- Email: [email protected]
Canadian media discourse about Fetal Alcohol Spectrum Disorder
Abstracts / Int. J. Devl Neuroscience 47 (2015) 1–131
dependent Coronin-1 expression increases permitting NGF-TrkA dependent calcium signaling which decreases axon growth rate and branching, ensuring that neurons terminate appropriately at their target organ. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.296 ISDN2014 0377 Canadian media discourse about Fetal Alcohol Spectrum Disorder J. Aspler 1,∗ , N. Zizzo 1 , E. Bell 1 , N. Di Pietro 2 , C. Green 3 , E. Racine 1 1 Institut de recherches cliniques de Montréal, Canada 2 National Core for Neuroethics, Canada 3 Canada FASD Research Network, Canada E-mail address: [email protected] (J. Aspler).
Fetal Alcohol Spectrum Disorder (FASD), a range of neurodevelopmental disabilities caused by exposure to alcohol in utero, could affect as many as 1 in 100 Canadians. Its actual prevalence remains unknown due to confounds such as inaccessible diagnostic services, the effects of stigma on willingness to report drinking during pregnancy, and uncertainty about more subtle alcohol-related neurodevelopmental effects. Some of these issues, amongst others, have been explored by the Canadian print media; however, the information presented is not always clear, precise, or accurate. Given the importance of informed public discourse on scientific and policy matters, we explored the information presented by the Canadian print media in detail. In order to identify and address informational gaps or contradictions in the Canadian media discourse, we have conducted a content analysis of 189 Canadian news articles published between 2003 and 2011 found using the Factiva research database. Major themes that emerged throughout the analysis included 1) descriptions of FASD (e.g., primary and secondary disabilities, severity); 2) systemic concerns (e.g., inadequate social services, inadequate criminal justice accommodation); 3) medical concerns (e.g., access to – and efficacy of – diagnoses, preventions, treatments); and 4) social concerns (e.g., criminality, stigma, race and class myths). Preliminary results indicate a wide variability in reported safe amounts of alcohol while pregnant and descriptions of FASD. This likely reflects disagreements in the literature itself, where these questions remain heavily debated, as well as the evolution of the diagnosis over time. Additionally, most information presented reflected the specific needs and the work of the provinces of Manitoba, Alberta, and British Columbia. Our final results will quantify the kind of information presented to the Canadian public so that we can better gauge public discourse about FASD.
109
ISDN2014 0378 Prenatal alcohol exposure alters the developmental methylation profile of the rat hypothalamus Alexandre Lussier 1,2,∗ , Wendy Comeau 1 , Tamara Bodnar 1 , Matthew Mingay 3 , Martin Hirst 3 , Michael S. Kobor 2 , Joanne Weinberg 1 1 Department of Cellular and Physiological Sciences, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada 2 Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada 3 Centre for High-Throughput Biology, Department of Microbiology & Immunology, University of British Columbia, Vancouver, British Columbia, Canada
Alcohol exposure during brain development causes a number of long-lasting neurobio-logical deficits, including a lifelong dysregulation of the stress response. In both animal models and children with FASD, hypothalamic-pituitary-adrenal (HPA) axis function is permanently altered following prenatal ethanol exposure, showing greater basal tone and increased responsivity to stressors. While the etiology of HPA axis reprogramming remains unknown, the persistence of deficits throughout life makes epigenetic modifications prime suspects to explain its molecular underpinnings. In the following study, we examine the effect of prenatal alcohol exposure on DNA methylation profiles of the hypothalamus and white blood cells at four developmental time-points. On gestation day (GD) 1, Sprague-Daley dams were randomly assigned to one of three groups: prenatal alcohol exposure (PAE) – ad libitum liquid ethanol diet; pair-fed (PF) – liquid control diet, maltose dextrin isocalorically substituted for ethanol, in the amount consumed by a PAE partner (g/kg/body weight/GD); control (C) – ad libitum standard rat chow. The hypothalamus of female offspring was collected at postnatal days 0, 8, 15, and 22 and white bloods cells (WBC) were collected from whole blood at postnatal day 22 only. DNA methylation analysis was performed by methylated DNA immunoprecipitation followed by next-generation sequencing on the Illumina HiSeq (MeDIP-seq). Preliminary results suggest that PAE alters hypothalamic and white blood cell DNA methylation profiles. Moreover, not only do baseline (control) methylation patterns vary over developmental ages, but changes induced by PAE also occur across development. Persistent DNA methylation changes in the hypothalamus may explain the HPA axis alterations observed in both animal models and clinical studies of prenatal alcohol exposure. Moreover, correlations between methylome alterations in peripheral tissue and the brain may prove critical to the development of an easily measurable signature of fetal alcohol spectrum disorder.
http://dx.doi.org/10.1016/j.ijdevneu.2015.04.297 http://dx.doi.org/10.1016/j.ijdevneu.2015.04.298
dependent Coronin-1 expression increases permitting NGF-TrkA dependent calcium signaling which decreases axon growth rate and branching, ensuring that neurons terminate appropriately at their target organ. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.296 ISDN2014 0377 Canadian media discourse about Fetal Alcohol Spectrum Disorder J. Aspler 1,∗ , N. Zizzo 1 , E. Bell 1 , N. Di Pietro 2 , C. Green 3 , E. Racine 1 1 Institut de recherches cliniques de Montréal, Canada 2 National Core for Neuroethics, Canada 3 Canada FASD Research Network, Canada E-mail address: [email protected] (J. Aspler).
