Inaugural Meeting of the Canadian DOHaD Society
February 14, 2017
Fairmont Chateau Montebello – Montebello, Québec
DOHaD CANADA is pleased to announce its 1st Annual Meeting to be held at Fairmont Le Chateau Montebello, Quebec, on the 14th of February 2017.
The program will consist of a number of keynote speakers from the DOHAD community, trainee talks and a DOHAD Canada business meeting. A detailed program will be released shortly.
The inaugural meeting will provide a venue for information exchange and dissemination, and a valuable opportunity for members to strategize and plan the society’s role in research, knowledge dissemination, and implementation of health policy. As a newly established society, the meeting will also be critical in establishing a core community, fostering collaborations and promoting engagement among members. In this regard, the success of the meeting will symbolize the value that DOHaD Canada brings to the research community. Therefore, to ensure the best possible attendance and reach of our message, our first meeting is scheduled to take place immediately before the Canadian Perinatal Research Meeting (CNPRM).
Due to the popularity of the Meeting, we had to now close subsidized registration.
You are welcome to register on-site or below at the cost of $100.00/registration.
DOHaD and human milk: can breastfeeding program lifelong health? The Canadian Healthy Infant Longitudinal Development (CHILD) Study (www.canadianchildstudy.ca) is following 3500 families across Canada, from pregnancy through early childhood. We are exploring the genetic and environmental factors that predispose or protect children from chronic diseases including asthma, allergies and obesity. Research in the Azad Lab (www.azadlab.ca) focuses on infant feeding practices and breast milk composition in the CHILD Study. Our results show that breastfeeding is associated with reduced risks of asthma and obesity in early childhood, and these effects differ depending on the mode of feeding (direct breastfeeding vs. expressed breast milk) as well as the timing and type of complementary feeding (formula vs. solid foods). To understand the biological mechanisms underlying these associations, we are analyzing breast milk samples from the CHILD cohort to measure multiple bioactive components, including oligosaccharides, microbiota, fatty acids and endocrine hormones. Our results to date have identified specific milk bioactives associated with infant body composition and allergic sensitization, and show that both fixed (eg. age, ethnicity) and modifiable (e.g. diet, BMI) maternal characteristics are associated with breast milk composition. Long-term associations are now being studied as the CHILD cohort reaches 5 years of age.
Dr. Amy Bombay is an Assistant Professor in the Department of Psychiatry and School of Nursing at Dalhousie University. Amy is a member of Rainy River First Nation (Anishinaabe kwe) and completed her MSc and PhD in Psychology and Neuroscience, followed by a postdoctoral fellowship at the University of Ottawa Institute of Mental Health Research. Her research focuses generally on issues related to the health and well-being of Indigenous peoples in Canada, with much of her projects being driven by the needs and objectives of Indigenous communities and organizations. Her primary areas of inquiry have explored the links between historical trauma, contemporary stressor exposure, and mental health and wellness among Indigenous peoples, and on the important role that cultural identity plays in relation to well-being. One of her main programs of research has explored the different pathways by which Indian Residential School trauma is transmitted across generations, which has garnered extensive media interest and has been influential in influencing policy and practice related to Indigenous health.
Reframing Indigenous Health Inequity: Resilience and well-Being in the context of Historical Trauma and the intergenerational effects of colonization. The forced removal of Indigenous children by the Canadian government to church-run Indian residential schools for over a century is one of many harmful aspects of colonization that has negatively affected individual and community well-being for Indigenous peoples. The current presentation will provide an overview of research exploring how familial residential school attendance is associated with various aspects of Indigenous well-being, and how these effects are transmitted across generations and perpetuated by ongoing government policies. At the same time, Indigenous peoples have shown extreme resilience in the face of chronic collective stress and trauma, and culture-related factors such as having cultural pride have shown to promote positive outcomes when faced with challenges among Indigenous populations, which will also be discussed.
