<?xml version="1.0" encoding="UTF-8"?><xml><records><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%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Addobbati, C</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Sotero Fragoso, T</style></author><author><style face="normal" font="default" size="100%">Tavares Dantas, A</style></author><author><style face="normal" font="default" size="100%">de Ataíde Mariz, H</style></author><author><style face="normal" font="default" size="100%">Ferreira da Rocha Junior, L</style></author><author><style face="normal" font="default" size="100%">Branco PintoDuarte, A L</style></author><author><style face="normal" font="default" size="100%">Coelho, A V C</style></author><author><style face="normal" font="default" size="100%">de Moura, R R</style></author><author><style face="normal" font="default" size="100%">Polesello, V</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author><author><style face="normal" font="default" size="100%">Sandrin Garcia, P</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comprehensive analysis of polymorphisms in the HLA-G 5' upstream regulatory and 3' untranslated regions in Brazilian patients with systemic lupus erythematosus.</style></title><secondary-title><style face="normal" font="default" size="100%">Tissue Antigens</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tissue Antigens</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 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">85</style></volume><pages><style face="normal" font="default" size="100%">458-65</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;This study aims to comprehensively analyze human leucocyte antigen (HLA)-G polymorphisms association with susceptibility to systemic lupus erythematosus (SLE) development and clinical manifestations. The HLA-G 5' upstream regulatory region (URR), 3' untranslated region (UTR) and a cytosine deletion at exon 3 (ΔC, HLA-G*0105N allele) were analyzed in 114 SLE patients and 128 healthy controls from North East Brazil. The +3003T&gt;C (rs1707) C allele and the HG010101c extended HLA-G allele were significantly more frequent in SLE patients than healthy controls (+3003C allele frequency: 12% in SLE patients vs 6% in controls; odds ratio (OR), 2.10, 95% confidence interval (CI), 1.06-4.28, P = 0.026; HG010101c frequency: 11.8% in SLE patients and 6.3% in controls; OR, 2.14, 95% CI, 1.01-4.51, P = 0.046) and were associated with susceptibility for disease development. Other polymorphisms were associated with different clinical manifestations. Although HLA-G role in SLE disease is far from being elucidated yet, our association study results along with a systematic review and meta-analysis suggest that HLA-G might be able to slightly modulate the complex SLE phenotype (pooled OR, 1.14, 95% CI, 1.02-1.27, P = 0.021).&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25762019?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%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Addobbati, C</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Sotero Fragoso, T</style></author><author><style face="normal" font="default" size="100%">Domingues Barbosa, A</style></author><author><style face="normal" font="default" size="100%">Tavares Dantas, A</style></author><author><style face="normal" font="default" size="100%">de Ataíde Mariz, H</style></author><author><style face="normal" font="default" size="100%">F da Rocha, L</style></author><author><style face="normal" font="default" size="100%">Branco Pinto Duarte, A L</style></author><author><style face="normal" font="default" size="100%">Monasta, L</style></author><author><style face="normal" font="default" size="100%">Sandrin-Garcia, P</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">HLA-G gene polymorphisms associated with susceptibility to rheumatoid arthritis disease and its severity in Brazilian patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Tissue Antigens</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tissue Antigens</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">3' Untranslated Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">5' Flanking Region</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis, Rheumatoid</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Progression</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mutational Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</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%">HLA-G Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk</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 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">84</style></volume><pages><style face="normal" font="default" size="100%">308-15</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 analyzed the possible association between human leukocyte antigen-G (HLA-G) genetic variants, supposed to regulate HLA-G expression, and the susceptibility to develop rheumatoid arthritis (RA) as well as its clinical manifestations. The 5'upstream regulatory region (5'URR) and 3'untranslated region (3'UTR) regions of the HLA-G gene were screened in 127 RA patients and 128 controls: 10 5'URR and 3 3'UTR HLA-G polymorphisms as well as two haplotypes were associated with risk for RA development, while a polymorphism in the 5'URR showed an association with the degree of disease activity. These findings, although the number of cases analyzed is limited and the P-values are modest, indicate a possible association between HLA-G gene polymorphisms and susceptibility to develop RA disease and its severity.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24957665?dopt=Abstract</style></custom1></record></records></xml>