W E R Ollier

Salford Royal NHS Foundation Trust, Salford, England, United Kingdom

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Publications (536)2266.3 Total impact

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    ABSTRACT: Cognitive abilities (memory, processing speed, vocabulary, and fluid intelligence) are correlated with educational attainment and occupational status, as well as physical and mental health. The variation in cognitive abilities observed within a population has a substantial genetic contribution (heritability ∼50%) and yet the identification of genetic polymorphisms from both genome-wide association and candidate studies have to date only uncovered a limited number of genetic variants that exert small genetic effects. Here we impute human leukocyte antigens (HLA) using existing genome-wide association data from 1,559 non-pathological elderly volunteers who have been followed for changes in cognitive functioning between a 12- and 18-year period. Specifically, we investigate DRB1*05 (*11/*12) and DRB1*01, which have previously been associated with cognitive ability. We also analyze DRB1*0801, which shares close sequence homology with DRB1*1101. Together with DRB1*1101, DRB1*0801 has been associated with several diseases including multiple sclerosis and primary biliary cirrhosis, which themselves are associated with cognitive impairment. We observed that both DRB1*0801 and DRB1*1101 were significantly associated with vocabulary ability (cross-sectional and longitudinal scores) and that the effects were in opposite directions with DRB1*0801 associated with lower score and faster decline. This opposing affect is similar to that reported by other groups in systemic lupus erythematosus, type 1 diabetes, and primary biliary cirrhosis. DRB1*0801 was also significantly associated with reduced memory ability. We observed no associations between cognitive abilities and DRB1*01 or DRB1*12. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 10/2015; DOI:10.1002/ajmg.b.32393 · 3.42 Impact Factor
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    ABSTRACT: Inbreeding depression refers to lower fitness among offspring of genetic relatives. This reduced fitness is caused by the inheritance of two identical chromosomal segments (autozygosity) across the genome, which may expose the effects of (partially) recessive deleterious mutations. Even among outbred populations, autozygosity can occur to varying degrees due to cryptic relatedness between parents. Using dense genome-wide single-nucleotide polymorphism (SNP) data, we examined the degree to which autozygosity associated with measured cognitive ability in an unselected sample of 4854 participants of European ancestry. We used runs of homozygosity—multiple homozygous SNPs in a row—to estimate autozygous tracts across the genome. We found that increased levels of autozygosity predicted lower general cognitive ability, and estimate a drop of 0.6 s.d. among the offspring of first cousins (P=0.003–0.02 depending on the model). This effect came predominantly from long and rare autozygous tracts, which theory predicts as more likely to be deleterious than short and common tracts. Association mapping of autozygous tracts did not reveal any specific regions that were predictive beyond chance after correcting for multiple testing genome wide. The observed effect size is consistent with studies of cognitive decline among offspring of known consanguineous relationships. These findings suggest a role for multiple recessive or partially recessive alleles in general cognitive ability, and that alleles decreasing general cognitive ability have been selected against over evolutionary time.
    Molecular Psychiatry 09/2015; DOI:10.1038/mp.2015.120 · 14.50 Impact Factor
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    ABSTRACT: Objectives: The idiopathic inflammatory myopathies (IIMs) are a heterogeneous group of rare autoimmune diseases characterised by muscle weakness and extramuscular manifestations such as skin rashes and interstitial lung disease. We genotyped 2566 IIM cases of Caucasian descent using the Immunochip; a custom array covering 186 established autoimmune susceptibility loci. The cohort was predominantly comprised of patients with dermatomyositis (DM, n=879), juvenile DM (JDM, n=481), polymyositis (PM, n=931) and inclusion body myositis (n=252) collected from 14 countries through the Myositis Genetics Consortium. Results: The human leucocyte antigen (HLA) and PTPN22 regions reached genome-wide significance (p<5×10(-8)). Nine regions were associated at a significance level of p<2.25×10(-5), including UBE2L3, CD28 and TRAF6, with evidence of independent effects within STAT4. Analysis of clinical subgroups revealed distinct differences between PM, and DM and JDM. PTPN22 was associated at genome-wide significance with PM, but not DM and JDM, suggesting this effect is driven by PM. Additional suggestive associations including IL18R1 and RGS1 in PM and GSDMB in DM were identified. HLA imputation confirmed that alleles HLA-DRB1*03:01 and HLA-B*08:01 of the 8.1 ancestral haplotype (8.1AH) are most strongly associated with IIM, and provides evidence that amino acids within the HLA, such as HLA-DQB1 position 57 in DM, may explain part of the risk in this locus. Associations with alleles outside the 8.1AH reveal differences between PM, DM and JDM. Conclusions: This work represents the largest IIM genetic study to date, reveals new insights into the genetic architecture of these rare diseases and suggests different predominating pathophysiology in different clinical subgroups.
