Connaissances et perceptions de la religion et du phénomène de la radicalisation chez les étudiant(e)s du collégial

Comprend des références bibliographiquesDiffusé avec l'aimable autorisation des auteurs. Le document original est également accessible en ligne : http://cefir.cegepmontpetit.ca/2018/05/16/connaissances-et-perceptions-de-la-religion-et-du-phenomene-de-la-radicalisation-chez-les-etudiantes-du-collegial-2018

Promoting New Approach Methodologies (NAMs) for research on skin color changes in response to environmental stress factors: tobacco and air pollution

Aging is one of the most dynamic biological processes in the human body and is known to carry significant impacts on individuals’ self-esteem. Skin pigmentation is a highly heritable trait made possible by complex, strictly controlled cellular and molecular mechanisms. Genetic, environmental and endocrine factors contribute to the modulation of melanin’s amount, type and distribution in the skin layers. One of the hallmarks of extrinsic skin aging induced by environmental stress factors is the alteration of the constitutive pigmentation pattern clinically defined as senile lentigines and/or melasma or other pigmentary dyschromias. The complexity of pollutants and tobacco smoke as environmental stress factors warrants a thorough understanding of the mechanisms by which they impact skin pigmentation through repeated and long-term exposure. Pre-clinical and clinical studies demonstrated that pollutants are known to induce reactive oxygen species (ROS) or inflammatory events that lead directly or indirectly to skin hyperpigmentation. Another mechanistic direction is provided by Aryl hydrocarbon Receptors (AhR) which were shown to mediate processes leading to skin hyperpigmentation in response to pollutants by regulation of melanogenic enzymes and transcription factors involved in melanin biosynthesis pathway. In this context, we will discuss a diverse range of New Approach Methodologies (NAMs) capable to provide mechanistic insights of the cellular and molecular pathways involved in the action of environmental stress factors on skin pigmentation and to support the design of raw ingredients and formulations intended to counter their impact and of any subsequently needed clinical studies

Prenatal Exposure to Organophosphate Pesticides and IQ in 7-Year-Old Children

Context: Organophosphate (OP) pesticides are neurotoxic at high doses. Few studies have examined whether chronic exposure at lower levels could adversely affect children’s cognitive development

Making the Grade through the Front Door: Evaluation and Innovation in a Registered Practical Nurse to Bachelor of Science in Nursing Program

Background: Education of nurses from a diploma to a degree is a global phenomenon. However, bridging is often seen as a ‘backdoor’ route to becoming a Registered Nurse and very little evaluation data exists to challenge this notion. Objectives: This research project was undertaken to explore student characteristics, academic performance, outcomes, and experiences in an RPN-to-BScN Bridging Program. Design: A mixed method design was employed. Student admission and registrarial data were examined in relation to student characteristics and academic performance. Secondary data analysis was conducted on focus group interviews with 110 students that explored their perceptions of the impact of the program on their lives. Setting: Data was collected through University databases and face to face focus groups. Participants: Admission and registrarial data for all students admitted to a nursing bridging program in Ontario, Canada, from 2005-2011 were analyzed. Participants in the qualitative focus group interviews included 110 students across all years of the program. Methods: Descriptive and analytical statistics provide insight into student performance and characteristics. Qualitative data analysis was conducted using NVivo 9 with multi-member teams. Results: Data analysis reveals important insights into student academic performance, including exploration of relevant variables such as ongoing and cumulative GPA, entrance GPA, and program completion. Qualitative analysis provides insight into how studying in the program affects students’ lives. Conclusions: RPN-to-BScN education is not a “back door” to a nursing degree. Rather, it is a front door, as rigorous and as personally and professionally transformative as we expect a 4-year BScN Degree to be

Correlates of overall and central obesity in adults from seven European countries: findings from the Food4Me Study