Stephen Lye Ph.D., is a Senior Investigator at the Lunenfeld-Tanenbaum Research Institute of Sinai Health System where he is the ScotiaBank Scientist in Child and Adolescent Development and the Women’s Auxiliary Chair in Women’s and Infants’ Health Research. Dr. Lye is Professor in the Departments of Obstetrics & Gynecology, Physiology and Medicine at the University of Toronto. Dr. Lye leads the Alliance for Human Development, a transdisciplinary initiative that seeks to improve the health and well-being of all children, everywhere, by focusing on optimizing their development in early-life. His research has integrated discovery, clinical and translational studies including the commercialization of discoveries in partnership with industry. Dr. Lye has established international research consortia focused on identifying interactions between an individual’s genetic make-up and their environment during the first 2000 days of life that underlie obesity and cardio-metabolic disorders. He has published over 230 research papers on pregnancy and maternal-child health with a special focus on mechanisms underlying preterm birth and other pregnancy complications. Dr. Lye has received numerous awards and honors, including Fellowship of the Canadian Academy of Health Sciences, Fellowship of the Royal College of Obstetricians and Gynaecologists (UK) and the President’s Scientific Achievement Award from the Society for Reproductive Investigation.
Precision Public Health: How DOHaD can drive science-based interventions to improve life-long health and wellbeing. Our research is focused on an emerging understanding of how early-life exposures interact with a child’s genetic blueprint to set developmental paths that impact a child’s life-long health, learning ability and behavior and social functioning. The genetic blueprint for development specifies how a single cell (the fertilized egg) develops over just 2000 days into the enthusiastic, active, questioning and thoughtful child on her first day of grade school. While genetic variations amongst all of us contribute to individual differences in our attributes and characteristics, genetics alone is insufficient in explaining the diversity of functioning and the degree to which our children achieve their potential. It is the interaction between an individual’s genetic make-up and the environments (pre- and postnatal) in which their development occurs that determines the trajectories that will establish their future health and wellbeing. Increasing data suggest that these interactions can occur at multiple levels; for example, through variations in response to environmental stimuli due to genetic polymorphisms or through environmental marking of DNA to produce variable gene expression, i.e., epigenetics. Epigenetic programming is particularly powerful and may explain how adverse exposures can have negative impacts across generations. Further, recent evidence indicates functional interactions between genetic polymorphisms and epigenetic marks that may explain why some individuals are resilient while others are particularly vulnerable to early-life exposures. With this new understanding and improved capabilities to detect DNA polymorphisms or epigenetic variants in large human populations, we are poised at the birth of a new era in developmental science. Not only can we gain an understanding of how the foundations of health and wellbeing are established, but through targeted early interventions, we will be positioned to increase the health, cognitive-social development and school readiness of our children.
Sophie Petropoulos, PhD has merged her expertise in the fields of physiology, developmental biology, epigenetics and single-cell genomics to gain an understanding of early preimplantation development. Her research interests focus on how early events such as parental or environmental exposures can result in fetal reprogramming, ultimately leading to the onset of disease or disorder later in life. Dr. Petropoulos completed her PhD in the Department of Physiology, University of Toronto and then joined the Department of Pharmacology and Therapeutics at McGill University where she specialized in epigenetics during her first postdoctoral training. She then moved to the Karolinska Institutet, Department of Clinical Science, Intervention and Technology and the Ludwig Cancer Research Institute where her studies investigated human preimplantation development using single-cell RNA-sequencing. Her recent publication in Cell catapulted the field by providing important insights into human preimplantation development; highlighting differences with mouse development in regard to lineage segregation and proposing a new mechanism of X-chromosome dosage compensation in the human embryo. Currently, Sophie is a Principal Investigator at the Karolinska Institutet, Department of Clinical Science, Intervention and Technology, where she is establishing a multi-level omics (transcriptome, small RNAs and methylome) profile of human preimplantation development and elucidating the effects of preimplantation exposures/stress (i.e. culture media, oxygen level, hormones, nutrients), as occurring during artificial reproductive technologies, on the human embryo. She hopes to identify key genes and pathways that are susceptible to reprogramming when faced with preimplantation stressors to gain an understanding of the mechanisms used by the embryo to sense and to adapt to different environments. These studies will provide important insights into human development, fetal programming, stem cell research and may improve current clinical practice. Ultimately, she envisions her research having a global impact on embryo development and future generations by ensuring that each child born via ART is provided with the optimal conditions for a healthy life.