    Annals of the rheumatic diseases 09/2015; DOI:10.1136/annrheumdis-2015-208119 · 10.38 Impact Factor
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    ABSTRACT: Hypothyroidism is a complex clinical condition found in both humans and dogs, thought to be caused by a combination of genetic and environmental factors. In this study we present a multi-breed analysis of predisposing genetic risk factors for hypothyroidism in dogs using three high-risk breeds—the Gordon Setter, Hovawart and the Rhodesian Ridgeback. Using a genome-wide association approach and meta-analysis, we identified a major hypothyroidism risk locus shared by these breeds on chromosome 12 (p = 2.1x10-11). Further characterisa-tion of the candidate region revealed a shared ~167 kb risk haplotype (4,915,018–5,081,823 bp), tagged by two SNPs in almost complete linkage disequilibrium. This breed-shared risk haplotype includes three genes (LHFPL5, SRPK1 and SLC26A8) and does not extend to the dog leukocyte antigen (DLA) class II gene cluster located in the vicinity. These three genes have not been identified as candidate genes for hypothyroid disease previously, but have functions that could potentially contribute to the development of the disease. Our results implicate the potential involvement of novel genes and pathways for the development of canine hypothyroidism, raising new possibilities for screening, breeding programmes and treatments in dogs. This study may also contribute to our understanding of the genetic etiology of human hypothyroid disease, which is one of the most common endocrine disorders in humans.
    PLoS ONE 09/2015; 10(8). DOI:10.1371/journal.pone.0134720 · 3.23 Impact Factor
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    ABSTRACT: Autoimmune muscle diseases (myositis) comprise a group of complex phenotypes influenced by genetic and environmental factors. To identify genetic risk factors in patients of European ancestry, we conducted a genome-wide association study (GWAS) of the major myositis phenotypes in a total of 1710 cases, which included 705 adult dermatomyositis, 473 juvenile dermatomyositis, 532 polymyositis and 202 adult dermatomyositis, juvenile dermatomyositis or polymyositis patients with anti-histidyl-tRNA synthetase (anti-Jo-1) autoantibodies, and compared them with 4724 controls. Single-nucleotide polymorphisms showing strong associations (P<5 × 10(-8)) in GWAS were identified in the major histocompatibility complex (MHC) region for all myositis phenotypes together, as well as for the four clinical and autoantibody phenotypes studied separately. Imputation and regression analyses found that alleles comprising the human leukocyte antigen (HLA) 8.1 ancestral haplotype (AH8.1) defined essentially all the genetic risk in the phenotypes studied. Although the HLA DRB1*03:01 allele showed slightly stronger associations with adult and juvenile dermatomyositis, and HLA B*08:01 with polymyositis and anti-Jo-1 autoantibody-positive myositis, multiple alleles of AH8.1 were required for the full risk effects. Our findings establish that alleles of the AH8.1 comprise the primary genetic risk factors associated with the major myositis phenotypes in geographically diverse Caucasian populations.Genes and Immunity advance online publication, 20 August 2015; doi:10.1038/gene.2015.28.
    Genes and immunity 08/2015; DOI:10.1038/gene.2015.28 · 2.91 Impact Factor
  • Angela L Holder · Lorna J Kennedy · William E R Ollier · Brian Catchpole ·
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    ABSTRACT: Administration of insulin for treatment of diabetes mellitus in dogs can stimulate an immune response, with a proportion of animals developing anti-insulin antibodies (AIA). For an IgG antibody response to occur, this would require B cell presentation of insulin peptides by major histocompatibility complex (MHC) class II molecules, encoded by dog leukocyte antigen (DLA) genes, in order to receive T-cell help for class switching. DLA genes are highly polymorphic in the dog population and vary from breed to breed. The aim of the present study was to evaluate AIA reactivity in diabetic dogs of different breeds and to investigate whether DLA genes influence AIA status.
