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.


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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.


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.


Lysandropoulos A.P.,Erasmus University College Brussels | Havrdova E.,Charles University
European Journal of Neurology | Year: 2015

Traditional outcome measures for patients with multiple sclerosis (MS), whether in clinical trials or clinical practice, are currently in question. The combination of relapses, physical disability progression and magnetic resonance imaging (MRI) disease activity reflect only part of the impact that MS has on a patient's daily life. Quality of life (QoL) is considered by many to be the ideal outcome measure. Since it captures the patient's own perspective of well-being, QoL should be the primary focus when evaluating a patient and the main objective of MS management. Nevertheless, whilst numerous instruments to measure QoL in MS patients are available or proposed, there is no current consensus regarding which is the best tool to use and under what circumstances. QoL in patients with MS is determined by several factors beyond the more obvious; these include coping with the MS diagnosis, understanding the disease and the disease process, dealing with so-called 'hidden' symptoms such as fatigue, cognitive impairment and sexual disturbances, and managing the many associated personal challenges such as social isolation, family issues and working difficulties. Evidence is emerging that psychological interventions may be beneficial in MS patients although more research is required to confirm their utility. This article examines some factors that influence QoL in MS patients which may be overlooked in the general busyness of routine clinical practice. © 2015 European Academy of Neurology.


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.


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.


Soupart A.,Jolimont Tubize Hospital | Soupart A.,Erasmus University College Brussels | Coffernils M.,Jolimont Tubize Hospital | Couturier B.,Erasmus University College Brussels | And 2 more authors.
Clinical Journal of the American Society of Nephrology | Year: 2012

Background and objectives Vaptans (vasopressin V 2-receptor antagonists) are a new approach for the treatment of hyponatremia. However, their indications remain to be determined, and their benefit compared with that of the usual treatments for the syndrome of inappropriate antidiuretic hormone secretion (SIADH) have not been evaluated. This prospective, long-term study compared the efficacy, tolerability, and safety of two oral vaptans with those of oral urea in patients with SIADH. Design, setting, participants, & measurements Patients with chronic SIADH of various origins were treated first with vaptans for 1 year. After an 8-day holiday period, they received oral urea for an additional 1-year follow-up. Serum sodium was measured every 2 months, and drug doses were adjusted accordingly. Results Thirteen participants were initially included in the study (serum sodium, 125±3 mEq/L); 12 completed the 2-year treatment period. Treatment with vaptans (satavaptan, 5-50 mg/d, n=10; tolvaptan, 30-60 mg/day, n=2) increased natremia (serum sodium, 135±3 mEq/L) during the 1-year vaptan period without escape. Hyponatremia recurred in the 12 participants when vaptans were stopped (holiday period). Urea improved the natremia with the same efficacy (serum sodium, 135±2 mEq/L) as vaptans during the 1-year urea treatment period. One participant treated with tolvaptan withdrew from the study early because of excessive thirst. Another patient receiving urea developed hypernatremia without complications. Conclusions Urea has efficacy similar to that of vaptans for treatment of chronic SIADH. Tolerance is generally good for both agents. © 2012 by the American Society of Nephrology.


Taccone F.S.,Erasmus University College Brussels | Citerio G.,NeuroIntensive Care Unit
Neurocritical Care | Year: 2014

Hemodynamic monitoring is widely used in critical care; however, the impact of such intervention in patients with acute brain injury (ABI) remains unclear. Using PubMed, a systematic review was performed (1966–August 2013), and 118 studies were included. Data were extracted using the PICO approach. The evidence was classified, and recommendations were developed according to the GRADE system. Electrocardiography and invasive monitoring of arterial blood pressure should be the minimal hemodynamic monitoring required in unstable or at-risk patients in the intensive care unit. Advanced hemodynamic monitoring (i.e., assessment of preload, afterload, cardiac output, and global systemic perfusion) could help establish goals that take into account cerebral blood flow and oxygenation, which vary depending on diagnosis and disease stage. Choice of techniques for assessing preload, afterload, cardiac output, and global systemic perfusion should be guided by specific evidence and local expertise. Hemodynamic monitoring is important and has specific indications among ABI patients. Further data are necessary to understand its potential for therapeutic interventions and prognostication. © 2014, Springer Science+Business Media New York.


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.


Montesinos I.,Erasmus University College Brussels | Eykmans J.,Erasmus University College Brussels | Delforge M.-L.,Erasmus University College Brussels
Journal of Clinical Virology | Year: 2014

Objectives: We have evaluated the recently Conformité Européenne (CE)-marked Bio-Rad Geenius human immunodeficiency virus (HIV)1/2 as a rapid and simple alternative to western blot for confirmation of HIV screening results. Methods: A total of 160 serum samples were tested: 44 HIV-1 reactive samples by a fourth-generation Murex HIV Ag/Ab and/or Vidas HIV Duo Ultra, five HIV-2 reactive samples, 15 HIV-1 non-B subtype samples and 11 confirmed HIV-1 early seroconversion samples, 72 nonreactive samples, eight indeterminate samples by MP HIV BLOT 2.2 confirmed negative after follow-up and five low-reactive samples by enzyme immunoassay (EIA) negative by MP HIV BLOT 2.2. The samples were tested according to the manufacturer's guidelines. Results: The overall sensitivity for Bio-Rad Geenius HIV1/2 assay was 92%. Five out of 11 early seroconversion samples were tested positive, four negative and two indeterminate. All HIV-1 non-B subtype samples were tested positive. Two out of the five HIV-2 reactive samples were tested positive HIV-2, two positive HIV-2 with HIV-1 cross-reaction and one HIV positive untypable. After excluding early seroconversion samples, the sensitivity of Bio-Rad Geenius HIV1/2 assay reached 100%. Overall specificity was 96%. All HIV negative serums by fourth-generation EIA were tested negative. All five low-reactive samples by EIA, negative by HIV BLOT 2.2 were tested negative by Bio-Rad Geenius HIV1/2. Two out of the eight indeterminate samples by MP HIV BLOT 2.2 that were confirmed negative after follow-up were tested indeterminate and one invalid, the other five were negative. After excluding these last 13 samples, the specificity of Bio-Rad Geenius HIV1/2 assay reached 100%. In comparison with MP HIV BLOT 2.2, the Bio-Rad Geenius HIV1/2 assay was markedly time saving, allowed full traceability, automatic reading and interpretation. Conclusions: The Bio-Rad Geenius HIV1/2 confirmatory system represents a reliable alternative to other confirmatory assays in HIV testing algorithms and provides clear improvement in quality management. © 2014 Elsevier B.V.


Eizirik D.L.,Free University of Colombia | Cnop M.,Free University of Colombia | Cnop M.,Erasmus University College Brussels
Science Signaling | Year: 2010

Secretory cells, such as pancreatic β cells, face the challenge of increasing protein synthesis severalfold during acute or chronic stimulation. This poses a burden on the endoplasmic reticulum (ER), the organelle where proinsulin synthesis and folding takes place. Thus, β cells use various adaptive mechanisms to adjust the functional capacity of the ER to the prevailing demand. These check-and-balance mechanisms are collectively known as the unfolded protein response (UPR). It remains unclear how UPR signaling is ultimately regulated and what delineates the boundaries between a physiological and a pathological response. New discoveries point to the divergent effects of acute and chronic metabolic fluxes and chemical ER stressors on the formation of complexes among UPR transducers, scaffold proteins, and phosphatases. These and other findings provide a first glimpse on how different signals trigger diverging UPR outcomes. Copyright 2008 the American Association for the Advancement of Science; all rights reserved.

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