Single-Cell RNA-Sequencing: Insights into human preimplantation development. Characterizing embryonic development during the first and arguably most critical week of human development is of great importance. During the first 7 days, the human embryo divides to form the first three lineages: trophectoderm (TE), primitive endoderm (PE), and pluripotent epiblast cells (EPI). To date, limited information exists pertaining to the transcriptional landscape and what drives lineage segregation and pluripotency in humans. Further, the status of X-inactivation in the human preimplantation embryo remains controversial. Using Smart-seq2 single-cell RNA-sequencing, we established a transcriptional road map consisting of 1529 cells from 88 human embryos, covering 8-cell stage to mature blastocyst at embryonic (E) day 7. Further, single molecule RNA FISH was utilized to confirm the status of X-chromosome dosage compensation. These data show that cells undergo an intermediate state of co-expression of lineage-specific genes, followed by a concurrent establishment of all three lineages during late E5, coinciding with blastocyst formation. Further, female cells of all three lineages undergo a dual X-chromosome dosage compensation prior to implantation, which is in contrast to that observed in the mouse. In addition, comparisons with the mouse embryo revealed numerous cross-species differences in early development, such as timing of lineage segregation and X-chromosome dosage compensation. Further we have now established lineage specific transcriptional blueprints and have identified several less studied markers such as ARGFX in the EPI and LINC00261 in the PE. Our data have profiled the global transcriptome in the preimplantation human embryo at single-cell resolution, shedding light onto the dynamics of and underlying pathways driving lineage segregation. We anticipate broad utility of this transcriptional atlas in future studies on human development as well as in stem cell research.
Kent L. Thornburg, PhD, is the M. Lowell Edwards Endowed Chair of Cardiovascular Medicine and Professor of Medicine in the Knight Cardiovascular Institute at the Oregon Health & Science University. He holds joint professorships in the Departments of Physiology & Pharmacology, Medical Informatics and Clinical Epidemiology and Obstetrics & Gynecology. He directs the Center for Developmental Health in the Knight Cardiovascular Institute and the OHSU Bob and Charlee Moore Institute for Nutrition & Wellness. He studies how women adapt to pregnancy and the roles of maternal diet and body composition in regulating fetal growth and lifelong health. He collaborates with epidemiologists and basic scientists in England, New Zealand, Switzerland, Finland, Australia and India. He oversees clinical studies in rural Oregon and Alaska. Kent Thornburg serves regularly on advisory panels at the National Institutes of Health, the American Heart Association and the Children’s Heart Foundation and serves on the scientific advisory board of the Preeclampsia Foundation. He is director of research training for the Knight Cardiovascular Institute and holds grants from the NIH. He recently co-chaired the task force to determine the 10 year vision of the developmental origins of health and disease for the National Institute of Child Health and Human Development.
Developmental Programming: Progress and Problems. In response to the finding by Professor David Barker and colleagues showing that mortality from heart disease among English men and women is related to their birthweight, a new field of medicine often called developmental programming, was born overnight. While many people originally doubted the veracity of this finding, a surge of basic animal studies demonstrated the plasticity of the developmental process that allows developing mammals to compromise organogenesis and organ maturation in the face of environmental adversities. The basic science findings lit the fire of enthusiasm for further investigation of the developmental origins of disease among basic, clinical and epidemiological scientists. To promote the work, a new international society was formed, the Society for the Developmental Origins of Health and Disease and subsidiary societies suggests that thousands of scientists are now in the field. Over the past 30 years, epidemiologists have discovered a host of relationships between birthweight, maternal body phenotype, male nutrition and long term chronic disease risk. Now, virtually every organ system in the body has a developmental link to adult-onset disease. Thus, a long list of chronic diseases are rooted in development through indicators like birthweight, maternal anatomical phenotype, and placental size and shape. The worsening health of western societies can now be examined in light of developmental compromises caused by malnutrition of mothers, fathers and infants, maternal toxic stress during pregnancy, social stress in early childhood, low oxygen during pregnancy and environmental toxins. The field is now on solid scientific footing and the next generation of investigation must include unravelling the epigenetic and sex dependent transgenerational component of programming and the peculiarities of adaptation by individual organs. On the social side, the entire discipline needs to penetrate and influence the many layers of governmental bureaucracy so that sensible policies can promote healthy diets and lifestyles for masses of people who are now suffering disease as a result of stresses before and after birth.
