18F-FDG-PET/CT in diagnosis of Q fever endocarditis

info:eu-repo/semantics/publishedVersio

Reliability of a questionnaire for diagnosing the severity of temporomandibular disorder

CONTEXTUALIZAÇÃO: Disfunção temporomandibular (DTM) é um termo coletivo que engloba vários problemas clínicos envolvendo a musculatura da mastigação, as articulações temporomandibulares (ATM) e suas estruturas associadas, com alta prevalência nas populações. OBJETIVOS: Sabendo-se que estudos brasileiros vêm utilizando o instrumento proposto por Da Fonseca et al. (1994) para diagnóstico da severidade desta disfunção, realizou-se este estudo com o objetivo de verificar e estimar a consistência interna e a reprodutibilidade do mesmo. MÉTODOS: O delineamento amostral adotado foi o probabilístico, e participaram 1230 indivíduos moradores da cidade de Ribeirão Preto (SP), maiores de 18 anos de idade. As entrevistas foram realizadas por um único entrevistador por meio de ligações telefônicas. Para estudo da consistência interna, calculou-se o Coeficiente de Kuder-Richardson (kr-20) e para estimar a reprodutibilidade, utilizou-se a estatística Kappa (κ). RESULTADOS: A consistência interna do formulário foi de 0,5594, apontando para uma validação abaixo do desejado. Observou-se maior contribuição das questões 1, 2, 3, 6 e 7 para o coeficiente kr-20 total e maior consistência do instrumento quando composto apenas pelas mesmas (0,7044). Observou-se reprodutibilidade "Boa" e "Ótima" para as questões. CONCLUSÕES: Frente ao exposto, sugere-se que o formulário proposto por Da Fonseca et al. (1994) seja adaptado, ficando composto apenas pelas questões 1, 2, 3, 6 e 7 da versão inicial, colaborando, assim, para aumento da confiabilidade do instrumento. Deve-se ressaltar ainda a necessidade da realização de estudos de validade para assegurar adequadas características psicométricas à nova versão do instrumento.BACKGROUND: Temporomandibular disorder (TMD) is a collective term that encompasses many clinical problems involving the masticatory muscles, temporomandibular joints (TMJ) and associated structures and it has high prevalence among populations. OBJECTIVES: Because Brazilian studies have used the instrument proposed by Da Fonseca et al. (1994) to diagnose the severity of TMD, this study was conducted to investigate and estimate the internal consistency and reproducibility of this method. METHODS: We used a probability sampling design to select 1230 participants over the age of 18 years who were living in the city of Ribeirão Preto, SP, Brazil. The interviews were conducted by a single interviewer over the phone. The internal consistency was analyzed by calculating the Kuder-Richardson coefficient (kr-20), and kappa statistics (κ) were used to estimate the reproducibility. RESULTS: The internal consistency of the questionnaire was 0.5594, thus indicating that validation was lower than desired. Questions 1, 2, 3, 6 and 7 had greater contribution towards the total kr-20 coefficient, and the consistency of the instrument was higher when it was composed only of these questions (0.7044). "Good" and "Excellent" reproducibility was observed for these same questions. CONCLUSIONS: Based on these data, it is suggested that the questionnaire proposed by Da Fonseca et al. (1994) should be adapted to include only questions 1, 2, 3, 6 and 7 of the initial version. This would help improve the reliability of the instrument. The need for validation studies must also be emphasized to ensure that the new version of the instrument has adequate psychometric characteristics

Impact of carvedilol on the mitochondrial damage induced by hypoxanthine and xantine oxidase: what role in myocardial ischemia and reperfusion?

OBJECTIVES: The cardioprotective effects of carvedilol (CV) may be explained in part by interactions with heart mitochondria. The objective of this work was to study the protection afforded by CV against oxidative stress induced in isolated heart mitochondria by hypoxanthine and xanthine oxidase (HX/XO), a well-known source of reactive oxygen species (ROS) in the cardiovascular system. METHODS: Mitochondria were isolated from Wistar rat hearts (n = 8) and incubated with HX/XO in the presence and in the absence of calcium. Several methods were used to assess the protection afforded by CV: evaluation of mitochondrial volume changes (by measuring changes in the optical density of the mitochondrial suspension), calcium uptake and release (with a fluorescent probe, Calcium Green 5-N) and mitochondrial respiration (with a Clark-type oxygen electrode). RESULTS: CV decreased mitochondrial damage associated with ROS production by HX and XO, as verified by the reduction of mitochondrial swelling and increase in mitochondrial calcium uptake. In the presence of HX and XO, CV also ameliorated mitochondrial respiration in the active phosphorylation state and prevented decrease in the respiratory control ratio (p < 0.05) and in mitochondrial phosphorylative efficiency (p < 0.001). CONCLUSIONS: The data indicate that CV partly protected heart mitochondria from oxidative damage induced by HX and XO, which may be useful during myocardial ischemia and reperfusion. It is also suggested that mitochondria may be a priority target for the protective action of some compounds

Coffee shops, a hub for TB clusters?