    Veterinary Immunology and Immunopathology 08/2015; 167(3). DOI:10.1016/j.vetimm.2015.07.014 · 1.54 Impact Factor
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    ABSTRACT: In common with several other autoimmune diseases, autoimmune Addison's disease (AAD) is thought to be caused by a combination of deleterious susceptibility polymorphisms in several genes, together with undefined environmental factors and stochastic events. To date, the strongest genomic association with AAD has been with alleles at the HLA locus, DR3-DQ2 and DR4. The contribution of other genetic variants has been inconsistent. We have studied the association of 16 single-nucleotide polymorphisms (SNPs) within the CD28-CTLA-4-ICOS genomic locus, in a cohort comprising 691 AAD patients of Norwegian and UK origin with matched controls. We have also performed a meta-analysis including 1002 patients from European countries. The G-allele of SNP rs231775 in CTLA-4 is associated with AAD in Norwegian patients (odds ratio (OR)=1.35 (confidence interval (CI) 1.10-1.66), P=0.004), but not in UK patients. The same allele is associated with AAD in the total European population (OR=1.37 (CI 1.13-1.66), P=0.002). A three-marker haplotype, comprising PROMOTER_1661, rs231726 and rs1896286 was found to be associated with AAD in the Norwegian cohort only (OR 2.43 (CI 1.68-3.51), P=0.00013). This study points to the CTLA-4 gene as a susceptibility locus for the development of AAD, and refines its mapping within the wider genomic locus.Genes and Immunity advance online publication, 23 July 2015; doi:10.1038/gene.2015.27.
    Genes and immunity 07/2015; 16(6). DOI:10.1038/gene.2015.27 · 2.91 Impact Factor
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    ABSTRACT: Cognitive deficits and reduced educational achievement are common in psychiatric illness; understanding the genetic basis of cognitive and educational deficits may be informative about the etiology of psychiatric disorders. A recent, large genome-wide association study (GWAS) reported a genome-wide significant locus for years of education, which subsequently demonstrated association to general cognitive ability ("g") in overlapping cohorts. The current study was designed to test whether GWAS hits for educational attainment are involved in general cognitive ability in an independent, large-scale collection of cohorts. Using cohorts in the Cognitive Genomics Consortium (COGENT; up to 20,495 healthy individuals), we examined the relationship between g and variants associated with educational attainment. We next conducted meta-analyses with 24,189 individuals with neurocognitive data from the educational attainment studies, and then with 53,188 largely independent individuals from a recent GWAS of cognition. A SNP (rs1906252) located at chromosome 6q16.1, previously associated with years of schooling, was significantly associated with g (P = 1.47 × 10(-4) ) in COGENT. The first joint analysis of 43,381 non-overlapping individuals for this a priori-designated locus was strongly significant (P = 4.94 × 10(-7) ), and the second joint analysis of 68,159 non-overlapping individuals was even more robust (P = 1.65 × 10(-9) ). These results provide independent replication, in a large-scale dataset, of a genetic locus associated with cognitive function and education. As sample sizes grow, cognitive GWAS will identify increasing numbers of associated loci, as has been accomplished in other polygenic quantitative traits, which may be relevant to psychiatric illness. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 07/2015; 168(5). DOI:10.1002/ajmg.b.32319 · 3.42 Impact Factor
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    ABSTRACT: Swallowing difficulties (dysphagia) affect a significant proportion of community dwelling older individuals, being more prevalent in age-associated neurological conditions such as stroke and Parkinson's disease. The genetic determinants of dysphagia are still being explored and have largely been studied through candidate gene analysis approaches. The aim of the study was to perform a genome-wide association study (GWAS) of common genetic single nucleotide polymorphisms (SNP) and self-reported swallowing impairments in a longitudinal cohort of community dwelling older adults. We performed a case-control genome-wide association study of self-reported swallowing symptoms using the Sydney Swallow Questionnaire. The analysis included 555 community dwelling, unrelated, older adults (mean years of age=81.4; SD=5.349) with known phenotype and genetic information consisting of 512,806 single nucleotide polymorphisms. Gene-based association analysis of these traits was also conducted. Analysis of the cohort confirmed European ancestry with no major population stratification. Further analysis for association with swallowing impairment identified one SNP rs17601696 which achieved genome-wide significance (P-value=5x10(-8)) within a non-coding region of chromosome 10. Gene-based analysis did not result in any genome-wide significant association. SNP rs17601696 may have an impact on swallowing impairment among elderly individuals. The results require replication in an independent cohort with appropriate phenotype/genotype data. Copyright © 2015. Published by Elsevier Inc.