Dr. Rudolf Uher is the Canada Research Chair in Early Intervention and a Professor in Psychiatry at Dalhousie University. Dr Uher studied medicine and neurosciences at Charles University in Prague and trained in Psychiatry at the Maudsley Hospital in London, UK. In 2013, Dr Uher launched the FORBOW program with the aim to prevent mental illness in youth (www.FORBOW.org; Twitter: @ProjectFORBOW). Dr. Uher is also the editor of the journal Depression and Anxiety and he consults for the World Health Organization on the classification of mental disorders and works on the 11th revision of the International Classification of Diseases. Dr. Uher is an author of 180 articles on mental illness, its causes and treatment, a recipient of the Max Hamilton Memorial Prize (2014) and the Royal-Mach-Gaensslen Prize for Mental Health Research (2016) and a Member of the College of New Scholars, Artists and Scientists of the Royal Society of Canada. Dr Uher treats people for depression and bipolar disorder at the Mood Disorders Program at the QEII hospital in Halifax, Nova Scotia.
Genes, environment and the development of mental illness. Severe mental illness including schizophrenia, bipolar disorder and depression is one of the most costly and burdensome health conditions to the affected individuals, their families and society. Severe mental illness tends to run in families with close biological relatives being at highest risks. It typically onsets in the second or third decade of life and is preceded by earlier milder psychopathology, including anxiety, and it in turns predicts physical morbidity in later life. IIndividuals present to services at a relatively late stage in the development of severe mental illness and that pre-emptive interventions at earlier stages may be needed to positively influence the brain development and prevent disability. The need for such early interventions raises the question of how early can we identify individuals who are at risk for developing severe mental illness. I will outline recent developments towards early indicated prevention of severe mental illness, including the Families Overcoming Risks and Building Opportunities for Well-Being (FORBOW) study of youth at risk. Youth aged 1-24 years have been enrolled through identified parents and followed up annually with diagnostic and risk assessments. One in two eligible youth are randomly selected to be offered the Skills for Wellness (SWELL), an individual skills-learning intervention based on cognitive-behavioral therapy. Antecedents including affective lability, anxiety, psychotic symptoms and basic symptoms were associated with family history of all types of severe mental illness (schizophrenia, bipolar disorder, severe major depressive disorder) and predicted new onsets of severe mental illness. SWELL is an acceptable intervention hat effectively targets these antecedents. Future work will include personalization, timing and tracking the long-term effects of early interventions on mental and physical health.
