<?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%">Toson, Bruno</style></author><author><style face="normal" font="default" size="100%">Dos Santos, Eduardo José</style></author><author><style face="normal" font="default" size="100%">Adelino, José Eduardo</style></author><author><style face="normal" font="default" size="100%">Sandrin-Garcia, Paula</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Louzada-Júnior, Paulo</style></author><author><style face="normal" font="default" size="100%">Oliveira, Renê Donizete Ribeiro</style></author><author><style face="normal" font="default" size="100%">Pedroza, Larysse Santa Rosa Aquino</style></author><author><style face="normal" font="default" size="100%">de Fátima Lobato Cunha Sauma, Maria</style></author><author><style face="normal" font="default" size="100%">de Lima, Clayton Pereira Silva</style></author><author><style face="normal" font="default" size="100%">Barbosa, Fabiola Brasil</style></author><author><style face="normal" font="default" size="100%">Brenol, Claiton Viegas</style></author><author><style face="normal" font="default" size="100%">Xavier, Ricardo Machado</style></author><author><style face="normal" font="default" size="100%">Chies, José Artur Bogo</style></author><author><style face="normal" font="default" size="100%">Veit, Tiago Degani</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CCR5Δ32 and the genetic susceptibility to rheumatoid arthritis in admixed populations: a multicentre study.</style></title><secondary-title><style face="normal" font="default" size="100%">Rheumatology (Oxford)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Rheumatology (Oxford)</style></alt-title></titles><keywords><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%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Consanguinity</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, CCR5</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 03 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">56</style></volume><pages><style face="normal" font="default" size="100%">495-497</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><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/28082621?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%">Cavalcanti, Catarina Addobbati Jordão</style></author><author><style face="normal" font="default" size="100%">De Azevêdo Silva, Jaqueline</style></author><author><style face="normal" font="default" size="100%">de Barros Pita, Will</style></author><author><style face="normal" font="default" size="100%">Veit, Tiago Degani</style></author><author><style face="normal" font="default" size="100%">Monticielo, Odirlei Andre</style></author><author><style face="normal" font="default" size="100%">Xavier, Ricardo Machado</style></author><author><style face="normal" font="default" size="100%">Brenol, João Carlos Tavares</style></author><author><style face="normal" font="default" size="100%">Brenol, Cleiton Viegas</style></author><author><style face="normal" font="default" size="100%">Fragoso, Thiago Sotero</style></author><author><style face="normal" font="default" size="100%">Barbosa, Alexandre Domingues</style></author><author><style face="normal" font="default" size="100%">Duarte, Ângela Luiza Branco Pinto</style></author><author><style face="normal" font="default" size="100%">Oliveira, Renê Donizeti Ribeiro</style></author><author><style face="normal" font="default" size="100%">Louzada-Júnior, Paulo</style></author><author><style face="normal" font="default" size="100%">Donadi, Eduardo Antônio</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Chies, José Artur Bogo</style></author><author><style face="normal" font="default" size="100%">Sandrin-Garcia, Paula</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Vitamin D receptor polymorphisms and expression profile in rheumatoid arthritis brazilian patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Biol Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol. Biol. Rep.</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 Dec 19</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation and important joint commitment, being the most common systemic autoimmune disease worldwide. RA displays important genetic background with a variety of genes contributing to the immune balance breakdown. Recent studies have demonstrated that vitamin D, through its receptor (VDR), is able to regulate the immune balance and suppress the autoimmunity process, being a potential target in autoimmune diseases. In the present genetic association study, we assessed 5 Tag single nucleotide polymorphisms (SNPs) (rs11168268, rs2248098, rs1540339, rs4760648 and rs3890733), which cover most of the VDR gene, in three different Brazilian populations (from Northeast, Southeast and South Brazil). We also evaluated the VDR expression profile in whole blood and monocytes from RA patients. For genotyping study, 428 RA patients and 616 healthy controls were genotyped with fluorogenic allele specific probes on an ABI7500 platform. For gene expression study, VDR mRNA levels of 15 RA patients and 26 healthy individuals were assessed by RT-PCR. Our results showed that SNPs rs4760648 and rs3890733 are associated to RA susceptibility (p value = 0.0026, OR 1.31 and p value = 0.0091, OR 1.28 with statistical power = 0.999 and 0.993, respectively). Regarding RA clinical features, the studied SNPs did not show significant associations. The gene expression assays showed that VDR mRNA levels were down regulated in both whole blood (-3.3 fold) and monocytes (-3.2 fold) of RA patients when compared to healthy controls. Our results, the first reported for distinct Brazilian populations, support a role of the VDR gene in the susceptibility to RA.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26686848?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%">da Silva, G K</style></author><author><style face="normal" font="default" size="100%">Vianna, Priscila</style></author><author><style face="normal" font="default" size="100%">Veit, Tiago Degani</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Catamo, Eulalia</style></author><author><style face="normal" font="default" size="100%">Cordero, Elvira Alicia Aparicio</style></author><author><style face="normal" font="default" size="100%">Mattevi, Vanessa Suñé</style></author><author><style face="normal" font="default" size="100%">Lazzaretti, Rosmeri Kuhmmer</style></author><author><style face="normal" font="default" size="100%">Sprinz, Eduardo</style></author><author><style face="normal" font="default" size="100%">Kuhmmer, Regina</style></author><author><style face="normal" font="default" size="100%">Chies, José Artur Bogo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Influence of HLA-G polymorphisms in human immunodeficiency virus infection and hepatitis C virus co-infection in Brazilian and Italian individuals.