    Experimental gerontology 06/2015; 69. DOI:10.1016/j.exger.2015.06.014 · 3.49 Impact Factor
  • D Nimmons · N Pendleton · A Payton · W Ollier · M Horan · J Wilkinson · S Hamdy ·
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    ABSTRACT: Catechol-O-methyl transferase (COMT) and brain-derived neurotrophic factor (BDNF) are neuro-modulatory proteins that have been demonstrated to affect cortical plasticity, which in turn has been shown to affect age-related changes and neuronal functioning in humans. Here, we tested the hypothesis that single nucleotide polymorphisms (SNP) within COMT and BDNF genes are associated with dysphagia in older adults. A total of 800 community-dwelling older individuals were sent the Sydney Oropharyngeal Dysphagia Questionnaire to identify swallowing difficulties. DNA from this population was available for study and used to genotype 18 COMT and 12 BDNF polymorphisms. Logistic regression statistical models were used to identify potential associations between dysphagia and the genotypes. A total of 638 individuals completed the questionnaire, giving an 80% response rate. Of these, 538 were genotyped for COMT and BDNF polymorphisms. Age was found to predict dysphagia (p = 0.018, OR = 1.08, CI = 1.01-1.14). The COMT polymorphism rs165599 and the BDNF polymorphism rs10835211 were found to predict dysphagia and have an interactive effect (p = 0.028), which varied according to the carrier status of the other. In the case of SNP rs10835211, the effect of heterozygosity was protective or harmful dependent on the respective status of rs165599. These results suggest that certain interactions between plasticity genes contribute to the development of dysphagia with increasing age. This highlights a possible role for genetic factors in future monitoring and treating individuals affected by dysphagia. © 2015 John Wiley & Sons Ltd.
    Neurogastroenterology and Motility 06/2015; 27(9). DOI:10.1111/nmo.12609 · 3.59 Impact Factor
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    ABSTRACT: Beagles are commonly used in vaccine trials as part of the regulatory approval process. Genetic restriction within this breed and the impact this might have on vaccine responses is rarely considered. This study was designed to characterise diversity of dog leucocyte antigen (DLA) class II genes in a breeding colony of laboratory Beagles, whose offspring are used in vaccine studies. DLA haplotypes were determined by PCR and sequence-based typing from genomic DNA extracted from blood. Breeding colony Beagles demonstrated significantly different DLA haplotype frequencies in comparison with pet Beagles and both groups showed limited DLA diversity. Restricted DLA class II genetic variability within Beagles might result in selective antigen presentation and vaccine responses that are not necessarily representative of those seen in other dog breeds.
    The Veterinary Journal 01/2015; 203(3). DOI:10.1016/j.tvjl.2014.12.032 · 1.76 Impact Factor
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    ABSTRACT: Objectives/HypothesisAge-related hearing loss has a genetic component, but there have been limited genetic studies in this field. Both N-acetyltransferase 2 and apolipoprotein E genes have previously been associated. However, these studies have either used small sample sizes, examined a limited number of polymorphisms, or have produced conflicting results. Here we use a haplotype tagging approach to determine association with age-related hearing loss and investigate epistasis between these two genes.Study DesignCandidate gene association study of a continuous phenotype.Methods We investigated haplotype tagging single nucleotide polymorphisms in the N-acetyltransferase 2 gene and the presence/absence of the apolipoprotein E ε4 allele for association with age-related hearing loss in a cohort of 265 Caucasian elderly volunteers from Greater Manchester, United Kingdom. Hearing phenotypes were generated using principal component analysis of the hearing threshold levels for the better ear (severity, slope, and concavity). Genotype data for the N-acetyltransferase 2 gene was obtained from existing genome-wide association study data from the Illumina 610-Quadv1 chip. Apolipoprotein E genotyping was performed using Sequenom technology. Linear regression analysis was performed using Plink and Stata software.ResultsNo significant associations (P value, > 0.05) were observed between the N-acetyltransferase 2 or apolipoprotein E gene polymorphisms and any hearing factor. No significant association was observed for epistasis analysis of apolipoprotein E ε4 and the N-acetyltransferase 2 single nucleotide polymorphism rs1799930 (NAT2*6A).Conclusion We found no evidence to support that either N-acetyltransferase 2 or apolipoprotein E gene polymorphisms are associated with age-related hearing loss in a cohort of 265 elderly volunteers.Level of EvidenceN/A. Laryngoscope, 2014