Effects of in utero and lactational exposure to new Generation “green” plasticizers in the male rat: A comparative study with Diethyl Hexyl Phthalate (DEHP). Phthalates, widely used plasticizers, leach out into the environment and are well established as anti-androgenic substances acting on the male reproductive system. Still, the use of phthalates in consumer products is poorly regulated, and there is a critical need for innocuous replacements. Our objective is to identify novel plasticizers that will meet the stringent demands of both industry and regulatory agencies. Out of 20 candidate compounds designed by McGill University’s Department of Chemical Engineering to mimic the plasticity properties of diethylhexyl phthalate (DEHP), we selected 2 compounds, 1,4-butanediol dibenzoate (BDD) and dioctyl succinate (DOS), that displayed the most innocuous profiles on a range of cell lines. We hypothesize that BDD and DOS exert fewer endocrine disrupting effects than existing phthalates on the male reproductive system after in utero and lactational exposure. Nine groups of Sprague Dawley dams were dosed daily with corn oil (vehicle), BDD or DOS from gestational day 8 to postnatal day 21 (PND21); DEHP and 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH, a current replacement of DEHP) served as reference compounds. Exposure to DEHP (300 mg/kg/day) induced endocrine disruption phenotypes such as a reduced anogenital index and multinucleated gonocytes at PND3, as well as a higher incidence of hemorrhagic testes at PND8. Similarly, DINCH produced a higher incidence of hemorrhagic testes at PND8. By contrast, neither of the “green” plasticizers showed significant effects on the weight of vital and reproductive organs, age or weight at puberty in the male offspring. These results indicate that BDD and DOS are safer plasticizers than DEHP or DINCH and that further studies are necessary to establish them as responsible replacement chemicals. Supported by CIHR-IHDCYH grant RHF100626.
Laura Marcela Reyes Martinez. I am a Colombian physician, from 2008 to 2010 I worked as a clinical research fellow in the field of clinical epidemiology. My research focused on determining the risk factors associated with pregnancy complications. In 2011, I joined the Davidge laboratory as a PhD student, where I learned in vitro and in vivo techniques (working heart preparation, wire myography, cardiomyocyte cell culture and echocardiography) that allowed me investigate the role of aerobic exercise as a therapeutic option to prevent the development of cardiovascular diseases in an animal model of intrauterine growth restriction. Throughout my PhD I have been funded by the Faculty of Medicine & Dentistry/Alberta Health Services Graduate Student Recruitment Studentships and the Mazankowski Graduate Studentship Award (2011). After the completion of these studentships, I received the Alberta Innovates–Health Solutions Studentship Award (2012-2017), I will be completing my PhD degree in June 2017.
The cardiovascular effects of aerobic exercise training in hypoxic-induced intrauterine growth restriction. Introduction Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. We have demonstrated that prenatal hypoxia leads to intrauterine growth restriction (IUGR) and impairs later-life endothelial-dependent vascular function. Cardiac performance in IUGR offspring is also affected after an ischemic event, demonstrating that fetal environment during early development is important for cardiovascular health. Early interventions are needed to ultimately reduce later life risk for cardiovascular disease. We tested whether aerobic exercise prevents the development of cardiovascular diseases in hypoxic-induced IUGR offspring. Methods Pregnant Sprague-Dawley rats were exposed to control (21% oxygen) or hypoxia (11% oxygen) conditions from gestational day 15 to 21. Male and female offspring from normoxic (control) and hypoxic (IUGR) pregnancies were randomized at 10 weeks of age to either an exercise-trained or sedentary group. After acclimatization, rats ran on a treadmill for 6 weeks; 5 days/week, 30 min/day at 20 m/min. After a recovery period of 24 hours, animals were euthanized and gastrocnemius muscle arteries were mounted on a wire myograph. Response curves to methacholine were performed in the absence or presence of L-NAME (nitric oxide synthase inhibitor), a combination of Apamin and TRAM-34 (potassium channel blockers), or indomethacin (cyclooxygenase inhibitor). On the same experimental day, hearts were perfused for 10 min in retrograde Langendorff mode. Hearts were then switched to working heart mode and global, normothermic flow ischemia was induced for 10 min. Following ischemia, hearts were reperfused for 40 min. Results Female IUGR offspring had reduced nitric oxide-mediated vasodilation and an increased prostaglandin-mediated vasoconstriction. Aerobic exercise training improved endothelium-derived hyperpolarization (EDH)-mediated vasodilation only in IUGR male offspring. Moreover, aerobic exercise training improved baseline cardiac performance and decreased superoxide generation in male control offspring while in IUGR offspring the opposite effect was observed. There was no effect of IUGR or exercise on cardiac function in female offspring. Conclusions Our findings demonstrated that in IUGR populations, a common preventive strategy such as aerobic exercise may represent a secondary stressor to the cardiovascular physiology. The results from the present study also highlight that when examining the mechanisms by which exercise impacts the cardiovascular system in a susceptible population, sexual dimorphism must be considered.
