Preface

UOJM Volume 4 Issue 2 marks a significant milestone for UOJM. For the first time, UOJM has sustained activity over the summer due to increased interest and submissions, which has resulted in the release of multiple issues in a year. Our second issue reflects an increase in awareness and support for UOJM both internally at the University of Ottawa and externally. We have made several infrastructure upgrades to accommodate the high volume of submissions, including the implementation of the Open Journal Systems platform hosted through the University of Ottawa Library as a peer review management platform, content manager, and digital archive. We have also expanded our effort to use social media platforms such as Facebook, Twitter, LinkedIn and Google+ to provide day-to-day communication to our followers around the world

Integrating Administration, the Clinic, and Research: An Interview with Dr. Jacques Bradwejn

ABSTRACT: Dr. Jacques Bradwejn is a Professor of Psychiatry, the Dean of the Faculty of Medicine, and a past Chair of the Department of Psychiatry at the University of Ottawa. He trained in Medicine at the University of Sherbrooke and in Psychiatry at McGill University. He completed a Research Fellowship in basic research in neuropsychopharmacology at Université de Montréal. He began his career as a clinician/researcher in the McGill University network and continued at University of Toronto, before coming to the University of Ottawa. He has also served as the Psychiatrist-in-chief at the Royal Ottawa Hospital and the head of Psychiatry at The Ottawa Hospital. In addition to his teaching and administrative engagement, Dr. Bradwejn has been extensively involved in translational neuropsychopharmacology research investigating the underlying biological etiology of anxiety disorders such as panic disorder and social phobia, as well as integrating clinical and psychological approaches towards the management of anxiety disorders. We were able to discuss with Dr. Bradwejn his dedication and extensive commitment to clinical care and advocacy, biomedical research, and administrative leadership, as well as his advice for medical students with regards to juggling a multitude of responsibilities and pursuing leadership roles within their careers. RÉSUMÉ: Dr. Jacques Bradwejn est professeur de psychiatrie, doyen de la Faculté de médecine, et un ancien président du Département de psychiatrie de l’Université d’Ottawa. Il a été formé en médecine à l’Université de Sherbrooke et en psychiatrie à l’Université McGill. Il a complété une bourse en recherche fondamentale en neuropsychopharmacologie à l’Université de Montréal. Il a commencé sa carrière en tant que clinicien-chercheur dans le réseau de l’Université McGill et a continué à l’Université de Toronto avant de venir à l’Université d’Ottawa. Il a également servi en tant que chef de psychiatrie à l’Hôpital Royal Ottawa et à l’Hôpital d’Ottawa. En plus de ses tâches d’enseignement et d’engagement administratif, le Dr. Bradwejn a été largement impliqué en recherche en neuropsychopharmacologie traductionnelle, enquêtant l’étiologie biologique sous-jacente des troubles anxieux tels que le trouble panique et la phobie sociale, ainsi que l’intégration des approches cliniques et psychologiques envers la gestion des troubles anxieux. Nous avons pu discuter avec le Dr. Bradwejn de son dévouement et de son engagement extensif aux soins cliniques et à son plaidoyer, à la recherche biomédicale, et au leadership administratif, ainsi que ses conseils aux étudiants en médecine en ce qui concerne jongler une multitude de responsabilités et poursuivre des rôles de leadership au sein de leur carrière

Type I interferon responses are impaired in latently HIV infected cells

Abstract Background The latent HIV-1 reservoir represents the primary barrier to the eradication of HIV-1 infection. The design of novel reservoir-clearance strategies, however, is impeded in part by the inability to distinguish latently HIV-infected cells from uninfected cells. Significant impairment of the type I interferon (IFN-I) response is observed during productive HIV-1 infection. Although this remains poorly described in the context of latent HIV-1 infection, presence of potential defects may serve as a novel therapeutic target. Therefore, IFN-I pathways were characterized using two latently HIV-1-infected cell lines, U1 and OM10.1, in comparison to their respective uninfected parental U937 and HL60 cell lines. Findings Constitutive expression and induction of important mediators of IFN-I signaling including IFNα/β cytokines, IFNAR1, MHC-I, ISG15, and PKR were evaluated following exogenous IFNα or poly(I:C) treatment. Differences in basal expression of IFNAR1, MHC-I, and PKR were observed between the latently HIV-1 infected and uninfected cell lines. In parallel, significant impairments in the induction of MHC-I, ISG15 and PKR, as well as secretion of IFNα/β cytokines were observed in response to appropriate exogenous stimulation within the two latently HIV-infected U1 and OM10.1 cells, relative to their HIV-uninfected parental cells. Conclusions In comparison to the HIV-uninfected U937 and HL60 cell lines, widespread defects in IFN-I responsiveness were observed within the latently HIV-infected U1 and OM10.1 cells. These impairments represent novel therapeutic targets, which may be amenable to strategies currently employed in cancer therapy

Coronary Artery Calcification, Cardiovascular Events, and Death: A Prospective Cohort Study of Incident Patients on Hemodialysis

Background: Coronary calcification in patients with end-stage renal disease (ESRD) is associated with an increased risk of cardiovascular outcomes and death from all causes. Previous evidence has been limited by short follow-up periods and inclusion of a heterogeneous cluster of events in the primary analyses. Objective: To describe coronary calcification in patients incident to ESRD, and to identify whether calcification predicts vascular events or death. Design: Prospective substudy of an inception cohort. Setting: Tertiary care haemodialysis centre in Ontario (St Joseph's Healthcare Hamilton). Participants: Patients starting haemodialysis who were new to ESRD. Measurements: At baseline, clinical characterization and spiral computed tomography (CT) to score coronary calcification by the Agatston-Janowitz 130 scoring method. A primary outcome composite of adjudicated stroke, myocardial infarction, or death. Methods: We followed patients prospectively to identify the relationship between cardiac calcification and subsequent stroke, myocardial infarction, or death, using Cox regression. Results: We recruited 248 patients in 3 centres to our main study, which required only biochemical markers. Of these 164 were at St Joseph's healthcare, and eligible to participate in the substudy; of these, 51 completed CT scanning (31 %). Median follow up was 26 months (Q 1 , Q 3 : 14, 34). The primary outcome occurred in 16 patients; 11 in the group above the median and 5 in the group below ( p = 0.086). There were 26 primary outcomes in 16 patients; 20 (77 %) events in the group above the coronary calcification median and 6 (23 %) in the group below ( p = 0.006). There were 10 deaths; 8 in the group above the median compared with 2 in the group below ( p = 0.04). The hazard ratios for coronary calcification above, compared with below the median, for the primary outcome composite were 2.5 (95 % CI 0.87, 7.3; p = 0.09) and 1.7 (95 % CI 0.55, 5.4; p = 0.4), unadjusted and adjusted for age, respectively. For death, the hazard ratios were 4.6 (95 % CI 0.98, 21.96; p = 0.054) and 2.4 (95 % CI 0.45, 12.97; p = 0.3) respectively. Limitations: We were limited by a small sample size and a small number of events. Conclusions: Respondent burden is high for additional testing around the initiation of dialysis. High coronary calcification in patients new to ESRD has a tendency to predict cardiovascular outcomes and death, though effects are attenuated when adjusted for age