To identify predictors of obesity in adults and investigate to what extent these predictors are independent of other major confounding factors. Data collected at baseline from 1441 participants from the Food4Me study conducted in seven European countries were included in this study. A food frequency questionnaire was used to measure dietary intake. Accelerometers were used to assess physical activity levels (PA), whereas participants self-reported their body weight, height and waist circumference via the internet. The main factors associated (p < 0.05) with higher BMI per 1-SD increase in the exposure were age (β:1.11 kg/m2), intakes of processed meat (β:1.04 kg/m2), red meat (β:1.02 kg/m2), saturated fat (β:0.84 kg/m2), monounsaturated fat (β:0.80 kg/m2), protein (β:0.74 kg/m2), total energy intake (β:0.50 kg/m2), olive oil (β:0.36 kg/m2), sugar sweetened carbonated drinks (β:0.33 kg/m2) and sedentary time (β:0.73 kg/m2). In contrast, the main factors associated with lower BMI per 1-SD increase in the exposure were PA (β:-1.36 kg/m2), intakes of wholegrains (β:-1.05 kg/m2), fibre (β:-1.02 kg/m2), fruits and vegetables (β:-0.52 kg/m2), nuts (β:-0.52 kg/m2), polyunsaturated fat (β:-0.50 kg/m2), Healthy Eating Index (β:-0.42 kg/m2), Mediterranean diet score (β:-0.40 kg/m2), oily fish (β:-0.31 kg/m2), dairy (β:-0.31 kg/m2) and fruit juice (β:-0.25 kg/m2). These findings are important for public health and suggest that promotion of increased PA, reducing sedentary behaviours and improving the overall quality of dietary patterns are important strategies for addressing the existing obesity epidemic and associated disease burden

Genome-wide association study of offspring birth weight in 86 577 women identifies five novel loci and highlights maternal genetic effects that are independent of fetal genetics

