ORCID Profile
0000-0002-3035-9386
Current Organisations
University of Southampton
,
Columbia University
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Publisher: Public Library of Science (PLoS)
Date: 11-12-2009
Publisher: Springer Science and Business Media LLC
Date: 11-10-2009
DOI: 10.1038/NG.467
Publisher: Elsevier BV
Date: 02-2014
Publisher: Elsevier BV
Date: 11-2012
Publisher: Springer Science and Business Media LLC
Date: 06-01-2008
DOI: 10.1038/NG.72
Abstract: Recently, two common sequence variants on 9p21, tagged by rs10757278-G and rs10811661-T, were reported to be associated with coronary artery disease (CAD) and type 2 diabetes (T2D), respectively. We proceeded to further investigate the contributions of these variants to arterial diseases and T2D. Here we report that rs10757278-G is associated with, in addition to CAD, abdominal aortic aneurysm (AAA odds ratio (OR) = 1.31, P = 1.2 x 10(-12)) and intracranial aneurysm (OR = 1.29, P = 2.5 x 10(-6)), but not with T2D. This variant is the first to be described that affects the risk of AAA and intracranial aneurysm in many populations. The association of rs10811661-T to T2D replicates in our s les, but the variant does not associate with any of the five arterial diseases examined. These findings extend our insight into the role of the sequence variant tagged by rs10757278-G and show that it is not confined to atherosclerotic diseases.
Publisher: Springer Science and Business Media LLC
Date: 15-01-2006
DOI: 10.1038/NG1732
Abstract: We have previously reported suggestive linkage of type 2 diabetes mellitus to chromosome 10q. We genotyped 228 microsatellite markers in Icelandic in iduals with type 2 diabetes and controls throughout a 10.5-Mb interval on 10q. A microsatellite, DG10S478, within intron 3 of the transcription factor 7-like 2 gene (TCF7L2 formerly TCF4) was associated with type 2 diabetes (P = 2.1 x 10(-9)). This was replicated in a Danish cohort (P = 4.8 x 10(-3)) and in a US cohort (P = 3.3 x 10(-9)). Compared with non-carriers, heterozygous and homozygous carriers of the at-risk alleles (38% and 7% of the population, respectively) have relative risks of 1.45 and 2.41. This corresponds to a population attributable risk of 21%. The TCF7L2 gene product is a high mobility group box-containing transcription factor previously implicated in blood glucose homeostasis. It is thought to act through regulation of proglucagon gene expression in enteroendocrine cells via the Wnt signaling pathway.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 2014
DOI: 10.1161/STROKEAHA.113.002707
Abstract: Ischemic stroke (IS) and coronary artery disease (CAD) share several risk factors and each has a substantial heritability. We conducted a genome-wide analysis to evaluate the extent of shared genetic determination of the two diseases. Genome-wide association data were obtained from the METASTROKE, Coronary Artery Disease Genome-wide Replication and Meta-analysis (CARDIoGRAM), and Coronary Artery Disease (C4D) Genetics consortia. We first analyzed common variants reaching a nominal threshold of significance ( P .01) for CAD for their association with IS and vice versa. We then examined specific overlap across phenotypes for variants that reached a high threshold of significance. Finally, we conducted a joint meta-analysis on the combined phenotype of IS or CAD. Corresponding analyses were performed restricted to the 2167 in iduals with the ischemic large artery stroke (LAS) subtype. Common variants associated with CAD at P .01 were associated with a significant excess risk for IS and for LAS and vice versa. Among the 42 known genome-wide significant loci for CAD, 3 and 5 loci were significantly associated with IS and LAS, respectively. In the joint meta-analyses, 15 loci passed genome-wide significance ( P ×10 −8 ) for the combined phenotype of IS or CAD and 17 loci passed genome-wide significance for LAS or CAD. Because these loci had prior evidence for genome-wide significance for CAD, we specifically analyzed the respective signals for IS and LAS and found evidence for association at chr12q24/SH2B3 ( P IS =1.62×10 −7 ) and ABO ( P IS =2.6×10 −4 ), as well as at HDAC9 ( P LAS =2.32×10 −12 ), 9p21 ( P LAS =3.70×10 −6 ), RAI1-PEMT-RASD1 ( P LAS =2.69×10 −5 ), EDNRA ( P LAS =7.29×10 −4 ), and CYP17A1-CNNM2-NT5C2 ( P LAS =4.9×10 −4 ). Our results demonstrate substantial overlap in the genetic risk of IS and particularly the LAS subtype with CAD.
Publisher: Elsevier BV
Date: 03-2014
Publisher: Springer Science and Business Media LLC
Date: 08-02-2009
DOI: 10.1038/NG.323
Abstract: Eosinophils are pleiotropic multifunctional leukocytes involved in initiation and propagation of inflammatory responses and thus have important roles in the pathogenesis of inflammatory diseases. Here we describe a genome-wide association scan for sequence variants affecting eosinophil counts in blood of 9,392 Icelanders. The most significant SNPs were studied further in 12,118 Europeans and 5,212 East Asians. SNPs at 2q12 (rs1420101), 2q13 (rs12619285), 3q21 (rs4857855), 5q31 (rs4143832) and 12q24 (rs3184504) reached genome-wide significance (P = 5.3 x 10(-14), 5.4 x 10(-10), 8.6 x 10(-17), 1.2 x 10(-10) and 6.5 x 10(-19), respectively). A SNP at IL1RL1 associated with asthma (P = 5.5 x 10(-12)) in a collection of ten different populations (7,996 cases and 44,890 controls). SNPs at WDR36, IL33 and MYB that showed suggestive association with eosinophil counts were also associated with atopic asthma (P = 4.2 x 10(-6), 2.2 x 10(-5) and 2.4 x 10(-4), respectively). We also found that a nonsynonymous SNP at 12q24, in SH2B3, associated significantly (P = 8.6 x 10(-8)) with myocardial infarction in six different populations (6,650 cases and 40,621 controls).
