Introdução: O número de indivíduos com sobrepeso e obesidade está aumentando, e a busca por entender mecanismo relacionados a esta doença se mostram cada vez mais importantes. O gene FTO foi o primeiro gene associado à obesidade, mas não se sabe muito a respeito de como é regulado e suas vias. MiRs são pequenos RNAs regulatórios que podem estar associados à obesidade, como também na regulação do gene FTO. Dessa forma, pretendemos identificar a relação do gene FTO e do hsamir-150 com sobrepeso/obesidade, perfil lipídico e glicemia de jejum. Métodos: Homens e mulheres (18 anos ou mais), com IMC > 25 kg/m2 participaram do presente estudo e foram analisadas a expressão do gene FTO, expressão do mir-150, parâmetros bioquímicos do sangue e antropometria. Resultados: Observamos a expressão do gene FTO estar relacionada à obesidade, LDL e glicemia de jejum. Conclusão: O gene FTO parece de fato estar relacionado à obesidade, LDL e glicemia de jejum, diferentemente do mir-150 / Introduction: The overweight population is growing in the entire world, and the search for obesity-associated mechanisms is important for a better understanding of this disease. The FTO gene was the first obesity associated gene. Otherwise, its pathways and how it can be regulated remain unknown. MiRs are small no coding RNAs that may be associated to obesity and FTO gene regulation. Thus, the aim of this study was to verify the relationship among the FTO gene and the mir-150 expression with overweight/obesity lipid profile and fast blood glucose. Methods: Men and woman (18 years older or above), with body mass index > 25 Kg/m2, were enrolled in the present work and the FTO gene and mir-150 expression, biochemical parameters of blood and anthropometric measure were analyzed. Results: The results highlight that the FTO gene expression is associated to obesity, LDL and fasting blood glucose. Conclusion: Indeed, the FTO gene seems to be related to obesity, LDL and blood fasting glucose, differently of the mir-150

Lymphomas are heterogenous class of diseases characterized by proliferation of a malignant lymphocyte clone. MicroRNA miR-155 was found to be a key molecule in immune response, namely in inflammation and germinal reaction of B cells. On the other hand, miR-155 can drive lymphoproliferation in mouse and its levels were found to be elevated in certain lymphoma types in human. MiR-155 down-regulates expression of its target gene PU.1, a hematopoietic transcription factor important for B cell differentiation. Expression of the gene encoding miR-155, known as MIR155HG, is controled by several transcription factors, among them MYB, a member of an oncogenic E-box protein family. Levels of MYB itself are controled by microRNA miR-150. In this study, we measured levels of miR-155, PU.1, MYB and miR-150 in lymph nodes of patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (B-CLL/SLL, N=20), diffuse large B-cell lymphoma (DLBCL, N=24), follicular lymphoma (FL, N=29), Hodgkin lymphoma (HL, N=25), marginal zone lymphoma (MZL, N=13), and mantle cell lymphoma (MCL, N=10). We also measured levels of these molecules in lymph nodes with the finding of strong inflammation (N=4). We found that patients of all the diagnoses except of MCL display heterogeneously elevated levels of miR-155 and correspondingly...

L’encéphalomyélite myalgique (EM) est une maladie complexe, multi-systémique et débilitante, dont l’étiologie est inconnue. D’une personne atteinte d’encéphalomyélite myalgique (PAEM) à l’autre, les symptômes varient en fréquence et en sévérité créant ainsi une grande hétérogénéité clinique entre les individus. Un sous-groupe de PAEM vivent des épisodes d’intolérance orthostatique (IO) ou vivent avec une comorbidité de syndrome de tachycardie orthostatique posturale (POTS), deux conditions qui sont mal comprises. Le malaise après-effort (PEM), un des symptômes phare de l’EM, survient après une activité physique ou mentale minimale. Le malaise après-effort entraîne une dégradation générale de l’état de l’individu, peut entraîner une exacerbation des autres symptômes et va durer de plusieurs heures à plusieurs jours. Chez les individus souffrant de POTS ou d’IO, le malaise après-effort peut déclencher des épisodes d’intolérance orthostatique. Le gène SLC6A2 codant pour le transporteur de norépinephrine NET a été identifié comme potentiel mécanisme dans pathophysiologie du POTS, tout comme les protéines impliquées dans la vasodilatation, comme la thrombospondine-1 (TSP-1). Notre laboratoire a identifié un panel de onze microARN (miARN) exprimés différentiellement chez les PAEM. Parmi ceux-ci, le miR-150-5p a comme cible prédite SLC6A2. Notre hypothèse était qu’une plus grande expression du miR-150-5p après un effort ou qu’une chute de thrombospondine-1 pourrait induire une vasodilatation soudaine contribuant aux symptômes d’IO ou de POTS. Nous avons mesuré les niveaux plasmatiques du miR-150-5p et de TSP-1 avant (T0) et après (T90) l’induction du malaise après-effort chez des PAEM avec POTS/IO (n = 20), chez des PAEM sans POTS/IO (n = 117) et chez des témoins sédentaires associés pour le sexe et l’âge (n = 48). Nous avons démontré que les sujets atteints de POTS/IO avaient des niveau plus importants du miR-150-5p et des symptômes plus sévères. Finalement, nous avons également utilisé la veste intelligente Hexoskin (Carré Technologies Inc., Montreal, Qué., Canada) pour suivre un sous-groupe d’individus (n = 10) sur une plus longue période après l’induction du malaise après-effort. Avec cet outil, nous avons pu monitorer les symptômes au quotidien, permettant un meilleur suivi clinique de ces patients. Ce projet de maîtrise a permis une meilleure compréhension de la pathophysiologie de l’EM et de celle du POTS. / Myalgic encephalomyelitis (ME) is a complex chronic disease with debilitating smyptoms and unknown etiology. Symptoms vary in frequency and severity from a person with ME (PwME) to another, thus creating a highly clinically heterogeneous patient population. Some PwME also experience orthostatic intolerance (OI) episodes or live with a comorbidity of postural orthostatic tachycardia syndrome (POTS), two conditions that are not well understood. Post-exertional malaise (PEM) causes patients to experience a worsening of their symptoms following an effort, whether it be physical or mental. PEM can last from a few hours to several days. In PwME with POTS/OI, PEM can trigger orthostatic intolerance episodes. SLC6A2 is a gene coding for the norepinephrine transporter NET. Its contribution to the POTS pathophysiology has been mentioned several times in literature. A biochemical milieu prone to vasodilation was also reported as a contributing element to POTS pathophysiology. Recently, our laboratory published an article identifying a panel of eleven microRNAs (miRNAs) differentially expressed in PwME. Among these miRNAs, miR-150-5p has been predicted to target SLC6A2. Our hypothesis was that higher expression of miR-150-5p following an effort or a decrease in circulating thrombospondin-1 (TSP-1) inducing vasodilation could contribute to POTS/OI symptoms. We measured circulating levels of miR-150-5p and TSP-1 before (T0) and after (T90) PEM induction in PwME (n = 117), PwME with POTS/OI (n = 20) and age and sex matched sedentary controls (n = 48). We demonstrated that PwME with POTS/OI have higher levels of miR-150-5p at both T0 and T90, while also having more severe symptoms. Furthermore, we used the connected vest Hexoskin (Carré Technologies Inc., Montreal, Qué., Canada) to follow a subgroup (n = 10) of patients for a longer period following PEM induction. With this tool, we were able to monitor symptoms on a daily basis, allowing better clinical follow-up. Overall, this project allowed better understanding of ME and POTS’ pathophysiology.