</style></title><secondary-title><style face="normal" font="default" size="100%">Infect Genet Evol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Infect. Genet. Evol.</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%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">African Continental Ancestry Group</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Coinfection</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Variation</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">Hepatitis C</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</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%">Italy</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%">Young Adult</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 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">21</style></volume><pages><style face="normal" font="default" size="100%">418-23</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;This study aimed to investigate the role of Human Leukocyte Antigen (HLA)-G in the susceptibility to HIV-1 infection through the analysis of the HLA-G 3' untranslated region (UTR) polymorphisms 14 bp insertion/deletion (rs66554220) and +3142C&gt;G (rs1063320).&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN: &lt;/b&gt;We analyzed 582 HIV-1 infected patients and 626 uninfected individuals from Brazil and Italy in a case-control study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;HLA-G polymorphisms were genotyped using PCR, PCR-RFLP assays or direct sequencing. All analyses were stratified by ethnicity. Genotypic, allelic and diplotypic frequencies were compared between HIV-1 infected subjects and controls using Chi-square or Fischer exact tests. Also, haplotypic frequencies were estimated using MLocus software.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;African-derived HIV-infected individuals presented a higher frequency of the 14 bp insertion allele as compared to non-infected individuals (0.468 versus 0.373, respectively; p(Bonf) = 0.010). A higher frequency of the 14 bp insertion +3142G (insG) haplotype (0.456 versus 0.346, p&lt;0.001) and the insG/insG diplotype (OR=1.88, 95%CI = 1.08-3.23, p=0.021) was observed among African-derived patients as compared to uninfected controls. Also, we observed a higher frequency of the ins/ins genotype among African-derived HIV patients co-infected with HCV (OR=2.78, 95%CI = 1.20-6.49, p = 0.008).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data point out to an increased frequency of alleles and genotypes associated with low HLA-G expression among African-derived patients, suggesting a potential role for HLA-G in the susceptibility to HIV-1 infection and HCV co-infection in those individuals.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24389119?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%">da Silva, Gabriela Kniphoff</style></author><author><style face="normal" font="default" size="100%">Guimarães, Rafael</style></author><author><style face="normal" font="default" size="100%">Mattevi, Vanessa Suñé</style></author><author><style face="normal" font="default" size="100%">Lazzaretti, Rosmeri Kuhmmer</style></author><author><style face="normal" font="default" size="100%">Sprinz, Eduardo</style></author><author><style face="normal" font="default" size="100%">Kuhmmer, Regina</style></author><author><style face="normal" font="default" size="100%">Brandão, Lucas</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Chies, José Artur Bogo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The role of mannose-binding lectin gene polymorphisms in susceptibility to HIV-1 infection in Southern Brazilian patients.</style></title><secondary-title><style face="normal" font="default" size="100%">AIDS</style></secondary-title><alt-title><style face="normal" font="default" size="100%">AIDS</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV-1</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Lectins, C-Type</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mannose-Binding Lectin</style></keyword><keyword><style  face="normal" font="default" size="100%">Mannose-Binding Lectins</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Promoter Regions, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Cell Surface</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Feb 20</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">411-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;This study investigates the role of mannose-binding lectin (MBL) in the susceptibility to HIV-1 infection analyzing polymorphisms located at the MBL2 promoter and exon 1 regions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;The prevalence of MBL2 variant alleles was investigated in 410 HIV-1-infected patients from the South Brazilian HIV cohort and in 345 unexposed uninfected healthy individuals. The promoter variants were genotyped using polymerase chain reaction with sequence-specific primers (PCR-SSP) and exon 1 variants were analyzed by real-time PCR using a melting temperature assay and were confirmed by PCR-restriction fragment length polymorphism (RFLP). MBL2 genotypic and allelic frequencies were compared between HIV-1-infected patients and controls using the chi-squared tests.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The analyses were performed subdividing the individuals according to their ethnic origin. Among Euro-derived individuals a higher frequency of the LX/LX genotype was observed in patients when compared to controls (P &lt; 0.001). The haplotypic analysis also showed a higher frequency of the haplotypes associated with lower MBL levels among HIV-1-infected patients (P = 0.0001). Among Afro-derived individuals the frequencies of LY/LY and HY/HY genotypes were higher in patients when compared to controls (P = 0.009 and P = 0.02).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;An increased frequency of MBL2 genotypes associated with low MBL levels was observed in Euro-derived patients, suggesting a potential role for MBL in the susceptibility to HIV-1 infection in Euro-derived individuals.&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/21192229?dopt=Abstract</style></custom1></record></records></xml>