Jessica Wallace is a Research Associate in the laboratory of Dr. Deborah M. Sloboda at McMaster University. She completed her MSc in Medical Sciences at McMaster University in September 2016. Her research focuses on investigating maternal intestinal microbial shifts during pregnancy and maternal obesity and the impacts to maternal intestinal and placental function. Through combining classical bench work, next-generation sequencing, and bioinformatics, Jessica hopes to better understand the role of the maternal intestinal microbiota as a factor influencing the developmental origins of obesity.
Maternal Obesity: Impacts on the Maternal Gut at Mid Gestation. Introduction: Despite the importance of the intestinal microbiota in mediating metabolism, its role in pregnancy is unclear. In animal models, we show that maternal obesity modifies pregnancy-induced changes in the maternal intestinal microbiota. Commensal bacteria and their metabolites are essential for the development and function of the immune system, the maintenance of gut epithelial barrier integrity, and the breakdown of nutrients. The factors mediating maternal intestinal microbial shifts during pregnancy are unknown, and the influence on maternal intestinal inflammation barrier function remain to be investigated. Objective: We investigated: 1) Whether shifts in maternal intestinal microbiota were mediated by steroid hormone fluctuations using a non-invasive model in non-pregnant female mice and 2) Whether maternal intestinal microbial shifts were associated with elevated maternal intestinal inflammation and impaired barrier function in the context of maternal obesity. Methods: 1) Fecal samples were collected at 3 distinct stages of the estrous cycle in 7-week-old individually housed non-pregnant female C57BL/6 mice, fed a control diet. Estrous stages were used as a proxy for circulaing steroid hormone levels and were determined by vaginal cytology. Microbial composition at distinct estrous stages over 3 estrous cycles were analyzed. 2) C57BL/6 female mice were fed a high-fat (HF; 60% kcal fat) or control (CON) diet 6 weeks prior to mating and throughout gestation (n=10). Maternal weight, food intake, and fecal samples were collected at gestational day (GD) 0.5, 6.5, 10.5, and 14.5. At GD14.5, dams underwent an intestinal permeability assay and maternal intestinal tissue was collected. Intestinal inflammation was assessed by NFκB p65 activity. All microbial analyses were performed via 16S rRNA genomic sequencing of the variable 3 (V3) region. Results: 1) Taxonomic summaries of intestinal microbial relative abundance revealed no significant shift in the non-pregnant female intestinal microbiota over the course of the estrous cycle. 2) At GD 14.5, maternal blood glucose, serum insulin, and leptin levels were higher in obese dams compared to controls. Pregnancy induced an intestinal microbial shift that was further modulated by maternal obesity. Akkermansia was observed to exhibit the largest increase in relative abundance with pregnancy and maternal obesity, while Ruminococcaceae and Lachnospiraceae abundance correlated with maternal glucose, insulin, and leptin levels. Maternal obesity was associated with increased intestinal mRNA levels of colonic mucin protein, Muc5ac, and elevated NFκB p65 activity although maternal intestinal permeability was similar between groups. Conclusions: The intestinal microbiota did not shift over the course of the estrous cycle in regularly cycling non-pregnant female mice. Future studies are required to fully investigate the factors mediating intestinal microbial shifts during pregnancy. Pregnancy and maternal obesity are associated with maternal intestinal microbial shifts characterized by taxa involved in intestinal mucus and short-chain fatty acid production. Maternal obesity is associated with increased intestinal NFκB mediated inflammation without a change in gut permeability. These data are suggestive of a microbial-immune interaction in mediating the impacts of obesity on maternal adaptation to pregnancy.
