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Rose C.F.,Center Hospitalier Of Luniversitede Montreal Crchum | Verkhratsky A.,University of Manchester | Parpura V.,University of Manchester | Parpura V.,University of Alabama at Birmingham | Parpura V.,University of Rijeka
Biochemical Society Transactions | Year: 2013

The multifunctional properties of astrocytes signify their importance in brain physiology and neurological function. In addition to defining the brain architecture, astrocytes are primary elements of brain ion, pH and neurotransmitter homoeostasis. GS (glutamine synthetase), which catalyses the ATP-dependent condensation of ammonia and glutamate to form glutamine, is an enzyme particularly found in astrocytes. GS plays a pivotal role in glutamate and glutamine homoeostasis, orchestrating astrocyte glutamate uptake/release and the glutamate-glutamine cycle. Furthermore, astrocytes bear the brunt of clearing ammonia in the brain, preventing neurotoxicity. The present review depicts the central function of astrocytes, concentrating on the importance of GS in glutamate/glutamine metabolism and ammonia detoxification in health and disease. © 2013 Biochemical Society. Source


Deng A.Y.,Center Hospitalier Of Luniversitede Montreal Crchum
Journal of Hypertension | Year: 2015

Essential hypertension is one of the most common disorders that underpin significant morbidity and mortality; however, underlying mechanisms remain elusive that either dictate the actions of individual quantitative trait loci (QTLs) or engineer the overall genetic architecture from them. Recent experimental evidence has unveiled that the genetic architecture determining blood pressure (BP) is assembled from QTL-building blocks by epistasis into regulatory hierarchies. BP, a polygenic and quantitative trait, is homeostasized via pathways participated by Mendelian constituents that operate distantly from endphase physiological genes. Epistasis genetics performed in the current article has mechanistically unravelled the order and regulatory relationships between certain BP QTLs, and is the first study ever conducted in a mammalian system in analysing a complex trait. The elucidation of the sequence of event and regulatory hierarchies of QTL actions in these pathways will facilitate mechanism-based diagnoses and cause-driven treatments for essential hypertension. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source


Lacasse A.,University of Quebec at Abitibi - Temiscamingue | Lacasse A.,Center Hospitalier Of Luniversitede Montreal Crchum | Ware M.A.,McGill University | Bourgault P.,Center Hospitalier Of Luniversitede Montreal Chum | And 7 more authors.
Clinical Journal of Pain | Year: 2016

Objectives: The validity of studies conducted with patient registries depends on the accuracy of the self-reported clinical data. As of now, studies about the validity of self-reported use of analgesics among chronic pain (CP) populations are scarce. The objective of this study was to assess the accuracy of self-reported prescribed analgesic medication use. This was attained by comparing the data collected in the Quebec Pain Registry (QPR) database to those contained in the Quebec administrative prescription claims database (Regie de l'assurance maladie du Quebec [RAMQ]). Methods: To achieve the linkage between the QPR and the RAMQ databases, the first 1285 patients who were consecutively enrolled in the QPR between October 31, 2008 and January 27, 2010 were contacted by mail and invited to participate in a study in which they had to provide their unique RAMQ health insurance number. Using RAMQ prescription claims as the reference standard, k coefficients, sensitivity, specificity, and their respective 95% confidence intervals were calculated for each therapeutic class of prescribed analgesic drugs that the participants reported taking currently and in the past 12 months. Results: A total of 569 QPR patients responded to the postal mailing, provided their unique health insurance number, and gave informed consent for the linkage (response proportion=44%). Complete RAMQ prescription claims over the 12 months before patient enrollment into the QPR were available for 272 patients, who constituted our validated study population. Regarding current self-reported prescribed analgesic use, k coefficients measuring agreement between the 2 sources of information ranged from 0.66 to 0.78 for COX-2-selective nonsteroidal anti-inflammatory drugs, anticonvulsants, antidepressants, skeletal muscle relaxants, synthetic cannabinoids, opiate agonists/partial agonists/antagonists, and antimigraine agents therapeutic classes. For the past 12-month self-reported prescribed analgesic use, QPR patients were less accurate regarding anticonvulsants (k=0.59), opiate agonists/partial agonists/antagonists (k=0.57), and antimigraine agents use (k=0.39). Discussion: Information about current prescribed analgesic medication use as reported by CP patients was accurate for the main therapeutic drug classes used in CP management. Accuracy of the past year self-reported prescribed analgesic use was somewhat lower but only for certain classes of medication, the concordance being good on all the others. © 2016 Wolters Kluwer Health, Inc. All rights reserved. Source


