Obliteration of Dentinal Tubules by Desensitizing Agents Based on Silver Fluoride/Potassium Iodide or Pre-Reacted Glass Particles: An in Vitro Study

Objective: To evaluate the efficacy of desensitizing agents for the obliteration of dentinal tubules subjected or not to a simulated oral environment. Material and Methods: Dentinal discs (n=8) treated with Riva-Star (RS) or PRG-Barrier-Coat (PRG) were submitted (cycled) or not submitted (control) to erosive-abrasive-thermal cycles and evaluated using scanning electron microscopy/energy dispersive spectroscopic analysis. The variables analyzed were tubule obliteration and dentin surface chemical composition. Data were analyzed by non-parametric tests (p<0.05). Results: The cycled and control groups did not differ significantly for the responses in each material. The PRG control and cycled groups had fewer visible tubules and a higher proportion of totally obliterated tubules than the RS groups. The percentages of silver coverage were higher in the RS-control than in the RS-cycled. There was a significant inverse correlation between the presence of silver and non-obliterated tubules (R=-0.791; p<0.001). The percentages of carbon, aluminum, strontium, and potassium were significantly higher in the PRG-control and PRG-cycled compared to the RS control. The percentages of calcium, phosphorus, and silver were significantly higher in the RS compared to the PRG groups. PRG-control showed a higher percentage of boron than RS-control. Conclusion: PRG promoted greater tubule obliteration than SR. Simulated stress did not affect the obliterating effect of each agent. Greater silver coverage corresponded to a lower proportion of non-obliterated tubules in RS. Carbon, aluminum, strontium, boron, and potassium predominated in the dentin surface treated with PRG, while calcium, phosphorus, and silver prevailed in RS groups

Physical Exercise Induces Immunoregulation of TREG, M2, and pDCs in a Lung Allergic Inflammation Model

The benefits of moderate aerobic physical exercise for allergic asthma are well-known, particularly that of the anti-inflammatory effect that occurs by reducing Th2 responses and lung remodeling. However, the mechanisms of this immunoregulation are still under investigation. In this study, we investigated the possible immunoregulatory mechanisms of lung inflammation induced by moderate aerobic exercise in an experimental asthma model. BALB/c mice were distributed into Control, Exercise (EX), OVA, and OEX groups. OVA and OEX groups were sensitized with ovalbumin (OVA) on days 0, 14, 21, 28, and 42 and were challenged with OVA aerosol three times a week from days 21 to 51. The EX and OEX groups underwent moderate aerobic physical exercise from days 21 to 51 (5 d/w, 1 h/d). The mice were euthanized on day 52. We evaluated pulmonary cytokine production, serum immunoglobulin levels, and the inflammatory cell profile in lung and mediastinal lymph nodes. OVA mice showed increased expression of IL-4, IL-6, IL-10, and TGF-β and decreased macrophage type 2 (M2) recruitment. Physical exercise did not affect the increased antibody production of IgG2a, IgG1, or IgE induced by OVA. Of note, physical exercise alone markedly increased production of anti-inflammatory cytokines such as IL-10 and TGF-β. Physical exercise in OVA-mice also increased the recruitment of M2 in the lungs, as well as the influx and activation of regulatory T cells (Tregs) and CD4 and CD8 lymphocytes. In the draining lymph nodes, it was also observed that physical exercise increased the activation of CD4 T cells, regardless of the presence of OVA. Notably, physical exercise decreased common dendritic cells' (cDCs; pro-inflammatory) expression of co-stimulatory molecules such as CD80, CD86, and ICOSL in the draining lymph nodes, as well as increased ICOSL in plasmacytoid dendritic cells (pDCs; anti-inflammatory). Together, these findings show that physical exercise modulates pulmonary allergic inflammation by increasing Treg and M2 recruitment, as well as pDCs activation, which leads to an increase in anti-inflammatory cytokines and a decrease in pro-inflammatory cells and mediators

Obliteration of Dentinal Tubules by Desensitizing Agents Based on Silver Fluoride/Potassium Iodide or Pre-Reacted Glass Particles: An in Vitro Study