|First name||Last Name||Affiliation|
|Kristi||Adamoemail@example.com||University of Ottawa|
|Meghan||Azad||meghan.azad@Umanitoba.ca||University of Manitoba|
|Jay||Baltzfirstname.lastname@example.org||Ottawa Hospital Research Institute, University of Ottawa|
|Rhonda||Bellemail@example.com||University of Alberta|
|Roberta||Bgeginskifirstname.lastname@example.org||Hospital de Clinicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Brazil|
|Stephane||Bourqueemail@example.com||University of Alberta|
|Christy||Cookefirstname.lastname@example.org <email@example.com>||University of Alberta|
|Denise||Daleyfirstname.lastname@example.org||University of British Columbia|
|Sandy||Davidgeemail@example.com||University of Alberta|
|Barbra||de Vrijerfirstname.lastname@example.org||University of Western Ontario//London Health Sciences Centre|
|Genevieve||Eastabrookemail@example.com||University of Western Ontario|
|Bénédicte||Fontaine-Bissonfirstname.lastname@example.org||University of Ottawa|
|Tracey||Gallowayemail@example.com||University of Toronto Mississauga|
|Gerry||Giesbrechtfirstname.lastname@example.org||University of Calgary|
|Sylvie||Girardemail@example.com||CHU Sainte-Justine/Universite de Montreal|
|Daniel||Goldowitzfirstname.lastname@example.org||University of British Columbia|
|Ruth||Grunauemail@example.com||University of British Columbia|
|Denise||Hemmingsfirstname.lastname@example.org||University of Alberta|
|Eileen K||Huttonemail@example.com||McMaster University|
|Padma||Kaulfirstname.lastname@example.org||University of Alberta|
|Robert||Levitanemail@example.com||CAMH, University of Toronto|
|Stephen||Lyefirstname.lastname@example.org||Lunenfeld-Tanenbaum Research Institute, Sinai Health System|
|Stephen||Matthews||Stephen.Matthews@utoronto.ca||University of Toronto|
|Serge||McGrawemail@example.com||CHU Ste-Justine Research Center, U. Montréal|
|Charles||McKenziefirstname.lastname@example.org||University of Western Ontario|
|Bryan||Mitchellemail@example.com||University of Alberta|
|Elisabeth||Murphyfirstname.lastname@example.org||University of Notre Dame, Sydney, Australia|
|Anne Monique||Nuytemail@example.com||CHU Sainte-Justine Université de Montréal|
|David M||Olsonfirstname.lastname@example.org||University of Alberta|
|Maria B.||Ospinaemail@example.com||University of Alberta|
|Timothy||Regnaultfirstname.lastname@example.org||University of Western Ontario|
|Bryan S||Richardsonemail@example.com||University of Western Ontario|
|Kent||Thornburgfirstname.lastname@example.org||Oregon Health & Science University|
|Suzanne||Toughemail@example.com||University of Calgary|
|Cathy||Vaillancourtfirstname.lastname@example.org||INRS-Institut Armand Frappier|
|First name||Last Name||Affiliation|
|Alireza||Akbariemail@example.com||University of Western Ontario|
|Océane||Albertfirstname.lastname@example.org||McGill University, Department of Pharmacology & Therapeutics|
|Marie-Eve||Brienemail@example.com||Universite de Montreal|
|Andrea||Constantinoffirstname.lastname@example.org||University of Toronto|
|Kathryn||Denizeemail@example.com||University of Ottawa|
|Cyntia||Duvalfirstname.lastname@example.org||Universite de Montreal|
|Zachary||Eastonemail@example.com||University of Western Ontario|
|Margaret Elizabeth||Engfirstname.lastname@example.org||University of Toronto|
|Aida||Eslamiemail@example.com||University of British Columbia|
|Evan||Formosafirstname.lastname@example.org||University of Western Ontario|
|Anne Marie||Gannonemail@example.com||Health Canada|
|Camille||Girard-Bockfirstname.lastname@example.org||CHU Sainte-Justine/Universite de Montreal|
|Stephanie||Gizaemail@example.com||University of Western Ontario|