Publisher: Elsevier BV
Date: 03-2012
Publisher: Springer Science and Business Media LLC
Date: 26-04-2007
DOI: 10.1038/NG2043
Abstract: We conducted a genome-wide association study for type 2 diabetes (T2D) in Icelandic cases and controls, and we found that a previously described variant in the transcription factor 7-like 2 gene (TCF7L2) gene conferred the most significant risk. In addition to confirming two recently identified risk variants, we identified a variant in the CDKAL1 gene that was associated with T2D in in iduals of European ancestry (allele-specific odds ratio (OR) = 1.20 (95% confidence interval, 1.13-1.27), P = 7.7 x 10(-9)) and in iduals from Hong Kong of Han Chinese ancestry (OR = 1.25 (1.11-1.40), P = 0.00018). The genotype OR of this variant suggested that the effect was substantially stronger in homozygous carriers than in heterozygous carriers. The ORs for homozygotes were 1.50 (1.31-1.72) and 1.55 (1.23-1.95) in the European and Hong Kong groups, respectively. The insulin response for homozygotes was approximately 20% lower than for heterozygotes or noncarriers, suggesting that this variant confers risk of T2D through reduced insulin secretion.
Publisher: Public Library of Science (PLoS)
Date: 31-07-2014
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 11-2010
DOI: 10.1161/ATVBAHA.109.201020
Abstract: Objective— Genetic studies might provide new insights into the biological mechanisms underlying lipid metabolism and risk of CAD. We therefore conducted a genome-wide association study to identify novel genetic determinants of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides. Methods and Results— We combined genome-wide association data from 8 studies, comprising up to 17 723 participants with information on circulating lipid concentrations. We did independent replication studies in up to 37 774 participants from 8 populations and also in a population of Indian Asian descent. We also assessed the association between single-nucleotide polymorphisms (SNPs) at lipid loci and risk of CAD in up to 9 633 cases and 38 684 controls. We identified 4 novel genetic loci that showed reproducible associations with lipids (probability values, 1.6×10 −8 to 3.1×10 −10 ). These include a potentially functional SNP in the SLC39A8 gene for HDL-C, an SNP near the MYLIP/GMPR and PPP1R3B genes for LDL-C, and at the AFF1 gene for triglycerides. SNPs showing strong statistical association with 1 or more lipid traits at the CELSR2 , APOB , APOE-C1-C4-C2 cluster, LPL , ZNF259-APOA5-A4-C3-A1 cluster and TRIB1 loci were also associated with CAD risk (probability values, 1.1×10 −3 to 1.2×10 −9 ). Conclusion— We have identified 4 novel loci associated with circulating lipids. We also show that in addition to those that are largely associated with LDL-C, genetic loci mainly associated with circulating triglycerides and HDL-C are also associated with risk of CAD. These findings potentially provide new insights into the biological mechanisms underlying lipid metabolism and CAD risk.
Publisher: Oxford University Press (OUP)
Date: 04-06-2013
DOI: 10.1093/HMG/DDT177
Publisher: Springer Science and Business Media LLC
Date: 08-2010
DOI: 10.1038/NATURE09270
Publisher: Elsevier BV
Date: 03-2013
Publisher: Informa UK Limited
Date: 16-07-2019
DOI: 10.1080/15402002.2019.1641501
Abstract: Children with Down syndrome (DS) commonly experience difficulties with executive function (EF). They are also vulnerable to obstructive sleep apnoea (OSA). OSA is associated with EF deficits in typically developing children. A recent study reported an association between OSA and cognitive deficits in 38 school-aged children with DS. We experimentally investigated EF behaviours in young children with DS, and their association with OSA. Children with DS were recruited to take part in a larger study of OSA (N = 202). Parents of 80 children (50 male) aged 36 to 71 months ( Obstructive apnoea/hypopnoea index was in the normal range (0-1.49/h) for 28 children but indicated OSA (≥1.5/h) in 41 children. Consistent with previous research, we found a large effect for children experiencing particular weaknesses in working memory, planning and organising, whilst emotional control was a relative strength. OSA was associated with poorer working memory (β = .23, R2 = .05, Findings suggest that known EF difficulties in DS are already evident at this young age. Children with DS already have limited cognitive reserve and can ill afford additional EF deficit associated with OSA. OSA is amenable to treatment and should be actively treated in these children to promote optimal cognitive development.
Publisher: Springer Science and Business Media LLC
Date: 06-10-2013
DOI: 10.1038/NG.2795
Publisher: Springer Science and Business Media LLC
Date: 06-10-2013
DOI: 10.1038/NG.2797
Publisher: Elsevier BV
Date: 04-2015
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Muredach Reilly.