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Tropical forcing of the recent rapid Arctic warming in northeastern Canada and Greenland
Ding, Qinghua,Wallace, John M.,Battisti, David S.,Steig, Eric J.,Gallant, Ailie J. E.,Kim, Hyung-Jin,Geng, Lei Nature Publishing Group, a division of Macmillan P 2014 Nature Vol.509 No.7499
Rapid Arctic warming and sea-ice reduction in the Arctic Ocean are widely attributed to anthropogenic climate change. The Arctic warming exceeds the global average warming because of feedbacks that include sea-ice reduction and other dynamical and radiative feedbacks. We find that the most prominent annual mean surface and tropospheric warming in the Arctic since 1979 has occurred in northeastern Canada and Greenland. In this region, much of the year-to-year temperature variability is associated with the leading mode of large-scale circulation variability in the North Atlantic, namely, the North Atlantic Oscillation. Here we show that the recent warming in this region is strongly associated with a negative trend in the North Atlantic Oscillation, which is a response to anomalous Rossby wave-train activity originating in the tropical Pacific. Atmospheric model experiments forced by prescribed tropical sea surface temperatures simulate the observed circulation changes and associated tropospheric and surface warming over northeastern Canada and Greenland. Experiments from the Coupled Model Intercomparison Project Phase 5 (ref. 16) models with prescribed anthropogenic forcing show no similar circulation changes related to the North Atlantic Oscillation or associated tropospheric warming. This suggests that a substantial portion of recent warming in the northeastern Canada and Greenland sector of the Arctic arises from unforced natural variability.
Lessard, Christopher J.,Adrianto, Indra,Kelly, Jennifer A.,Kaufman, Kenneth M.,Grundahl, Kiely M.,Adler, Adam,Williams, Adrienne H.,Gallant, Caroline J.,Anaya, Juan-Manuel,Bae, Sang-Cheol,Boackle, Sus Elsevier 2011 American journal of human genetics Vol.88 No.1
<P>Systemic lupus erythematosus (SLE) is considered to be the prototypic autoimmune disease, with a complex genetic architecture influenced by environmental factors. We sought to replicate a putative association at 11p13 not yet exceeding genome-wide significance (p < 5 × 10<SUP>−8</SUP>) identified in a genome-wide association study (GWAS). Our GWA scan identified two intergenic SNPs located between <I>PDHX</I> and <I>CD44</I> showing suggestive evidence of association with SLE in cases of European descent (rs2732552, p = 0.004, odds ratio [OR] = 0.78; rs387619, p = 0.003, OR = 0.78). The replication cohort consisted of >15,000 subjects, including 3562 SLE cases and 3491 controls of European ancestry, 1527 cases and 1811 controls of African American (AA) descent, and 1265 cases and 1260 controls of Asian origin. We observed robust association at both rs2732552 (p = 9.03 × 10<SUP>−8</SUP>, OR = 0.83) and rs387619 (p = 7.7 × 10<SUP>−7</SUP>, OR = 0.83) in the European samples with p<SUB>meta</SUB> = 1.82 × 10<SUP>−9</SUP> for rs2732552. The AA and Asian SLE cases also demonstrated association at rs2732552 (p = 5 × 10<SUP>−3</SUP>, OR = 0.81 and p = 4.3 × 10<SUP>−4</SUP>, OR = 0.80, respectively). A meta-analysis of rs2732552 for all racial and ethnic groups studied produced p<SUB>meta</SUB> = 2.36 × 10<SUP>−13</SUP>. This locus contains multiple regulatory sites that could potentially affect expression and functions of <I>CD44</I>, a cell-surface glycoprotein influencing immunologic, inflammatory, and oncologic phenotypes, or PDHX, a subunit of the pyruvate dehydrogenase complex.</P>
Evaluation of <i>TRAF6</i> in a large multiancestral lupus cohort
Namjou, Bahram,Choi, Chan‐,Bum,Harley, Isaac T. W.,Alarcó,n‐,Riquelme, Marta E.,Kelly, Jennifer A.,Glenn, Stuart B.,Ojwang, Joshua O.,Adler, Adam,Kim, Kwangwoo,Gallant, Caroline J.,B Wiley Subscription Services, Inc., A Wiley Company 2012 Vol.64 No.6
<P><B>Abstract</B></P><P><B>Objective</B></P><P>Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease with significant immune system aberrations resulting from complex heritable genetics as well as environmental factors. We undertook to study the role of <I>TRAF6</I> as a candidate gene for SLE, since it plays a major role in several signaling pathways that are important for immunity and organ development.</P><P><B>Methods</B></P><P>Fifteen single‐nucleotide polymorphisms (SNPs) across <I>TRAF6</I> were evaluated in 7,490 SLE patients and 6,780 control subjects from different ancestries. Population‐based case–control association analyses and meta‐analyses were performed. <I>P</I> values, false discovery rate q values, and odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated.</P><P><B>Results</B></P><P>Evidence of associations was detected in multiple SNPs. The best overall <I>P</I> values were obtained for SNPs rs5030437 and rs4755453 (<I>P</I> = 7.85 × 10<SUP>−5</SUP> and <I>P</I> = 4.73 × 10<SUP>−5</SUP>, respectively) without significant heterogeneity among populations (<I>P</I> = 0.67 and <I>P</I> = 0.50, respectively, in Q statistic). In addition, SNP rs540386, which was previously reported to be associated with rheumatoid arthritis (RA), was found to be in linkage disequilibrium with these 2 SNPs (r<SUP>2</SUP> = 0.95) and demonstrated evidence of association with SLE in the same direction (meta‐analysis <I>P</I> = 9.15 × 10<SUP>−4</SUP>, OR 0.89 [95% CI 0.83–0.95]). The presence of thrombocytopenia improved the overall results in different populations (meta‐analysis <I>P</I> = 1.99 × 10<SUP>−6</SUP>, OR 0.57 [95% CI 0.45–0.72], for rs5030470). Finally, evidence of family‐based association in 34 African American pedigrees with the presence of thrombocytopenia was detected in 1 available SNP (rs5030437) with a Z score magnitude of 2.28 (<I>P</I> = 0.02) under a dominant model.</P><P><B>Conclusion</B></P><P>Our data indicate the presence of association of <I>TRAF6</I> with SLE, consistent with the previous report of association with RA. These data provide further support for the involvement of <I>TRAF6</I> in the pathogenesis of autoimmunity.</P>