Subjetividade e formação do leitor: o problema da ausência da leitura literária nos livros didáticos do Ciclo 1 do Ensino Fundamental

A formação do leitor exige processos de subjetivação. Não há possibilidade de enlaçar o sujeito à prática leitora sem que seja tocada sua memória afetiva, tramada a partir dos muitos discursos que a constituem, vários deles tensionados pela linguagem poética. Logo, compreende-se que a leitura significativa apenas se efetiva quando é permitido ao leitor atuar por meio da subjetividade, fazendo verter do texto lido o encontro de si com outras possibilidades discursivas. Nesse sentido, a presença do texto literário desde os primeiros anos do ensino fundamental torna-se fulcral, na medida em que se trata de campo privilegiado para o reposisionamento subjetivo pela apropriação dos letramentos de prestígio. Entretanto, boa parte da ação escolar que objetiva a formação de leitores parece desconsiderar a vinculação entre subjetividade e leitura e, consequentemente, a relevância da leitura literária em seu espaço. Tal concepção conduz à aplicação de atividades centradas na apropriação de operações que habilitam a criança a esquadrinhar os textos sem comprometê-la efetivamente com a leitura em seu potencial formativo. Submetem, portanto, os sujeitos à condição de leitores funcionais, imobilizando posições discursivas construídas historicamente. Essas constatações resultam de pesquisa focada nas propostas de leitura veiculadas pelos livros didáticos (LD) de língua portuguesa do ciclo 1 do Ensino Fundamental. Tendo em vista que o LD é importante objeto difusor de discursos, a pesquisa alerta para a necessidade de rever os fundamentos das abordagens concernentes à formação do leitor, sobretudo no momento inaugural de sua jornada

Additional file 1: of Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

Supplementary materials and methods. (PDF 348 kb

Additional file 5: Figure S1. of Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes

Comparison of different linear models. (PDF 109 kb

IL-6Rα protein expression in skeletal muscle tissue biopsies and in He, Ob and DM myocytes in response to IL-6.

<p>(A) Protein expression of IL-6Rα was assessed in skeletal muscle biopsies from the vastus lateralis muscle of non-obese (n = 10) or obese (n = 10) normal glucose tolerant (NGT) subjects and non-obese (n = 10) or obese (n = 9) subjects with type 2 diabetes (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0039657#pone-0039657-t001" target="_blank">Table 1</a>), using western blot analysis. Due to the variability in these <i>in vivo</i> samples, all blots are presented in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0039657#pone.0039657.s001" target="_blank">Figure S1</a>. A two-way ANOVA was performed, comparing the effect of obesity and the effect of diabetes on IL-6Rα protein expression. (B) Protein expression of IL-6Rα was assessed in satellite cells isolated from healthy (He) (n = 7), obese (Ob) (n = 7) and obese people (n = 7) with type 2 diabetes (DM) (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0039657#pone-0039657-t002" target="_blank">Table 2</a>). Satellite cells were differentiated into myocytes and treated with IL-6 (100 ng/ml) or control (PBS) for 30, 60 and 120 min. (C) Baseline IL-6Rα protein expression was normalized to total protein expression (as determined by reactive brown staining) and compared between groups by two-way ANOVAs. (D) IL-6 induced IL-6Rα protein expression was normalized to total protein and compared between groups by two-way ANOVAs and effect of time within groups was assessed with one-way ANOVAs. Data are presented as fold change (FC) between the control samples presented in B and C and samples treated with IL-6 (100 ng/ml). Data are mean ± SE. Groups were compared in pairs (i.e. He vs Ob, He vs DM and Ob vs DM) by two-way ANOVAs. Results from ANOVAs are marked in the figures with connecting capped arcs. *Results from Bonferroni post-tests, relative to He myocytes; *P<0.05, **P<0.01, ***P<0.001.</p

AMPK activity in response to IL-6 in myocytes from healthy and people with type 2 diabetes.