Objective: To evaluate the efficacy of desensitizing agents for the obliteration of dentinal tubules subjected or not to a simulated oral environment. Material and Methods: Dentinal discs (n=8) treated with Riva-Star (RS) or PRG-Barrier-Coat (PRG) were submitted (cycled) or not submitted (control) to erosive-abrasive-thermal cycles and evaluated using scanning electron microscopy/energy dispersive spectroscopic analysis. The variables analyzed were tubule obliteration and dentin surface chemical composition. Data were analyzed by non-parametric tests (p<0.05). Results: The cycled and control groups did not differ significantly for the responses in each material. The PRG control and cycled groups had fewer visible tubules and a higher proportion of totally obliterated tubules than the RS groups. The percentages of silver coverage were higher in the RS-control than in the RS-cycled. There was a significant inverse correlation between the presence of silver and non-obliterated tubules (R=-0.791; p<0.001). The percentages of carbon, aluminum, strontium, and potassium were significantly higher in the PRG-control and PRG-cycled compared to the RS control. The percentages of calcium, phosphorus, and silver were significantly higher in the RS compared to the PRG groups. PRG-control showed a higher percentage of boron than RS-control. Conclusion: PRG promoted greater tubule obliteration than SR. Simulated stress did not affect the obliterating effect of each agent. Greater silver coverage corresponded to a lower proportion of non-obliterated tubules in RS. Carbon, aluminum, strontium, boron, and potassium predominated in the dentin surface treated with PRG, while calcium, phosphorus, and silver prevailed in RS groups

Medical students’ quality of life: does the learning environment matter?

Introdução: A qualidade de vida e a saúde mental dos estudantes de medicina podem afetar o seu desempenho acadêmico, suas habilidades e atitudes com pacientes. Evidências recentes confirmam a importância do ambiente educacional como um dos determinantes da saúde mental e qualidade de vida. Este estudo teve o objetivo de avaliar diferentes aspectos da qualidade de vida dos estudantes de medicina brasileiros em todos os anos do curso. Casuística e Métodos: Estudo transversal de abrangência nacional, com a utilização de questionário validado de qualidade de vida específico para o estudante da área da saúde (Veras-q). Resultados: De uma amostra aleatória de 1.650 estudantes, em 22 escolas médicas de diferentes regiões do país, 1.350 (81,8%) participaram do estudo. Os coeficientes de alfa Cronbach dos domínios do Veras-q variaram entre 0,77 e 0,82. Estudantes do sexo feminino apresentaram menores escores de qualidade de vida nos domínios físico, psicológico e uso do tempo, quando comparadas a seus colegas do sexo masculino (p&lt;0,05; d&lt;0,5). A percepção de qualidade de vida relacionada ao ambiente de ensino também foi menor entre estudantes dos últimos anos do curso (p&lt;0,001; f&lt;0,25), principalmente entre as mulheres (p&lt;0,001; f=0,22). Conclusões: Estudantes do sexo feminino apresentaram pior percepção de qualidade de vida do que seus colegas do sexo masculino. Estudantes dos anos mais avançados do curso, principalmente as mulheres, apresentaram pior percepção de qualidade de vida no domínio ambiente de ensino quando comparados aos estudantes dos anos iniciais. Este estudo demonstra o impacto do ambiente educacional na qualidade de vida dos estudantes de Medicina e sugere que intervenções institucionais que aprimorem o ambiente, estimulem a formação de redes de suporte e promovam o bem-estar dos estudantes devem ser implementadas e avaliadas.Introduction: Medical students’ quality of life and mental health may affect their academic performance and their attitudes towards medical care. Recent evidence shows a preponderant role of the learning environment in the quality of life of medical students. This study aimed to assess Brazilian medical students’ quality of life throughout all years of medical school. Methods: Cross-sectional multi-centric study with the&nbsp;use of a quality of life questionnaire, validated for specific use among health sciences students (Veras-q). RESULTS: From a random sample of 1,650 students, 1,350 (81.8%) participated in the study. Cronbach’s alpha coefficients for Veras-q domains ranged from 0.77 to 0.82. Female students had lower scores on physical, psychological and time management domains of quality of life compared to male students (p&lt;0.05; d&lt;0.5). Perceptions of quality of life on the learning environment were also lower among students in the final years of medical school (p&lt;0.001; f&lt;0.25), especially among female students (p&lt;0.001; f= 0.22). CONCLUSIONS: Female students showed worse perception of quality of life than their male counterparts. Students from more advanced years of medical school, especially women, also showed lower perception of quality of life in the learning environment domain. Institutional interventions directed to students at higher risk of low quality of life should be implemented and evaluated in further studies. This study demonstrates the impact of the learning environment on medical students’ quality of life, suggesting that institutional interventions designed to improve students’ well being such as the supporting networks must be adequately implemented and assessed

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear un derstanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5–7 vast areas of the tropics remain understudied.8–11 In the American tropics, Amazonia stands out as the world’s most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepre sented in biodiversity databases.13–15 To worsen this situation, human-induced modifications16,17 may elim inate pieces of the Amazon’s biodiversity puzzle before we can use them to understand how ecological com munities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple or ganism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region’s vulnerability to environmental change. 15%–18% of the most ne glected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lostinfo:eu-repo/semantics/publishedVersio