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An investigation of TB infection and reinfection among stone quarry workers

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Advantages in the use of carvedilol versus propranolol for the protection of cardiac mitochondrial function

BACKGROUND: Carvedilol is a neurohormonal antagonist of multiple action which is used in clinical practice for the treatment of congestive heart failure, mild to moderate hypertension and myocardial infarction. Previous results from our group have demonstrated that one of the main targets for the protective effect of carvedilol is the cardiac mitochondrial network. In-this work, we compare the effect of carvedilol with propranolol in different models of mitochondrial dysfunction and in the generation of transmembrane electric potential (EP). We further tested if carvedilol was able to inhibit the mitochondrial permeability transition (MPT) induced by doxorubicin and calcium-dependent cytochrome c release, a phenomenon frequently associated with apoptotic cell death. METHODS: Cardiac mitochondria were isolated by differential centrifugation. Oxygen consumption and mitochondrial EP were determined using an oxygen electrode and a tetraphenylphosphonium-sensitive electrode, respectively. Changes in mitochondrial volume and the release of cytochrome c were measured with spectrophotometric techniques. RESULTS: Propranolol, compared with carvedilol, had only a marginal effect, not only in protection against MPT induction, but also against oxygen consumption linked to the oxidation of external NADH, a process that is considered by several authors as key in the cardiotoxicity of doxorubicin. Regarding EP generation, propranolol had no effect, in contrast to carvedilol, which was confirmed to act as a protonophore. For the first time we also show that carvedilol inhibits the MPT induced by doxorubicin and calcium-dependent cytochrome c release. CONCLUSIONS: With this work, we further support the notion that carvedilol is effective in several models of mitochondrial dysfunction, particularly those involving oxidative stress. The results demonstrate that for some pathological conditions, carvedilol and propranolol have different mechanisms of action at the sub-cellular level, as propranolol seems to lack effectiveness in the protection of cardiac mitochondria

Dynamic Quantile Linear Models: A Bayesian Approach

The paper introduces a new class of models, named dynamic quantile linear models, which combines dynamic linear models with distribution-free quantile regression producing a robust statistical method. Bayesian estimation for the dynamic quantile linear model is performed using an efficient Markov chain Monte Carlo algorithm. The paper also proposes a fast sequential procedure suited for high-dimensional predictive modeling with massive data, where the generating process is changing over time. The proposed model is evaluated using synthetic and well-known time series data. The model is also applied to predict annual incidence of tuberculosis in the state of Rio de Janeiro and compared with global targets set by the World Health Organization

Modulation of CD4 T cell function via CD6-targeting

In recent years molecules involved on the immune synapse became successful targets for therapeutic immune modulation. CD6 has been extensively studied, yet, results regarding CD6 biology have been controversial, in spite of the ubiquitous presence of this molecule on virtually all CD4 T cells. We investigated the outcome of murine and human antibodies targeting CD6 domain 1. We found that CD6-targeting had a major impact on the functional specialization of CD4 cells, both human and murine. Differentiation of CD4 T cells towards a Foxp3+ Treg fate was prevented with increasing doses of anti-CD6, while Th1 polarization was favoured. No impact was observed on Th2 or Th17 specialization. These in vitro results provided an explanation for the dose-dependent outcome of in vivo anti-CD6 administration where the anti-inflammatory action is lost at the highest doses. Our data show that therapeutic targeting of the immune synapse may lead to paradoxical dose-dependent effects due to modification of T cell fate.Funded by UID/BIM/50005/2019, project funded by Fundação para a Ciência e a Tecnologia (FCT) / Ministério da Ciência, Tecnologia e Ensino Superior (MCTES) throught Fundos do Orçamento do Estado, pela Fundação para a Ciência e a Tecnologia (FCT) ( PTDC/DTP-FTO/3080/2014 ); and by the project SRecognite Infect - ERA/0003/2015 using national funds through FCT . Funders did not have a role in study design, data collection, analysis, and interpretation, or in the writing of the manuscript

The Effects of Dasatinib in Experimental Acute Respiratory Distress Syndrome Depend on Dose and Etiology

Background/Aims: Evidence suggests that tyrosine-kinase inhibitors may attenuate lung inflammation and fibrosis in experimental acute respiratory distress syndrome (ARDS). We hypothesized that dasatinib, a tyrosine-kinase inhibitor, might act differently depending on the ARDS etiology and the dose. Methods: C57/BL6 mice were divided to be pre-treated with dasatinib (1mg/kg or 10mg/kg) or vehicle (1% dimethyl-sulfoxide) by oral gavage. Thirty-minutes after pre-treatment, mice were subdivided into control (C) or ARDS groups. ARDS animals received Escherichia coli lipopolysaccharide intratracheally (ARDSp) or intraperitoneally (ARDSexp). A new dose of dasatinib or vehicle was administered at 6 and 24h. Results: Forty-eight hours after ARDS induction, dasatinib 1mg/kg yielded: improved lung morphofunction and reduced cells expressing toll-like receptor (TLR)-4 in lung, independent of ARDS etiology; reduced neutrophil and levels of interleukin (IL)-6, IL-10 and transforming growth factor (TGF)-β in ARDSp. The higher dose of dasatinib caused no changes in lung mechanics, diffuse alveolar damage, neutrophil, or cells expressing TLR4, but increased IL-6, vascular endothelial growth factor (VEGF), and cells expressing Fas receptor in lung in ARDSp. In ARDSexp, it improved lung morphofunction, increased VEGF, and reduced cells expressing TLR4. Conclusion: Dasatinib may have therapeutic potential in ARDS independent of etiology, but careful dose monitoring is required. © 2015 S. Karger AG, Basel