Funding Information: Researchers were funded by investment from the European Regional Development Fund (ERDF) and the European Social Fund (ESF) Convergence Programme for Cornwall and the Isles of Scilly [J.T.]; European Research Council (ERC) [grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC to T.M.F., A.R.W.], [ERC Consolidator Grant, ERC-2014-CoG-648916 to V.W.V.J.], [P.R.N.]; University of Bergen, KG Jebsen and Helse Vest [P.R.N.]; Wellcome Trust Senior Investigator Awards [A.T.H. (WT098395), M.I.M. (WT098381)]; National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0611–10219); Sir Henry Dale Fellowship (Wellcome Trust and Royal Society grant: WT104150) [R.M.F., R.N.B.]; 4-year studentship (Grant Code: WT083431MF) [R.C.R]; the European Research Council under the European Union’s Seventh Framework Programme (FP/2007– 2013)/ERC Grant Agreement (grant number 669545; Develop Obese) [D.A.L.]; US National Institute of Health (grant: R01 DK10324) [D.A.L, C.L.R]; Wellcome Trust GWAS grant (WT088806) [D.A.L] and NIHR Senior Investigator Award (NF-SI-0611–10196) [D.A.L]; Wellcome Trust Institutional Strategic Support Award (WT097835MF) [M.A.T.]; The Diabetes Research and Wellness Foundation Non-Clinical Fellowship [J.T.]; Australian National Health and Medical Research Council Early Career Fellowship (APP1104818) [N.M.W.]; Daniel B. Burke Endowed Chair for Diabetes Research [S.F.A.G.]; UK Medical Research Council Unit grants MC_UU_12013_5 [R.C.R, L.P, S.R, C.L.R, D.M.E., D.A.L.] and MC_UU_12013_4 [D.M.E.]; Medical Research Council (grant: MR/M005070/1) [M.N.W., S.E.J.]; Australian Research Council Future Fellowship (FT130101709) [D.M.E] and (FT110100548) [S.E.M.]; NIHR Oxford Biomedical Research Centre (BRC); Oak Foundation Fellowship and Novo Nordisk Foundation (12955) [B.F.]; FRQS research scholar and Clinical Scientist Award by the Canadian Diabetes Association and the Maud Menten Award from the Institute of Genetics– Canadian Institute of Health Research (CIHR) [MFH]; CIHR— Frederick Banting and Charles Best Canada Graduate Scholarships [C.A.]; FRQS [L.B.]; Netherlands Organization for Health Research and Development (ZonMw–VIDI 016.136.361) [V.W.V.J.]; National Institute on Aging (R01AG29451) [J.M.M.]; 2010–2011 PRIN funds of the University of Ferrara—Holder: Prof. Guido Barbujani, Supervisor: Prof. Chiara Scapoli—and in part sponsored by the European Foundation for the Study of Diabetes (EFSD) Albert Renold Travel Fellowships for Young Scientists, ‘5 per mille’ contribution assigned to the University of Ferrara, income tax return year 2009 and the ENGAGE Exchange and Mobility Program for ENGAGE training funds, ENGAGE project, grant agreement HEALTH-F4–2007-201413 [L.M.]; ESRC (RES-060–23-0011) [C.L.R.]; National Institute of Health Research ([S.D., M.I.M.], Senior Investigator Award (NF-SI-0611–10196) [D.A.L]); Australian NHMRC Fellowships Scheme (619667) [G.W.M]. For study-specific funding, please see Supplementary Material. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Funding to pay the Open Access publication charges for this article was provided by the Charity Open Access Fund (COAF). Funding Information: We are extremely grateful to the participants and families who contributed to all of the studies and the teams of investigators involved in each one. These include interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists and nurses. This research has been conducted using the UK Biobank Resource (Application numbers 7036 and 12703). For additional study-specific acknowledgements, please see Supplementary Material. Conflict of Interest statement. D.A.L. has received support from Roche Diagnostics and Medtronic for biomarker research unrelated to the work presented here. Funding Researchers were funded by investment from the European Regional Development Fund (ERDF) and the European Social Fund (ESF) Convergence Programme for Cornwall and the Isles of Scilly [J.T.]; European Research Council (ERC) [grant: SZ-245 50371-GLUCOSEGENES-FP7-IDEAS-ERC to T.M.F., A.R.W.], [ERC Consolidator Grant, ERC-2014-CoG-648916 to V.W.V.J.], [P.R.N.]; University of Bergen, KG Jebsen and Helse Vest [P.R.N.]; Wellcome Trust Senior Investigator Awards [A.T.H. (WT098395), M.I.M. (WT098381)]; National Institute for Health Research (NIHR) Senior Investigator Award (NF-SI-0611-10219); Sir Henry Dale Fellowship (Wellcome Trust and Royal Society grant: WT104150) [R.M.F., R.N.B.]; 4-year studentship (Grant Code: WT083431MF) [R.C.R]; the European Research Council under the European Union's Seventh Framework Programme (FP/2007-2013)/ERC Grant Agreement (grant number 669545; Develop Obese) [D.A.L.]; US National Institute of Health (grant: R01 DK10324) [D.A.L, C.L.R]; Wellcome Trust GWAS grant (WT088806) [D.A.L] and NIHR Senior Investigator Award (NF-SI-0611-10196) [D.A.L]; Wellcome Trust Institutional Strategic Support Award (WT097835MF) [M.A.T.]; The Diabetes Research and Wellness Foundation Non-Clinical Fellowship [J.T.]; Australian National Health and Medical Research Council Early Career Fellowship (APP1104818) [N.M.W.]; Daniel B. Burke Endowed Chair for Diabetes Research [S.F.A.G.]; UK Medical Research Council Unit grants MC_UU_12013_5 [R.C.R, L.P, S.R, C.L.R, D.M.E., D.A.L.] and MC_UU_12013_4 [D.M.E.]; Medical Research Council (grant: MR/M005070/1) [M.N.W., S.E.J.]; Australian Research Council Future Fellowship (FT130101709) [D.M.E] and (FT110100548) [S.E.M.]; NIHR Oxford Biomedical Research Centre (BRC); Oak Foundation Fellowship and Novo Nordisk Foundation (12955) [B.F.]; FRQS research scholar and Clinical Scientist Award by the Canadian Diabetes Association and the Maud Menten Award from the Institute of Genetics-Canadian Institute of Health Research (CIHR) [MFH]; CIHR-Frederick Banting and Charles Best Canada Graduate Scholarships [C.A.]; FRQS [L.B.]; Netherlands Organization for Health Research and Development (ZonMw-VIDI 016.136.361) [V.W.V.J.]; National Institute on Aging (R01AG29451) [J.M.M.]; 2010-2011 PRIN funds of the University of Ferrara-Holder: Prof. Guido Barbujani, Supervisor: Prof. Chiara Scapoli-and in part sponsored by the European Foundation for the Study of Diabetes (EFSD) Albert Renold Travel Fellowships for Young Scientists, '5 per mille' contribution assigned to the University of Ferrara, income tax return year 2009 and the ENGAGE Exchange and Mobility Program for ENGAGE training funds, ENGAGE project, grant agreement HEALTH-F4-2007-201413 [L.M.]; ESRC (RES-060-23-0011) [C.L.R.]; National Institute of Health Research ([S.D., M.I.M.], Senior Investigator Award (NFSI-0611-10196) [D.A.L]); Australian NHMRC Fellowships Scheme (619667) [G.W.M]. For study-specific funding, please see Supplementary Material. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health. Funding to pay the Open Access publication charges for this article was provided by the Charity Open Access Fund (COAF). Publisher Copyright: © The Author(s) 2018.Genome-wide association studies of birth weight have focused on fetal genetics, whereas relatively little is known about the role of maternal genetic variation. We aimed to identify maternal genetic variants associated with birth weight that could highlight potentially relevant maternal determinants of fetal growth. We meta-analysed data on up to 8.7 million SNPs in up to 86 577 women of European descent from the Early Growth Genetics (EGG) Consortium and the UK Biobank. We used structural equation modelling (SEM) and analyses of mother-child pairs to quantify the separate maternal and fetal genetic effects. Maternal SNPs at 10 loci (MTNR1B, HMGA2, SH2B3, KCNAB1, L3MBTL3, GCK, EBF1, TCF7L2, ACTL9, CYP3A7) were associated with offspring birth weight at P<5 x 10(-8). In SEM analyses, at least 7 of the 10 associations were consistent with effects of the maternal genotype acting via the intrauterine environment, rather than via effects of shared alleles with the fetus. Variants, or correlated proxies, at many of the loci had been previously associated with adult traits, including fasting glucose (MTNR1B, GCK and TCF7L2) and sex hormone levels (CYP3A7), and one (EBF1) with gestational duration. The identified associations indicate that genetic effects on maternal glucose, cytochrome P450 activity and gestational duration, and potentially on maternal blood pressure and immune function, are relevant for fetal growth. Further characterization of these associations in mechanistic and causal analyses will enhance understanding of the potentially modifiable maternal determinants of fetal growth, with the goal of reducing the morbidity and mortality associated with low and high birth weights.Peer reviewe

