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Brussels, Belgium

The Erasmushogeschool Brussel is an institute of higher education based in Brussels, Belgium.Like the EU student exchange programme ERASMUS, Erasmus University College Brussels is named after the humanistic philosopher and author Desiderius Erasmus, who resided in Anderlecht, a municipality of Brussels. Wikipedia.


Cnop M.,Free University of Colombia | Cnop M.,Erasmus University College Brussels | Foufelle F.,University Pierre and Marie Curie | Velloso L.A.,University of Campinas
Trends in Molecular Medicine | Year: 2012

The endoplasmic reticulum (ER) stress response, also commonly known as the unfolded protein response (UPR), is an adaptive response used to align ER functional capacity with demand. It is activated in various tissues under conditions related to obesity and type 2 diabetes. Hypothalamic ER stress contributes to inflammation and leptin/insulin resistance. Hepatic ER stress contributes to the development of steatosis and insulin resistance, and components of the UPR regulate liver lipid metabolism. ER stress in enlarged fat tissues induces inflammation and modifies adipokine secretion, and saturated fats cause ER stress in muscle. Finally, prolonged ER stress impairs insulin synthesis and causes pancreatic β cell apoptosis. In this review, we discuss ways in which ER stress operates as a common molecular pathway in the pathogenesis of obesity and diabetes. © 2011 Elsevier Ltd. Source


Cnop M.,Free University of Colombia | Cnop M.,Erasmus University College Brussels | Mulder H.,Lund University | Igoillo-Esteve M.,Free University of Colombia
Journal of Neurochemistry | Year: 2013

Diabetes is a common metabolic disorder in patients with Friedreich ataxia. In this Supplement article, we review the clinical data on diabetes in Friedreich ataxia, and the experimental data from rodent and in vitro models of the disease. Increased body adiposity and insulin resistance are frequently present in Friedreich ataxia, but pancreatic β cell dysfunction and death are a conditio sine qua non for the loss of glucose tolerance and development of diabetes. The loss of frataxin function in mitochondria accounts for these pathogenic processes in Friedreich ataxia. Mitochondria are essential for the sensing of nutrients by the β cell and for the generation of signals that trigger and amplify insulin secretion, known as stimulus-secretion coupling. Moreover, in the intrinsic pathway of apoptosis, pro-apoptotic signals converge on mitochondria, resulting in mitochondrial Bax translocation, membrane permeabilization, cytochrome c release and caspase cleavage. How and at which level frataxin deficiency impacts on these processes in β cells is only partially understood. A better understanding of the molecular mechanisms mediating β cell demise in Friedreich ataxia will pave the way for new therapeutic approaches. © 2013 International Society for Neurochemistry. Source


Eizirik D.L.,Laboratory of Experimental Medicine | Cnop M.,Laboratory of Experimental Medicine | Cnop M.,Erasmus University College Brussels
Cell Metabolism | Year: 2012

Pancreatic β cell failure is central in the pathogenesis of type 2 diabetes (T2D), but the mechanisms involved remain unclear. Mahdi and colleagues (2012) couple global evaluation of gene expression with coexpression network analysis of human islets from T2D patients to identify SFRP4 as an early mediator of b cell dysfunction in T2D. © 2012 Elsevier Inc. Source


Velloso L.A.,University of Campinas | Eizirik D.L.,Laboratory of Experimental Medicine | Cnop M.,Erasmus University College Brussels
Nature Reviews Endocrinology | Year: 2013

Inflammation-induced inhibition of the insulin signalling pathway can lead to insulin resistance and contribute to the development of type 2 diabetes mellitus (T2DM). Obesity and insulin resistance are associated with a chronic but subclinical inflammatory process that impairs insulin action in most tissues and could also hamper pancreatic β-cell function. The involvement of monocytic cells and the profiles of the chemokines and cytokines induced by this inflammation suggest an innate immune response. However, emerging data indicate that elements of the adaptive immune system could also be involved. As activation of an adaptive response requires antigen specificity, some researchers have hypothesized that T2DM evolves from an innate immune response to an autoimmune condition. In this Perspectives article, we present the arguments for and against this hypothesis and discuss which mechanisms could be involved in a putative switch from innate immunity to autoimmunity. © 2013 Macmillan Publishers Limited. Source


Kovacs G.,Medical University of Graz | Kovacs G.,Ludwig Boltzmann Research Institute | Avian A.,Medical University of Graz | Avian A.,Ludwig Boltzmann Research Institute | And 4 more authors.
American Journal of Respiratory and Critical Care Medicine | Year: 2014

The accuracy of pulmonary vascular pressure measurements is of great diagnostic and prognostic relevance. However, there is variability of zero leveling procedures, and the current recommendation of end-expiratory reading may not always be adequate. A review of physiological and anatomical data, supported by recent imaging, leads to the practical recommendation of zero leveling at the cross-section of three transthoracic planes, which are, respectively midchest frontal, transverse through the fourth intercostal space, and midsagittal. As for the inevitable respiratory pressure swings, end-expiratory reading at functional residual capacity allows for minimal influence of elastic lung recoil on pulmonary pressure reading. However, hyperventilation is associated with changes in end-expiratory lung volume and increased intrathoracic pressure, eventually exacerbated by expiratory muscle contraction and dynamic hyperinflation, all increasing pulmonary vascular pressures. This problem is amplified in patients with obstructed airways. With the exception of dynamic hyperinflation states, it is reasonable to assume that negative inspiratory and positive expiratory intrathoracic pressures cancel each other out, so averaging pulmonary vascular pressures over several respiratory cycles is most often preferable. This recommendation may be generalized for the purpose of consistency and makes sense, as pulmonary blood flow measurements are not corrected for phasic inspiratory and expiratory changes in clinical practice. Copyright © 2014 by the American Thoracic Society. Source

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