Pervasive gaps in Amazonian ecological research

Biodiversity loss is one of the main challenges of our time,1,2 and attempts to address it require a clear understanding of how ecological communities respond to environmental change across time and space.3,4 While the increasing availability of global databases on ecological communities has advanced our knowledge of biodiversity sensitivity to environmental changes,5,6,7 vast areas of the tropics remain understudied.8,9,10,11 In the American tropics, Amazonia stands out as the world's most diverse rainforest and the primary source of Neotropical biodiversity,12 but it remains among the least known forests in America and is often underrepresented in biodiversity databases.13,14,15 To worsen this situation, human-induced modifications16,17 may eliminate pieces of the Amazon's biodiversity puzzle before we can use them to understand how ecological communities are responding. To increase generalization and applicability of biodiversity knowledge,18,19 it is thus crucial to reduce biases in ecological research, particularly in regions projected to face the most pronounced environmental changes. We integrate ecological community metadata of 7,694 sampling sites for multiple organism groups in a machine learning model framework to map the research probability across the Brazilian Amazonia, while identifying the region's vulnerability to environmental change. 15%–18% of the most neglected areas in ecological research are expected to experience severe climate or land use changes by 2050. This means that unless we take immediate action, we will not be able to establish their current status, much less monitor how it is changing and what is being lost

Effects of residual diesel oil fly ash (ROFA) and pulmonary allergic chronic inflammation in tree lines of mice

Neste estudo, foram realizados três experimentos distintos (1) analisando os efeitos da administração de material particulado em camundongos BALB/c com inflamação pulmonar alérgica crônica induzida por ovalbumina; (2) comparando camundongos AIRmax e AIRmin com inflamação pulmonar alérgica crônica induzida por ovalbumina; (3) comparando camundongos AIRmax e AIRmin que receberam material particulado (resíduo da queima de óleo diesel - ROFA) por via intranasal. Para a indução da inflamação pulmonar alérgica crônica, os camundongos foram sensibilizados com ovalbumina (OVA) através de duas injeções intraperitoneais de alérgeno com o adjuvante hidróxido de alumínio (dias 0 e 14) e quatro inalações de OVA 1% (dias 22, 24, 26 e 28). Os animais que foram expostos ao material particulado, receberam ROFA (60 ?g) nos dias 0, 2, 4 e 6 no experimento do efeito do material particulado ou nos dias dos desafios com OVA no experimento do efeito da administração de material particulado em animais com inflamação pulmonar induzida pela OVA. Os grupos controle foram tratados com solução salina 0,9 % seguindo o mesmo protocolo. Quarenta e oito horas após o último desafio, a responsividade pulmonar foi medida por broncoprovocação àr metacolina através da pletismografia de corpo inteiro, após a qual os animais foram sacrificados e tiveram os pulmões removidos para analise histológica. O estudo realizado com animais BALB/c para análise dos efeitos do material particulado sobre a resposta inflamatória induzida pela ovalbumina mostrou um aumento de responsividade nos animais inflamados e co-expostos ao material particulado, sem efeito sobre a inflamação ou remodelamento epitelial induzidos pela OVA. A exposição ao material particulado por si só levou a uma diminuição da área ocupada por células ciliadas e a um aumento da responsividade pulmonar. O experimento realizado com camundongos das linhagens AIRmax e AIRmin para estudar eventuais diferenças entre a resposta destas linhagens à inflamação pulmonar crônica induzida pela OVA mostrou uma maior susceptibilidade dos animais AIRmin, com maior infiltrado eosinofílico nas vias aéreas e responsividade pulmonar. Por outro lado, o estudo realizado para verificar a ação do material particulado nas linhagens AIRmax e AIRmin mostrou um intenso remodelamento epitelial, com infiltrado macrofágico ao redor das vias aéreas de ambas as linhagens, porém os animais AIRmin apresentaram maior responsividade pulmonar que os AIRmax quando expostos ao material particulado. Assim pudemos concluir que (1) a exposição ao material particulado na presença de inflamação pulmonar alérgica crônica amplifica o remodelamento epitelial e a responsividade pulmonar; o background genético influencia (2) a inflamação eosinofílica e a responsividade pulmonar induzidas pela inflamação alérgica crônica bem como (3) a responsividade pulmonar induzida pela exposição ao material particulado.In this study, three distinct experiments were performed (1) examining the effects of administration of particulate matter in BALB/c mice with chronic allergic pulmonary inflammation induced by ovalbumin; (2) comparing AIRmax and AIRmin mice with chronic allergic pulmonary inflammation induced by ovalbumin; (3) comparing AIRmax and AIRmin mice receiving particulate matter (residue from the burning of diesel oil - ROFA) intranasally. For the induction of chronic allergic pulmonary inflammation, the mice were sensitized to ovalbumin (OVA) through two intraperitoneal injections of allergen with adjuvant aluminum hydroxide (days 0 and 14) and four inhalations of OVA 1% (days 22, 24, 26 and 28). The animals that were exposed to particulate matter received ROFA (60 ?g) on days 0, 2, 4 and 6 in the study of the effect of the particulate matter or after the challenges with OVA in experiment of the effect of administration of particulate matter in animals with pulmonary inflammation induced by OVA. The control groups were treated with saline 0.9% following the same protocol. Forty eight hours after the last challenge, pulmonary responsiveness was measured through broncoprovocation to methacholine by whole body plethysmography, after which the animals were sacrificed and the lungs were removed for histologic analysis. The study conducted on animals BALB/c for analysis of the effects of particulate matter on the inflammatory response induced by ovalbumin showed an increase of responsiveness in animals with allergic inflammation and exposed to the particulate matter, without effects on inflammation or epithelial remodeling induced by OVA. Exposure to particulate matter led to a reduction in the area occupied by ciliated cells and increased lung responsiveness. The experiment in AIRmax AIRmin mice to study possible differences in the response of these strains to chronic lung inflammation induced by OVA showed greater susceptibility of AIRmin, with more eosinophilic infiltration in airway and greater lung responsiveness. The study to check the action of particulate matter in the lines AIRmax and AIRmin showed an intense epithelial remodeling, with macrophagic infiltrate around the airways of both strains. However, AIRmin mice had higher pulmonary responsiveness than AIRmax when exposed to particulate matter. We conclude that (1) exposure to particulate matter in the presence of chronic allergic pulmonary inflammation amplifies the epithelial remodeling and pulmonary responsiveness; the genetic background influences (2) the pulmonary responsiveness and eosinophilic inflammation induced by chronic allergic inflammation and (3) the pulmonary responsiveness induced by exposure to particulate matter