    The Laryngoscope 01/2015; 125(1). DOI:10.1002/lary.24898 · 2.14 Impact Factor
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    ABSTRACT: Wear particle-induced inflammatory bone loss (osteolysis) is the leading cause of total hip arthroplasty (THA) failure. Individual susceptibility to osteolysis is modulated by genetic variation. In this 2-stage case-control association study we examined whether variation within candidate genes in inflammatory and bone turnover signaling pathways associates with susceptibility to osteolysis and time to prosthesis failure. We examined two cohorts, comprising 758 (347 male) Caucasian subjects who had undergone THA with a metal on polyethylene bearing couple; 315 of whom had developed osteolysis. Key genes within inflammatory, bone resorption, and bone formation pathways were screened for common variants by pairwise-SNP tagging using a 2-stage association analysis approach. In the discovery cohort four SNPs within RANK, and one each within KREMEN2, OPG, SFRP1, and TIRAP (p < 0.05) were associated with osteolysis susceptibility. Two SNPs within LRP6, and one each within LRP5, NOD2, SOST, SQSTM1, TIRAP, and TRAM associated with time to implant failure (p < 0.05). Meta-analysis of the two cohorts identified four SNPs within RANK, and one each within KREMEN2, OPG, SFRP1, and TIRAP associated with osteolysis susceptibility (p < 0.05). Genetic variation within inflammatory signaling and bone turnover pathways may play a role in susceptibility to osteolysis. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res
    Journal of Orthopaedic Research 11/2014; 33(2). DOI:10.1002/jor.22755 · 2.99 Impact Factor
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    Stephen McGowan · J A Lamb · D Gerrard · H Chinoy · W Ollier ·
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    ABSTRACT: Background / Purpose: The focus of this investigation was to elucidate molecular mimicry as a plausible model for idiopathic inflammatory myopathy (IIM) aetiology through systematic, computational experimentation using a previously developed molecular mimicry identification pipeline package. Main conclusion: The investigation found no direct association between molecular mimicry and IIM, however, the investigation successfully identified a catalogue of mimicry candidates possessed by bacterial, protist and viral infectious agent which can provide a platform for further analysis, not only for IIM, but for a range of diseases associated with these infectious agents where molecular mimicry is a theorised pathogenesis.
    Rheumatology 2013; 08/2014
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    ABSTRACT: Cognitive abilities vary among people. About 40-50% of this variability is due to general intelligence (g), which reflects the positive correlation among individuals' scores on diverse cognitive ability tests. g is positively correlated with many life outcomes, such as education, occupational status, and health, motivating the investigation of its underlying biology. In psychometric research, a distinction is made between general fluid intelligence (gF) - the ability to reason in novel situations - and general crystallized intelligence (gC) - the ability to apply acquired knowledge. This distinction is supported by developmental and cognitive neuroscience studies. Classical epidemiological studies and recent genome-wide association studies (GWASs) have established that these cognitive traits have a large genetic component. However, no robust genetic associations have been published thus far due largely to the known polygenic nature of these traits and insufficient sample sizes. Here, using two GWAS datasets, in which the polygenicity of gF and gC traits was previously confirmed, a gene- and pathway-based approach was undertaken with the aim of characterizing and differentiating their genetic architecture. Pathway analysis, using genes selected on the basis of relaxed criteria, revealed notable differences between these two traits. gF appeared to be characterized by genes affecting the quantity and quality of neurons and therefore neuronal efficiency, whereas long term depression (LTD) seemed to underlie gC. Thus, this study supports the gF-gC distinction at the genetic level and identifies functional annotations and pathways worthy of further investigation.