<p>Muscle precursor cells derived from the vastus lateralis muscle of healthy (He) (n = 5), and obese people with type 2 diabetes (DM) (n = 5) (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0039657#pone-0039657-t003" target="_blank">Table 3</a>), were differentiated into myocytes and were treated with recombinant IL-6 for 30 or 60 minutes. Controls (Ctrl) were treated with PBS for 60 minutes. Protein was isolated and AMPK activity was measured (A) AMPK α1 activity in response to IL-6 was compared between groups by a two-way ANOVA. (B) AMPK α2 activity in response to IL-6 was compared between groups by a two-way ANOVA. While there was no effect of group, there was an interaction (P<0.01) and thus Bonferroni post-tests were performed. Effect of treatment within groups was performed by one-way ANOVAs. Data are mean ± SE. *Results from Bonferroni post-tests, relative to He myocytes; *P<0.05, **P<0.01, ***P<0.001.</p

IL-6 induction of IL-6 mRNA in human myocytes.

<p>Muscle precursor cells derived from the vastus lateralis muscle of healthy (He), and obese people with type 2 diabetes (DM) (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0039657#pone-0039657-t003" target="_blank">Table 3</a>) (A) He myocytes (n = 5) and DM myocytes (n = 5) were treated with recombinant IL-6 or PBS for 60 minutes and IL-6 mRNA expression was assessed using qPCR. (B) Muscle precursor cells derived from healthy (n = 4), and obese people with type 2 diabetes (n = 4) were differentiated into myocytes and, during the last two days of differentiation transfected with siRNA targeting IL-6Rα. IL-6Rα knockdown was assessed using qPCR following 48 hrs of transfection. (C) IL-6 mRNA expression following IL-6Rα knockdown was assessed using qPCR following 48 hrs of transfection. Data were normalized to control treated samples within each cell subject and differences between groups were assessed using paired t-tests of dCT values. Data are mean ± SE *P<0.05, **P<0.01, ***P<0.001.</p

DNA methylation and gene expression of <i>TXNIP</i> in adult offspring of women with diabetes in pregnancy

<div><p>Background</p><p>Fetal exposure to maternal diabetes increases the risk of type 2 diabetes (T2DM), possibly mediated by epigenetic mechanisms. Low blood <i>TXNIP</i> DNA methylation has been associated with elevated glucose levels and risk of T2DM, and increased skeletal muscle <i>TXNIP</i> gene expression was reported in subjects with impaired glucose metabolism or T2DM. Subcutaneous adipose tissue (SAT) and skeletal muscle play a key role in the control of whole body glucose metabolism and insulin action. The extent to which <i>TXNIP</i> DNA methylation levels are decreased and/or gene expression levels increased in SAT or skeletal muscle of a developmentally programmed at-risk population is unknown.</p><p>Objective and methods</p><p>The objective of this study was to investigate <i>TXNIP</i> DNA methylation and gene expression in SAT and skeletal muscle, and DNA methylation in blood, from adult offspring of women with gestational diabetes (O-GDM, n = 82) or type 1 diabetes (O-T1DM, n = 67) in pregnancy compared with offspring of women from the background population (O-BP, n = 57).</p><p>Results</p><p>SAT <i>TXNIP</i> DNA methylation was increased (p = 0.032) and gene expression decreased (p = 0.001) in O-GDM, but these differences were attenuated after adjustment for confounders. Neither blood/muscle <i>TXNIP</i> DNA methylation nor muscle gene expression differed between groups.</p><p>Conclusion</p><p>We found no evidence of decreased <i>TXNIP</i> DNA methylation or increased gene expression in metabolic target tissues of offspring exposed to maternal diabetes. Further studies are needed to confirm and understand the paradoxical SAT <i>TXNIP</i> DNA methylation and gene expression changes in O-GDM subjects.</p></div

Baseline clinical characteristics in adult offspring of women with gestational diabetes (O-GDM) or type 1 diabetes (O-T1DM) compared to offspring of women from the background population (O-BP).

<p>Baseline clinical characteristics in adult offspring of women with gestational diabetes (O-GDM) or type 1 diabetes (O-T1DM) compared to offspring of women from the background population (O-BP).</p