mucocele in the frontal sinus (with/without other paranasal sinuses), considering successful outcomes and recurrence. We aimed to conduct a literature review for articles published between 1997 and 2015. For this, we accessed articles in the SciELO database, as well as LILACS, PubMed, and Google Scholar databases. Were identified 32 work-related injuries in the paranasal sinuses; 2 of these were not related to mucoceles or mucopyocele, 4 had no relation to the frontal sinus, 9 were related to the frontal sinus and other paranasal sinuses, 4 were related to mucocele associated with other sinuses, and 13 involved only the frontal sinus. Endoscopic techniques decrease intra- and postoperative morbidity, reducing the operative time, allow a larger view of the lesion and surrounding anatomical structures, and decrease chances of recurrence. Thus, the successful outcomes have been beneficial to both the surgeon and the patient.

Abstract-This study evaluated modulators of apoptosis in the myocardium of rats subjected to exercise training. Rats were assigned to non-trained and exercise-trained groups, respectively. The animals ran for 1 h per day, 6 times per week and, for a total of 13 weeks. The left ventricle was processed for analysis of gene and protein anti-(Bcl-2, c-IAP1, c-IAP2, Survivin, ILK, Akt and pAkt) and pro-(Bad) apoptotic expression by real-time PCR (except for Akt and pAkt) and Western blot, respectively. The Bad mRNA (p<0.05), but not the protein expression (p = 0.19), was significantly lower after training. The exercise training significantly increased the gene and protein expression for all anti-apoptotic factors. However, a significant change in the c-IAP2 was seen only for gene expression (p<0.05). The present findings indicate that exercise can create a favorable milieu for the survival of cardiomyocytes when apoptosis is increased. Keywords: apoptosis, exercise training, myocardialResumo-"Treinamento físico aeróbico induz ambiente anti-apoptótico em tecido miocárdico." Este estudo analisou moduladores de apoptose no miocárdio de ratos submetidos a treinamento físico. Os ratos foram distribuídos nos seguintes grupos, respectivamente: não treinados; treinados. Os animais realizaram exercício em esteira (60 min./dia; 6 x semana) por 13 semanas. O ventrículo esquerdo foi processado para análise da expressão gênica e protéica de fatores anti-apoptóticos (Bcl-2, c-IAP1, c-IAP2, Survivina, ILK, Akt e pAkt) e pro-apoptóticos (Bad) por PCR em tempo real (exceto Akt e pAkt) e Western blot, respectivamente. O teor de RNAm da Bad (p<0,05) foi significativamente reduzido após treinamento. Porém, a expressão protéica da Bad não foi diferente entre os grupos. A expressão gênica e proteica de todos os fatores anti-apoptóticos foi significativamente aumentada com o treinamento. A exceção foi para c-IAP2, que aumentou somente em nível transcripcional (p<0,05). Os achados deste estudo indicam que o exercício cria um ambiente favorável para sobrevivência dos cardiomiócitos a apoptose. Palavras-chave: apoptose, treinamento físico, miocárdioResumen-"La práctica de ejercicio aeróbico induce un ambiente anti-apoptótico en tejido miocárdico." El estudio analizó moduladores de la apoptosis en el miocardio de ratas entrenadas físicamente. Las ratas se dividieron en no entrenado y entrenadas. Los animales se ha ejecutado (60 por día x 6 semanas) a las 13 semanas. El ventrículo izquierdo se procesan para el análisis de la expresión de sus genes y proteínas que inhiben (Bcl-2, c-IAP1, c-IAP2, survivina, ILK, Akt y pAkt) y causa (Bad) de la apoptosis por PCR en tiempo real (excepto Akt y pAkt) y Western blot. El nivel de ARNm de Bad (p<0,05) se redujo después de la entrenamiento, pero no era diferente de proteína. La expresión de los inhibidores de la apoptosis fue significativamente mayor con la entrenamiento. La excepción fue para c-IAP2, que aumentó sólo en el nivel transcripcional (p<0,05). Los resultados de este estudio indican que el eje...