Maille E.,Center Hospitalier Of Luniversitede Montreal Crchum | Maille E.,University of Montreal | Trinh N.T.N.,Center Hospitalier Of Luniversitede Montreal Crchum | Trinh N.T.N.,University of Montreal | And 7 more authors.
American Journal of Physiology - Lung Cellular and Molecular Physiology | Year: 2011

Chronic infection and inflammation have been associated with progressive airway epithelial damage in patients with cystic fibrosis (CF). However, the effect of inflammatory products on the repair capacity of respiratory epithelia is unclear. Our objective was to study the regulation of repair mechanisms by tumor necrosis factor-α (TNF-α), a major component of inflammation in CF, in a model of mechanical wounding, in two bronchial cell lines, non-CF NuLi and CF CuFi. We observed that TNF-α enhanced the NuLi and CuFi repair rates. Chronic exposure (24-48 h) to TNF-α augmented this stimulation as well as the migration rate during repair. The cellular mechanisms involved in this stimulation were then evaluated. First, we discerned that TNF-α induced metalloproteinase-9 release, epidermal growth factor (EGF) shedding, and subsequent EGF receptor transactivation. Second, TNF-α-induced stimulation of the NuLi and CuFi wound-closure rates was prevented by GM6001 (metalloproteinase inhibitor), EGF antibody (to titrate secreted EGF), and EGF receptor tyrosine kinase inhibitors. Furthermore, we recently reported a relationship between the EGF response and Kα channel function, both controlling bronchial repair. We now show that TNF-α enhances KvLQT1 and KATP currents, while their inhibition abolishes TNF-α-induced repair stimulation. These results indicate that the effect of TNF-α is mediated, at least in part, through EGF receptor transactivation and Kα channel stimulation. In contrast, cell proliferation during repair was slowed by TNF-α, suggesting that TNF-α could exert contrasting actions on repair mechanisms of CF airway epithelia. Finally, the stimulatory effect of TNF-α on airway wound repair was confirmed on primary airway epithelial cells, from non-CF and CF patients. © 2011 by the American Physiological Society. Source


Danalache B.A.,Center Hospitalier Of Luniversitede Montreal Crchum | Yu C.,Center Hospitalier Of Luniversitede Montreal Crchum | Gutkowska J.,Center Hospitalier Of Luniversitede Montreal Crchum | Gutkowska J.,University of Montreal | And 2 more authors.
Journal of Endocrinology | Year: 2014

The functional oxytocin (OT) system is expressed in the human and rodent hearts. OT stimulates differentiation of cardiac stem cells into contracting cardiomyocytes (CM). In this study, we investigated OT receptors (OTR) expressed in the cells of cardiac side population (SP) and the abilities of these cells to differentiate into CM in response to the treatment with OT-Gly-Lys-Arg (OT-GKR), a dominant and biologically active form of OT, in the fetal rodent heart. Immunocytochemistry of whole rat embryo at mid gestation (E11) revealed parallel staining in the heart of OTR and the ATP-binding cassette sub-family G member 2 (brcp1) antigen the marker of the SP phenotype. Using flow cytometry, the SP cells were selected from the newborn CM stained with Hö echst 33342: 5.32%±0.06% of SP and 15.2%±1.10 of main population expressed OTR on the cell surface. The OTR was detected in CD29 (6.6%) and then in CD31 (4.7%) but less frequently in CD45 (0.7%) positive SP cell subpopulations. Specifically, the phenotype of SP CD31K cell, but not SP CD31C+ cells, proliferates in the presence of OT-GKR and develops large cell aggregates. Then, OT-GKR treatment induced the apparition of beating cell colonies after 11 days (10±2.78%), which increased until day 16 (52±1.21%). The cells in contractile colonies expressed the markers of a CM phenotype, such as troponin, cardiac myosin light chain-2, and actinin. Finally, SP cells stimulated by OT-GKR induced endothelial phenotype. These results suggest that the C-terminally extended OT molecule stimulates cardiac differentiation of SP CD31K cells and is involved in heart growth. © 2014 Society for Endocrinology. Source

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