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Abstract Multiple sclerosis is an autoimmune disease that affects the myelinated central nervous system (CNS) neurons and triggers physical and cognitive disabilities. Conventional therapy is based on disease-modifying drugs that control disease severity but can also be deleterious. Complementary medicines have been adopted and evidence indicates that yeast supplements can improve symptoms mainly by modulating the immune response. In this investigation, we evaluated the therapeutic potential of Saccharomyces cerevisiae and its selenized derivative (Selemax) in experimental autoimmune encephalomyelitis (EAE). Female C57BL/6 mice submitted to EAE induction were orally supplemented with these yeasts by gavage from day 0 to day 14 after EAE induction. Both supplements determined significant reduction in clinical signs concomitantly with diminished Th1 immune response in CNS, increased proportion of Foxp3+ lymphocytes in inguinal and mesenteric lymph nodes and increased microbiota diversity. However, Selemax was more effective clinically and immunologically; it reduced disease prevalence more sharply, increased the proportion of CD103+ dendritic cells expressing high levels of PD-L1 in mesenteric lymph nodes and reduced the intestinal inflammatory process more strongly than S. cerevisiae. These results suggest a clear gut-brain axis modulation by selenized S. cerevisiae and suggest their inclusion in clinical trials.

Experimental autoimmune encephalomyelitis (EAE) is an animal model to study multiple sclerosis (MS). Considering the tolerogenic effects of active vitamin D, we evaluated the therapeutic effect of myelin oligodendrocyte glycoprotein (MOG) associated with active vitamin D in EAE development. EAE was induced in female C57BL/6 mice by immunization with MOG emulsified with Complete Freund's Adjuvant plus Mycobacterium tuberculosis. Animals also received two intraperitoneal doses of Bordetella pertussis toxin. One day after immunization, mice were treated with 0,1 μg of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) every other day during 15 days (on days 1, 3, 5, 7, 9, 11, 13 and 15). MOG (150 μg) was co-administered on days 3 and 11. The administration of 1,25(OH)2D3 or MOG determined significant reduction in EAE incidence and in clinical scores. When MOG was associated with 1,25(OH)2D3 the animals did not develop EAE. Spleen and central nervous system (CNS) cell cultures from this group produced less IL-6 and IL-17 upon stimulation with MOG in comparison to the EAE control group. In addition, this treatment inhibited dendritic cells maturation in the spleen and reduced inflammatory infiltration in the CNS. The association of MOG with 1,25(OH)2D3 was able to control EAE development.

Aim of this study is analyze the effects of dental occlusion on postural stability in patients with previous whiplash and normal occlusion. Materials and methods: 36 adult patients with previous whiplash and normal occlusion (good alignment, 1 st class or mild 2 nd class deep bite for mandibular retrusion) were selected. The patients were suffering from masticatory muscles pain caused by clenching during sleep. Exclusion criteria: use of psych drugs. To simulate the conditions of sleep (with a reduction of proprio-and esteroceptive inputs for postural management performed by CNS), we used postural Romberg analysis (feet together, closed eyes)on stabilometric platform changing occlusal parameters only, under the following conditions: 1) in occlusal rest position, 2) in centric occlusion, 3) in clenching, 4) with occlusal disengage with cotton rolls and 5) in clenching on cotton rolls. Time of each test: 15 seconds. It was performed a statistical analysis with T-test comparing between them the mean of all tests. Results: stabilometry data (postural ball and ellipse) show better postural performances in centric occlusion and clenching in centric occlusion, and a worsening in all tests with occlusal disengage (with statistically significant difference - p

24 patients are selected and 30 teeth in vestibular mucosae, without keratinized gingiva. No active periodontal disease (no BOP and gingival recessions). No BOP and CAL loss at the start of the orthodontic treatment. Every patient was treated with self ligating appliances (Time2/Time3, American Orthodontics). In every orthodontic session (each 30 days as average) the patient was treated with Nd: Yag laser biostimulation, for 90 seconds, with 320 micron fiber section, on utilizing the Biostimulating machine paremeters. No termical effects were produced by lasers applications. At the moment of debonding, 30 teeth involved in the research were evaluated in terms of quality and quantity of attached gingiva. BOP and CAL loss were also investigated. Every tooth considerated, at the end of orthodontic treatment showed a attached gingiva around the crown: the average of keratinized gingiva at the end of the study was 2,7 mm and the mean increasing at each month was 0,45 mm. The combination between self ligating appliances and laser's biostimulation could improve the differentiation of periodontal ligaments stem cells in fibroblasts, able to promote attached gingiva around the crown of the teeth erupted in oral vestibular mucosae.

IntroductionMicronutrient deficiency is observed in heart failure patients. Taurine, for example, represents 50% of total free amino acids in the heart, and in vivo studies have linked taurine deficiency with cardiomyopathy.MethodsThirty-four male Wistar rats (body weight = 100 g) were weighed and randomly assigned to one of two groups: Control (C) or taurine-deficient (T (-)). Beta-alanine at a concentration of 3% was added to the animals' water to induce taurine deficiency in the T (-) group. On day 30, the rats were individually submitted to echocardiography; morphometrical and histopathological evaluation and metalloproteinase activity, oxidative stress and inflammation evaluation were performed. Tissue samples were collected to determine the taurine concentration in the heart.ResultsTaurine deficiency led to decreases in: ventricular wall thickness, left ventricle dry weight, myocyte sectional area, left ventricle posterior wall thickness and ventricular geometry. With regard to heart function, the velocity of the A wave, the ratio between the E and A wave, the ejection fraction, fractional shortening and cardiac output values were decreased in T (-) rats, suggesting abnormal diastolic and systolic function. Increased fibrosis, inflammation and increased activation of metalloproteinases were not observed. Oxidative stress was increased in deficient animals.ConclusionsThese data suggest that taurine deficiency promotes structural and functional cardiac alterations with unique characteristics.