Cigarette Smoke Increases CD8α+ Dendritic Cells in an Ovalbumin-Induced Airway Inflammation

Asthma is an allergic lung disease and, when associated to cigarette smoke exposition, some patients show controversial signs about lung function and other inflammatory mediators. Epidemiologic and experimental studies have shown both increasing and decreasing inflammation in lungs of subjects with asthma and exposed to cigarette smoke. Therefore, in this study, we analyzed how cigarette smoke affects pro-inflammatory and anti-inflammatory mediators in a murine model of allergic pulmonary inflammation. We sensitized Balb/c mice to ovalbumin (OVA) with two intraperitoneal injections. After sensitization, the animals were exposed to cigarette smoke twice a day, 30 min per exposition, for 12 consecutive days. In order to drive the cell to the lungs, four aerosol challenges were performed every 48 h with the same allergen of sensitization. OVA sensitization and challenge developed pulmonary Th2 characteristic response with increased airway responsiveness, remodeling, increased levels of IgE, interleukin (IL)-4, and IL-13. Cigarette smoke, unexpectedly, reduced the levels of IL-4 and IL-13 and simultaneously decreased anti-inflammatory cytokines as IL-10 and transforming growth factor (TGF)-β in sensitized and challenged animals. OVA combined with cigarette smoke exposition decreased the number of eosinophils in bronchoalveolar lavage and increased the number of neutrophils in lung. The combination of cigarette smoke and lung allergy increased recruitment of lymphoid dendritic cells (DCs) into lymph nodes, which may be the leading cause to an increase in number and activation of CD8+ T cells in lungs. In addition, lung allergy and cigarette smoke exposure decreased an important regulatory subtype of DC such as plasmacytoid DC as well as its activation by expression of CD86, PDL2, and ICOSL, and it was sufficient to decrease T regs influx and anti-inflammatory cytokines release such as IL-10 and TGF-β but not enough to diminish the structural changes. In conclusion, we observed, in this model, that OVA sensitization and challenge combined with cigarette smoke exposure leads to mischaracterization of the Th2 response of asthma by decreasing the number of eosinophils, IL-4, and IL-13 and increasing number of neutrophils, which is related to the increased number of CD8ɑ+ DCs and CD8+ T cells as well as reduction of the regulatory cells and its released cytokines