Effects of ocean sprawl on ecological connectivity: impacts and solutions

The growing number of artificial structures in estuarine, coastal and marine environments is causing “ocean sprawl”. Artificial structures do not only modify marine and coastal ecosystems at the sites of their placement, but may also produce larger-scale impacts through their alteration of ecological connectivity - the movement of organisms, materials and energy between habitat units within seascapes. Despite the growing awareness of the capacity of ocean sprawl to influence ecological connectivity, we lack a comprehensive understanding of how artificial structures modify ecological connectivity in near- and off-shore environments, and when and where their effects on connectivity are greatest. We review the mechanisms by which ocean sprawl may modify ecological connectivity, including trophic connectivity associated with the flow of nutrients and resources. We also review demonstrated, inferred and likely ecological impacts of such changes to connectivity, at scales from genes to ecosystems, and potential strategies of management for mitigating these effects. Ocean sprawl may alter connectivity by: (1) creating barriers to the movement of some organisms and resources - by adding physical barriers or by modifying and fragmenting habitats; (2) introducing new structural material that acts as a conduit for the movement of other organisms or resources across the landscape; and (3) altering trophic connectivity. Changes to connectivity may, in turn, influence the genetic structure and size of populations, the distribution of species, and community structure and ecological functioning. Two main approaches to the assessment of ecological connectivity have been taken: (1) measurement of structural connectivity - the configuration of the landscape and habitat patches and their dynamics; and (2) measurement of functional connectivity - the response of organisms or particles to the landscape. Our review reveals the paucity of studies directly addressing the effects of artificial structures on ecological connectivity in the marine environment, particularly at large spatial and temporal scales. With the ongoing development of estuarine and marine environments, there is a pressing need for additional studies that quantify the effects of ocean sprawl on ecological connectivity. Understanding the mechanisms by which structures modify connectivity is essential if marine spatial planning and eco-engineering are to be effectively utilised to minimise impacts

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD