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Myron</style></author><author><style face="normal" font="default" size="100%">Bis, Joshua C</style></author><author><style face="normal" font="default" size="100%">Franke, Lude</style></author><author><style face="normal" font="default" size="100%">Franco, Oscar H</style></author><author><style face="normal" font="default" size="100%">Benjamin, Emelia J</style></author><author><style face="normal" font="default" size="100%">Chasman, Daniel I</style></author><author><style face="normal" font="default" size="100%">Dupuis, Josée</style></author><author><style face="normal" font="default" size="100%">Snieder, Harold</style></author><author><style face="normal" font="default" size="100%">Dehghan, Abbas</style></author><author><style face="normal" font="default" size="100%">Alizadeh, Behrooz Z</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">LifeLines Cohort Study</style></author><author><style face="normal" font="default" size="100%">CHARGE Inflammation Working Group</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Genome Analyses of &gt;200,000 Individuals Identify 58 Loci for Chronic Inflammation and Highlight Pathways that Link Inflammation and Complex Disorders.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Hum Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Hum. Genet.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Nov 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">691-706</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;C-reactive protein (CRP) is a sensitive biomarker of chronic low-grade inflammation and is associated with multiple complex diseases. The genetic determinants of chronic inflammation remain largely unknown, and the causal role of CRP in several clinical outcomes is debated. We performed two genome-wide association studies (GWASs), on HapMap and 1000 Genomes imputed data, of circulating amounts of CRP by using data from 88 studies comprising 204,402 European individuals. Additionally, we performed in silico functional analyses and Mendelian randomization analyses with several clinical outcomes. The GWAS meta-analyses of CRP revealed 58 distinct genetic loci (p &lt; 5 × 10). After adjustment for body mass index in the regression analysis, the associations at all except three loci remained. The lead variants at the distinct loci explained up to 7.0% of the variance in circulating amounts of CRP. We identified 66 gene sets that were organized in two substantially correlated clusters, one mainly composed of immune pathways and the other characterized by metabolic pathways in the liver. Mendelian randomization analyses revealed a causal protective effect of CRP on schizophrenia and a risk-increasing effect on bipolar disorder. Our findings provide further insights into the biology of inflammation and could lead to interventions for treating inflammation and its clinical consequences.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30388399?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Sidore, Carlo</style></author><author><style face="normal" font="default" size="100%">Busonero, Fabio</style></author><author><style face="normal" font="default" size="100%">Maschio, Andrea</style></author><author><style face="normal" font="default" size="100%">Porcu, Eleonora</style></author><author><style face="normal" font="default" size="100%">Naitza, Silvia</style></author><author><style face="normal" font="default" size="100%">Zoledziewska, Magdalena</style></author><author><style face="normal" font="default" size="100%">Mulas, Antonella</style></author><author><style face="normal" font="default" size="100%">Pistis, Giorgio</style></author><author><style face="normal" font="default" size="100%">Steri, Maristella</style></author><author><style face="normal" font="default" size="100%">Danjou, Fabrice</style></author><author><style face="normal" font="default" size="100%">Kwong, Alan</style></author><author><style face="normal" font="default" size="100%">Ortega Del Vecchyo, Vicente Diego</style></author><author><style face="normal" font="default" size="100%">Chiang, Charleston W K</style></author><author><style face="normal" font="default" size="100%">Bragg-Gresham, Jennifer</style></author><author><style face="normal" font="default" size="100%">Pitzalis, Maristella</style></author><author><style face="normal" font="default" size="100%">Nagaraja, Ramaiah</style></author><author><style face="normal" font="default" size="100%">Tarrier, Brendan</style></author><author><style face="normal" font="default" size="100%">Brennan, Christine</style></author><author><style face="normal" font="default" size="100%">Uzzau, Sergio</style></author><author><style face="normal" font="default" size="100%">Fuchsberger, Christian</style></author><author><style face="normal" font="default" size="100%">Atzeni, Rossano</style></author><author><style face="normal" font="default" size="100%">Reinier, Frederic</style></author><author><style face="normal" font="default" size="100%">Berutti, Riccardo</style></author><author><style face="normal" font="default" size="100%">Huang, Jie</style></author><author><style face="normal" font="default" size="100%">Timpson, Nicholas J</style></author><author><style face="normal" font="default" size="100%">Toniolo, Daniela</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Malerba, Giovanni</style></author><author><style face="normal" font="default" size="100%">Dedoussis, George</style></author><author><style face="normal" font="default" size="100%">Zeggini, Eleftheria</style></author><author><style face="normal" font="default" size="100%">Soranzo, Nicole</style></author><author><style face="normal" font="default" size="100%">Jones, Chris</style></author><author><style face="normal" font="default" size="100%">Lyons, Robert</style></author><author><style face="normal" font="default" size="100%">Angius, Andrea</style></author><author><style face="normal" font="default" size="100%">Kang, Hyun M</style></author><author><style face="normal" font="default" size="100%">Novembre, John</style></author><author><style face="normal" font="default" size="100%">Sanna, Serena</style></author><author><style face="normal" font="default" size="100%">Schlessinger, David</style></author><author><style face="normal" font="default" size="100%">Cucca, Francesco</style></author><author><style face="normal" font="default" size="100%">Abecasis, Goncalo R</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Genome sequencing elucidates Sardinian genetic architecture and augments association analyses for lipid and blood inflammatory markers.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat. Genet.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">47</style></volume><pages><style face="normal" font="default" size="100%">1272-81</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We report ∼17.6 million genetic variants from whole-genome sequencing of 2,120 Sardinians; 22% are absent from previous sequencing-based compilations and are enriched for predicted functional consequences. Furthermore, ∼76,000 variants common in our sample (frequency &gt;5%) are rare elsewhere (&lt;0.5% in the 1000 Genomes Project). We assessed the impact of these variants on circulating lipid levels and five inflammatory biomarkers. We observe 14 signals, including 2 major new loci, for lipid levels and 19 signals, including 2 new loci, for inflammatory markers. The new associations would have been missed in analyses based on 1000 Genomes Project data, underlining the advantages of large-scale sequencing in this founder population.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26366554?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">O'Connell, Jared</style></author><author><style face="normal" font="default" size="100%">Gurdasani, Deepti</style></author><author><style face="normal" font="default" size="100%">Delaneau, Olivier</style></author><author><style face="normal" font="default" size="100%">Pirastu, Nicola</style></author><author><style face="normal" font="default" size="100%">Ulivi, Sheila</style></author><author><style face="normal" font="default" size="100%">Cocca, Massimiliano</style></author><author><style face="normal" font="default" size="100%">Traglia, Michela</style></author><author><style face="normal" font="default" size="100%">Huang, Jie</style></author><author><style face="normal" font="default" size="100%">Huffman, Jennifer E</style></author><author><style face="normal" font="default" size="100%">Rudan, Igor</style></author><author><style face="normal" font="default" size="100%">McQuillan, Ruth</style></author><author><style face="normal" font="default" size="100%">Fraser, Ross M</style></author><author><style face="normal" font="default" size="100%">Campbell, Harry</style></author><author><style face="normal" font="default" size="100%">Polasek, Ozren</style></author><author><style face="normal" font="default" size="100%">Asiki, Gershim</style></author><author><style face="normal" font="default" size="100%">Ekoru, Kenneth</style></author><author><style face="normal" font="default" size="100%">Hayward, Caroline</style></author><author><style face="normal" font="default" size="100%">Wright, Alan F</style></author><author><style face="normal" font="default" size="100%">Vitart, Veronique</style></author><author><style face="normal" font="default" size="100%">Navarro, Pau</style></author><author><style face="normal" font="default" size="100%">Zagury, Jean-Francois</style></author><author><style face="normal" font="default" size="100%">Wilson, James F</style></author><author><style face="normal" font="default" size="100%">Toniolo, Daniela</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Soranzo, Nicole</style></author><author><style face="normal" font="default" size="100%">Sandhu, Manjinder S</style></author><author><style face="normal" font="default" size="100%">Marchini, Jonathan</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A general approach for haplotype phasing across the full spectrum of relatedness.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS Genet.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chromosome Mapping</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Effect</style></keyword><keyword><style  face="normal" font="default" size="100%">Family</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombination, Genetic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">e1004234</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Many existing cohorts contain a range of relatedness between genotyped individuals, either by design or by chance. Haplotype estimation in such cohorts is a central step in many downstream analyses. Using genotypes from six cohorts from isolated populations and two cohorts from non-isolated populations, we have investigated the performance of different phasing methods designed for nominally 'unrelated' individuals. We find that SHAPEIT2 produces much lower switch error rates in all cohorts compared to other methods, including those designed specifically for isolated populations. In particular, when large amounts of IBD sharing is present, SHAPEIT2 infers close to perfect haplotypes. Based on these results we have developed a general strategy for phasing cohorts with any level of implicit or explicit relatedness between individuals. First SHAPEIT2 is run ignoring all explicit family information. We then apply a novel HMM method (duoHMM) to combine the SHAPEIT2 haplotypes with any family information to infer the inheritance pattern of each meiosis at all sites across each chromosome. This allows the correction of switch errors, detection of recombination events and genotyping errors. We show that the method detects numbers of recombination events that align very well with expectations based on genetic maps, and that it infers far fewer spurious recombination events than Merlin. The method can also detect genotyping errors and infer recombination events in otherwise uninformative families, such as trios and duos. The detected recombination events can be used in association scans for recombination phenotypes. The method provides a simple and unified approach to haplotype estimation, that will be of interest to researchers in the fields of human, animal and plant genetics.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24743097?dopt=Abstract</style></custom1></record></records></xml>