    Genes Brain and Behavior 06/2014; 13(7). DOI:10.1111/gbb.12152 · 3.66 Impact Factor
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    ABSTRACT: Background Idiopathic inflammatory myopathies (IIM) may present as a primary disorder, or may overlap with connective tissue diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) or systemic sclerosis. The aetiology of IIM is largely unknown, but is thought to include a combination of genetic and environmental factors. To generate ethnically homogeneous IIM cohorts of sufficient size given its rarity, one of the largest European IIM initiatives has enabled Europe wide ascertainment of cases with EUMYONET. Numerous genome-wide association studies (GWAS) have identified many genetic variants associated with autoimmune disorders, several common to multiple disorders. This is supported by our recent dermatomyositis (DM) GWAS, suggesting genetic overlap with other autoimmune disorders1. Objectives We sought to identify additional novel genetic risk factors in adult and juvenile polymyositis (PM) and DM (not previously identified by DM GWAS), shared with other autoimmune disorders. Methods SNPs significantly associated with SLE, RA, juvenile idiopathic arthritis, coeliac disease, Crohn's disease, ulcerative colitis, psoriasis, type 1 diabetes, multiple sclerosis or systemic sclerosis were identified from published Caucasian GWAS and from the national human genome research institute catalogue of published GWAS. 233 unique SNPs were identified (p <5×10-8), of which 99 had not been directly genotyped or captured through our MYOGEN GWAS1. SNPs were genotyped by Sequenom in a sample of 1001 European Caucasian individuals with definite or probable adult or juvenile PM or DM. 83 SNPs passed quality control criteria. GWAS data from EU contributors was imputed to the 1000G_phase1integrated_v3 reference panel. Association tests for IIM subgroups and random-effects meta-analysis of the individual country datasets were performed. Results Samples with >5% missing genotype data were excluded, resulting in 1149 cases and 3572 controls. Outside the MHC region, a non-synonymous SNP rs2304256 in the TYK2 gene was identified reaching Bonferroni-corrected significance in IIM and DM (β= -0.21, p value=0.00027; β= -0.25, p value=0.00020 respectively). Two further SNPs within the BLK gene and 2335bp 5' of BLK were associated with DM (rs2618476, β=0.24, p value=0.00062; rs13277113, β=0.25 p value=0.00045 respectively) but not with PM, supporting the results of our DM GWAS. Conclusions We have identified TYK2 as a novel association for DM, suggesting genetic overlap of DM with other autoimmune disorders, and indicating genetic heterogeneity between PM and DM. TYK2 has been associated previously with SLE, type 1 diabetes and multiple sclerosis. Further associations of the BLK gene with DM, suggests a role of B cells in its development. References Acknowledgements Funding: Arthritis Research UK (grants 18474; 14518), Intramural Research Program of the NIH, Wellcome Trust (076113; 085860). We thank all other members of the EUMYONET and Myositis Genetics Consortium (MYOGEN). Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.2877
    Annals of the Rheumatic Diseases 06/2014; 73(Suppl 2):151-151. DOI:10.1136/annrheumdis-2014-eular.2877 · 10.38 Impact Factor

Publication Stats

16k Citations
2,266.30 Total Impact Points


  • 2015
    • Salford Royal NHS Foundation Trust
      Salford, England, United Kingdom
  • 1990-2015
    • The University of Manchester
      • • Centre for Integrated Genomic Medical Research (CIGMR)
      • • School of Translational Medicine
      • • Manchester Medical School
      Manchester, England, United Kingdom
    • Evangelismos Hospital
      Athínai, Attica, Greece
  • 2013
    • Manchester University
      North Manchester, Indiana, United States
  • 2012
    • Worcestershire Acute Hospitals NHS Trust
      Worcester, England, United Kingdom
    • Western General Hospital
      Edinburgh, Scotland, United Kingdom
    • Autonomous University of Barcelona
      • Faculty of Veterinary
      Cerdanyola del Vallès, Catalonia, Spain
  • 2011
    • Central Manchester University Hospitals NHS Foundation Trust
      Manchester, England, United Kingdom
  • 2001-2011
    • University of Liverpool
      • School of Veterinary Science
      Liverpool, England, United Kingdom
  • 2009
    • Kerman University of Medical Sciences
      Carmana, Kermān, Iran
  • 2008
    • The University of Edinburgh
      • Department of Psychology
      Edinburgh, Scotland, United Kingdom
  • 2007
    • University of Pittsburgh
      Pittsburgh, Pennsylvania, United States
  • 1999-2004
    • Keele University
      • Institute for Science and Technology in Medicine
      Newcastle-under-Lyme, England, United Kingdom
  • 1995-2001
    • Arthritis Research UK
      Chesterfield, England, United Kingdom
  • 1997
    • Ahmadu Bello University Teaching Hospital
      Заря, Kaduna, Nigeria
  • 1994
    • Memorial University of Newfoundland
      St. John's, Newfoundland and Labrador, Canada
    • St. James University
      Сент-Джеймс, New York, United States
    • Cornell University
      Ithaca, New York, United States
  • 1993-1994
    • Imperial College Healthcare NHS Trust
      Londinium, England, United Kingdom
  • 1992
    • Ealing, Hammersmith & West London College
      Londinium, England, United Kingdom