Institution
Memorial University of Newfoundland
Education•St. John's, Newfoundland and Labrador, Canada•
About: Memorial University of Newfoundland is a education organization based out in St. John's, Newfoundland and Labrador, Canada. It is known for research contribution in the topics: Population & Context (language use). The organization has 13818 authors who have published 27785 publications receiving 743594 citations. The organization is also known as: Memorial University & Memorial University of Newfoundland and Labrador.
Topics: Population, Context (language use), Health care, Gadus, Computer science
Papers published on a yearly basis
Papers
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TL;DR: A significant genetic correlation with schizophrenia and association of ASD with several neurodevelopmental-related genes such as EXT1, ASTN2, MACROD2, and HDAC4 is identified and identified.
Abstract: Background: Over the past decade genome-wide association studies (GWAS) have been applied to aid in the
understanding of the biology of traits. The success of this approach is governed by the underlying effect sizes carried
by the true risk variants and the corresponding statistical power to observe such effects given the study design and
sample size under investigation. Previous ASD GWAS have identified genome-wide significant (GWS) risk loci; however,
these studies were of only of low statistical power to identify GWS loci at the lower effect sizes (odds ratio (OR) <1.15).
Methods: We conducted a large-scale coordinated international collaboration to combine independent genotyping
data to improve the statistical power and aid in robust discovery of GWS loci. This study uses genome-wide
genotyping data from a discovery sample (7387 ASD cases and 8567 controls) followed by meta-analysis of summary
statistics from two replication sets (7783 ASD cases and 11359 controls; and 1369 ASD cases and 137308 controls).
Results: We observe a GWS locus at 10q24.32 that overlaps several genes including PITX3, which encodes a transcription
factor identified as playing a role in neuronal differentiation and CUEDC2 previously reported to be associated with social
skills in an independent population cohort. We also observe overlap with regions previously implicated in schizophrenia
which was further supported by a strong genetic correlation between these disorders (Rg = 0.23; P=9 ×10−6). We further
combined these Psychiatric Genomics Consortium (PGC) ASD GWAS data with the recent PGC schizophrenia GWAS to
identify additional regions which may be important in a common neurodevelopmental phenotype and identified 12
novel GWS loci. These include loci previously implicated in ASD such as FOXP1 at 3p13, ATP2B2 at 3p25.3, and a
‘neurodevelopmental hub’ on chromosome 8p11.23.
Conclusions: This study is an important step in the ongoing endeavour to identify the loci which underpin the common
variant signal in ASD. In addition to novel GWS loci, we have identified a significant genetic correlation with schizophrenia
and association of ASD with several neurodevelopmental-related genes such as EXT1, ASTN2, MACROD2, and HDAC4.
458 citations
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McMaster University1, University of Pennsylvania2, University of Calgary3, Libin Cardiovascular Institute of Alberta4, Dalhousie University5, University of Alberta6, Alexandra Hospital7, Laval University8, University of Ottawa9, Concordia University10, Ottawa Hospital11, University of British Columbia12, Heart and Stroke Foundation of Canada13, Florida International University14, Queen's University15, University of Toronto16, Alberta Health Services17, Centre for Addiction and Mental Health18, University Health Network19, University of Minnesota20, York University21, Université de Sherbrooke22, Centre Hospitalier Universitaire de Sherbrooke23, Simon Fraser University24, Vancouver Island Health Authority25, Foothills Medical Centre26, University of Saskatchewan27, Population Health Research Institute28, St. Michael's Hospital29, St. John's University30, Memorial University of Newfoundland31
TL;DR: Obesity is a complex chronic disease in which abnormal or excess body fat (adiposity) impairs health, increases the risk of long-term medical complications and reduces lifespan.
Abstract: KEY POINTS
Obesity is a complex chronic disease in which abnormal or excess body fat (adiposity) impairs health, increases the risk of long-term medical complications and reduces lifespan.[1][1] Epidemiologic studies define obesity using the body mass index (BMI; weight/height2), which can stratify
457 citations
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TL;DR: Cultured and wild sea bass may be differentiated using total lipid content, fatty acid proportions and trace mineral compositions and these differences may be attributed to the constituents of the diet of the fish.
456 citations
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TL;DR: Results clearly show that postischemic hypothermia provides effective and long-lasting neuroprotection, which depends upon the delay to initiation, duration, and degree of cooling and survival time.
Abstract: In the gerbil, brief global forebrain ischemia induces profound habituation and working memory impairments that stem from delayed hippocampal CA1 death. Short duration postischemic hypothermia has been shown to reduce CA1 loss, but such reports are controversial, as it is thought that protection may be transient. The purpose of this study was to investigate whether prolonged postischemic hypothermia provided long- term CA1 and functional neuroprotection. Previously, 90% of anterior CA1 neurons were rescued (30 d survival) when 24 hr of hypothermia (32 degrees C) was induced 1 hr following a 5 min occlusion that otherwise produced more than 95% loss (Colbourne and Corbett, 1994). We now find about 70% CA1 savings with this same hypothermic treatment in gerbils that survived for 6 months postischemia. While this is a significant reduction from 30 day survival (medial CA1 only), it nonetheless shows, for the first time, persistent, if not permanent neuroprotection, especially in middle and lateral CA1. In addition, in non-treated animals, ischemia impaired learning in an open field and T-maze for up to 6 months. Postischemic hypothermia significantly reduced these deficits. Hypothermia (32 degrees), when initiated 4 hr after ischemia, rescued approximately 12% of CA1 neurons at 6 months with a slight behavioral benefit. Milder hypothermia (34 degrees C, 1–25 hr postischemia, 30 d survival) also reduced habituation impairments and saved approximately 60% of CA1 neurons. Similar trends were found at more caudal CA1 levels. These results clearly show that postischemic hypothermia provides effective and long-lasting neuroprotection, which depends upon the delay to initiation, duration, and degree of cooling and survival time. The protracted functional and histological benefit observed justifies further basic and clinical investigation.
453 citations
Authors
Showing all 13990 results
Name | H-index | Papers | Citations |
---|---|---|---|
Daniel Levy | 212 | 933 | 194778 |
Rakesh K. Jain | 200 | 1467 | 177727 |
Peter W.F. Wilson | 181 | 680 | 139852 |
Martin G. Larson | 171 | 620 | 117708 |
Peter B. Jones | 145 | 1857 | 94641 |
Dafna D. Gladman | 129 | 1036 | 75273 |
Guoyao Wu | 122 | 764 | 56270 |
Fereidoon Shahidi | 119 | 951 | 57796 |
David Harvey | 115 | 738 | 94678 |
Robert C. Haddon | 112 | 577 | 52712 |
Se-Kwon Kim | 102 | 763 | 39344 |
John E. Dowling | 94 | 305 | 28116 |
Mark J. Sarnak | 94 | 393 | 42485 |
William T. Greenough | 93 | 200 | 29230 |
Soottawat Benjakul | 92 | 891 | 34336 |