"Eu queria aprender a ser docente": sobre a formação de mestres nos programas de pós-graduação do campo da Alimentação e Nutrição no Brasil

Objetivo: O presente estudo tem como objetivo problematizar o campo científico da Alimentação e Nutrição, a partir do olhar de egressos de cursos de mestrado no Brasil, colocando em exame aspectos relativos às relações sociais nas quais está mergulhada a formação para o ensino. Norteia o estudo o conceito de campo científico de Pierre Bourdieu, para quem a produção do conhecimento não se dá de maneira pura ou neutra, e os consensos ocorrem em função de interesses em circulação na sociedade. Métodos: Participaram da pesquisa 177 mestres, formados em programas de pós-graduação inseridos na área de avaliação Nutrição, na Coordenação de Aperfeiçoamento de Pessoal de Nível Superior. O grupo respondeu a perguntas abertas e fechadas, em questionários enviados pela internet.Resultados: A grande maioria era composta por nutricionistas do sexo feminino, que ingressaram no mestrado com idade média de 28 anos e aproximadamente quatro anos e meio de conclusão da graduação. A docência destacouse dentre as expectativas ao ingressar no mestrado. Conforme aproximadamente metade dos entrevistados, suas expectativas foram plenamente alcançadas ou até mesmo superadas, tanto em razão de seu aprimoramento científico quanto da boa qualificação do corpo docente. Em contraposição, o pouco tempo, as pressões para a conclusão do mestrado e a insuficiência no preparo para a docência foram críticas presentes.Conclusão: A conformação de novas regras no jogo científico - de modelo produtivista -, impõe que se reconheça a existência de problemas sérios nos cursos de pós-graduação stricto sensu, com repercussão sobre a formação de docentes e, por conseguinte, de nutricionistas. Nesse processo, a avaliação da produção científica por meio de métricas de mercado está no rol dos modelos a serem profundamente questionados

Association of PPP2CA polymorphisms with systemic lupus erythematosus susceptibility in multiple ethnic groups.

OBJECTIVE: T cells from patients with systemic lupus erythematosus (SLE) express increased amounts of PP2Ac, which contributes to decreased production of interleukin-2 (IL-2). Because IL-2 is important in the regulation of several aspects of the immune response, it has been proposed that PP2Ac contributes to the expression of SLE. This study was designed to determine whether genetic variants of PPP2AC are linked to the expression of SLE and specific clinical manifestations and account for the increased expression of PP2Ac. METHODS: We conducted a trans-ethnic study of 8,695 SLE cases and 7,308 controls of 4 different ancestries. Eighteen single-nucleotide polymorphisms (SNPs) across PPP2CA were genotyped using an Illumina custom array. PPP2CA expression in SLE and control T cells was analyzed by real-time polymerase chain reaction. RESULTS: A 32-kb haplotype comprising multiple SNPs of PPP2CA showed significant association with SLE in Hispanic Americans, European Americans, and Asians, but not in African Americans. Conditional analyses revealed that SNP rs7704116 in intron 1 showed consistently strong association with SLE across Asian, European American, and Hispanic American populations (odds ratio 1.3 [95% confidence interval 1.14-1.31], meta-analysis P=3.8 710(-7)). In European Americans, the largest ethnic data set studied, the risk A allele of rs7704116 was associated with the presence of renal disease, anti-double-stranded DNA, and anti-RNP antibodies. PPP2CA expression was 3c2-fold higher in SLE patients carrying the rs7704116 AG genotype than those carrying the GG genotype (P=0.007). CONCLUSION: Our data provide the first evidence of an association between PPP2CA polymorphisms and elevated PP2Ac transcript levels in T cells, which implicates a new molecular pathway for SLE susceptibility in European Americans, Hispanic Americans, and Asians

Evaluation of TRAF6 in a large multiancestral lupus cohort

OBJECTIVE: 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 TRAF6 as a candidate gene for SLE, since it plays a major role in several signaling pathways that are important for immunity and organ development. METHODS: Fifteen single-nucleotide polymorphisms (SNPs) across TRAF6 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. P values, false discovery rate q values, and odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated. RESULTS: Evidence of associations was detected in multiple SNPs. The best overall P values were obtained for SNPs rs5030437 and rs4755453 (P = 7.85 × 10(-5) and P = 4.73 × 10(-5) , respectively) without significant heterogeneity among populations (P = 0.67 and P = 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(2) = 0.95) and demonstrated evidence of association with SLE in the same direction (meta-analysis P = 9.15 × 10(-4) , OR 0.89 [95% CI 0.83-0.95]). The presence of thrombocytopenia improved the overall results in different populations (meta-analysis P = 1.99 × 10(-6) , 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 (P = 0.02) under a dominant model. CONCLUSION: Our data indicate the presence of association of TRAF6 with SLE, consistent with the previous report of association with RA. These data provide further support for the involvement of TRAF6 in the pathogenesis of autoimmunity