Fetal Alcohol Spectrum Disorder (FASD), a range of neurodevelopmental disabilities caused by exposure to alcohol in utero, could affect as many as 1 in 100 Canadians. Its actual prevalence remains unknown due to confounds such as inaccessible diagnostic services, the effects of stigma on willingness to report drinking during pregnancy, and uncertainty about more subtle alcohol-related neurodevelopmental effects. Some of these issues, amongst others, have been explored by the Canadian print media; however, the information presented is not always clear, precise, or accurate. Given the importance of informed public discourse on scientific and policy matters, we explored the information presented by the Canadian print media in detail. In order to identify and address informational gaps or contradictions in the Canadian media discourse, we have conducted a content analysis of 189 Canadian news articles published between 2003 and 2011 found using the Factiva research database. Major themes that emerged throughout the analysis included 1) descriptions of FASD (e.g., primary and secondary disabilities, severity); 2) systemic concerns (e.g., inadequate social services, inadequate criminal justice accommodation); 3) medical concerns (e.g., access to – and efficacy of – diagnoses, preventions, treatments); and 4) social concerns (e.g., criminality, stigma, race and class myths). Preliminary results indicate a wide variability in reported safe amounts of alcohol while pregnant and descriptions of FASD. This likely reflects disagreements in the literature itself, where these questions remain heavily debated, as well as the evolution of the diagnosis over time. Additionally, most information presented reflected the specific needs and the work of the provinces of Manitoba, Alberta, and British Columbia. Our final results will quantify the kind of information presented to the Canadian public so that we can better gauge public discourse about FASD.
109
ISDN2014 0378 Prenatal alcohol exposure alters the developmental methylation profile of the rat hypothalamus Alexandre Lussier 1,2,∗ , Wendy Comeau 1 , Tamara Bodnar 1 , Matthew Mingay 3 , Martin Hirst 3 , Michael S. Kobor 2 , Joanne Weinberg 1 1 Department of Cellular and Physiological Sciences, Life Sciences Institute, University of British Columbia, Vancouver, BC, Canada 2 Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada 3 Centre for High-Throughput Biology, Department of Microbiology & Immunology, University of British Columbia, Vancouver, British Columbia, Canada
Alcohol exposure during brain development causes a number of long-lasting neurobio-logical deficits, including a lifelong dysregulation of the stress response. In both animal models and children with FASD, hypothalamic-pituitary-adrenal (HPA) axis function is permanently altered following prenatal ethanol exposure, showing greater basal tone and increased responsivity to stressors. While the etiology of HPA axis reprogramming remains unknown, the persistence of deficits throughout life makes epigenetic modifications prime suspects to explain its molecular underpinnings. In the following study, we examine the effect of prenatal alcohol exposure on DNA methylation profiles of the hypothalamus and white blood cells at four developmental time-points. On gestation day (GD) 1, Sprague-Daley dams were randomly assigned to one of three groups: prenatal alcohol exposure (PAE) – ad libitum liquid ethanol diet; pair-fed (PF) – liquid control diet, maltose dextrin isocalorically substituted for ethanol, in the amount consumed by a PAE partner (g/kg/body weight/GD); control (C) – ad libitum standard rat chow. The hypothalamus of female offspring was collected at postnatal days 0, 8, 15, and 22 and white bloods cells (WBC) were collected from whole blood at postnatal day 22 only. DNA methylation analysis was performed by methylated DNA immunoprecipitation followed by next-generation sequencing on the Illumina HiSeq (MeDIP-seq). Preliminary results suggest that PAE alters hypothalamic and white blood cell DNA methylation profiles. Moreover, not only do baseline (control) methylation patterns vary over developmental ages, but changes induced by PAE also occur across development. Persistent DNA methylation changes in the hypothalamus may explain the HPA axis alterations observed in both animal models and clinical studies of prenatal alcohol exposure. Moreover, correlations between methylome alterations in peripheral tissue and the brain may prove critical to the development of an easily measurable signature of fetal alcohol spectrum disorder.
http://dx.doi.org/10.1016/j.ijdevneu.2015.04.297 http://dx.doi.org/10.1016/j.ijdevneu.2015.04.298