|Laetitia||Guillemettefirstname.lastname@example.org||University of Manitoba|
|Farrah||Jabaremail@example.com||Children’s Hospital Research Institute of Manitoba, University of Manitoba|
|Megan||Jarmanfirstname.lastname@example.org||University of Alberta|
|Stephanie||Kereliukemail@example.com||Children’s Hospital Research Institute of Manitoba/University of Manitoba|
|Yohei||Makifirstname.lastname@example.org||University of Western Ontario|
|Daniel||McCooeyeemail@example.com||University of Western Ontario|
|Shuhiba||Mohammadfirstname.lastname@example.org||University of Ottawa|
|Alexandros||Mouratidisemail@example.com||University of Toronto|
|Brittany||Moycefirstname.lastname@example.org||University of Manitoba|
|Pinki||Nandiemail@example.com||University of Western Ontario|
|Muhammad||Oneeb Rehman Mianfirstname.lastname@example.org||University of Montreal, Research Center of Sainte-Justine Hospital|
|Julia||Palaciosemail@example.com||Universite de Montreal|
|Janet||Poplawskifirstname.lastname@example.org||University of Lethbridge|
|Jonathan||Rankinemail@example.com||University of Ottawa|
|Laura Marcela||Reyes Martinezfirstname.lastname@example.org||University of Alberta|
|Conrad||Rockelemail@example.com||University of Western Ontario|
|Jennifer||Schneiderfirstname.lastname@example.org||Children’s Hospital Research Institute of Manitoba, University of Manitoba|
|Natalie||Scimeemail@example.com||University of Western Ontario|
|Kevin||Sinclairfirstname.lastname@example.org||University of Western Ontario|
|Rachel||Skowemail@example.com||University of Alberta|
|Lauren||Smithfirstname.lastname@example.org||University of Western Ontario|
|Frances||Sobierajskiemail@example.com||University of Alberta|
|Floor||Spaansfirstname.lastname@example.org||University of Alberta|
|Maria||Sqapiemail@example.com||University of Toronto|
|Lorena||Vehlingfirstname.lastname@example.org||University of Manitoba/Laurentian University|
|Abdul||Wajidemail@example.com||University of Calgary|
|Ashley||Weeksfirstname.lastname@example.org||University of Ottawa|
|Amanda||Weileremail@example.com||University of Lethbridge|
|Andrew||Woodmanfirstname.lastname@example.org||University of Alberta|
Ian C.G. Weaver, Ph.D.
Depts. Psychology & Neuroscience, and Psychiatry
Atlantic Canada Chapter Chair, Canadian Developmental Origins of Health and Disease Network
Tel: 902-494-1133 | Fax: 902-494-4013
Stephane Bourque, Ph.D.
Depts. Anesthesiology & Pain Medicine and Pharmacology
Women and Children’s Health Research Institute
University of Alberta
Tel: 780-492-6000 | Fax: 780-492-0723
Vasilis G. Moisiaids
Department of Physiology
University of Toronto
Fairmont Le Château Montebello, Quebec
392 Notre-Dame, Montebello, QC J0V 1L0
Tel #: (819) 423-6341
Fax #: (819) 423-5106
Please register through this page: http://www.cnprm.org/presentation-guidelines/
If you are also attending the CNPRM 2017 meeting, you only need to make 1 hotel reservation that includes the appropriate dates. (However, you still need to register for both meetings!)
There are a couple of options for transport to Montebello:
Allante Airport Transportation Services – http://aats.limo/ or (613) 741-7111
Maestro Limousines – http://www.maestrolimousine.com/ or (819) 246-5081
Shuttle Jet Services – http://www.shuttlejetservices.com/chateau-montebello-hotel-taxi-shuttle-limousine.html or (613) 315-2505
These are the only services that run in the area.
Other options: Rent a vehicle
Take the Greyhound to Montebello. There is a shuttle available from the Greyhound drop-off in Montebello to the Fairmont. If you choose this option, you would need to call the Fairmont to get them to sent the shuttle upon your arrival at the Montebello drop-off at (819) 423-6341.