Étude comparative des pratiques d’enseignement de la lecture en 4e primaire : des questions de didactique pointées par l’étude internationale PIRLS 2011

Cette étude vise à mettre en lumière des pratiques d‘enseignement de la lecture susceptibles de rendre compte des disparités de performances observées dans différents systèmes éducatifs. Les comparaisons portent sur les pratiques d’enseignement de la lecture déclarées par les enseignant.e.s de huit systèmes éducatifs contrastés tant au plan de la langue enseignée (français, anglais, allemand) qu’au plan des performances moyennes obtenues à l’épreuve PIRLS 2011. Les résultats mettent en évidence des différences parfois importantes dans la fréquence à laquelle sont mises en place certaines facettes de l’enseignement de la lecture et plus spécifiquement de la compréhension. Ces pratiques témoignent de visions contrastées, parfois éloignées de ce que l’on pourrait attendre d’un enseignement de la lecture experte.Peer reviewe

Additional file 2: of Susceptibility to Ebbinghaus and MĂźller-Lyer illusions in autistic children: a comparison of three different methods

Results of robustness checks for Bayesian analyses. Results of robustness checks for Bayesian independent sample t tests in experiments 1 and 3 and for the Bayesian contingency test in experiment 2. (PDF 92 kb

Additional file 1: of Susceptibility to Ebbinghaus and Müller-Lyer illusions in autistic children: a comparison of three different methods

Results with no replacement of outliers. Means, standard deviations and t-test statistics for group differences in bias in the Ebbinghaus and Müller-Lyer tasks in experiment 1 and Müller-Lyer context-free judgments in experiment 3 when outliers were not replaced. (PDF 9 kb

Effect of ML-190 on the attenuation of NF-κB/p65 nuclear translocation by DYN 1–17 and the N-terminal fragments in LPS-stimulated THP-1 cells.

<p>The LPS-stimulated THP-1 cells were pre-treated with ML-190, a KOP receptor antagonist (1 μM, 1 hour) followed by co-treatment of the DYN 1–17 and the N-terminal fragments (10 nM) or U50,488H (10 nM) with ML-190 (1 μM, 1 hour). The treated cells were fixed with paraformaldehyde (3.7%) and immunolabelled with primary anti-NF-κB/p65 rabbit monoclonal antibody and visualized using Alexa Fluor 555^® secondary antibody. DAPI staining was used to identify the nuclei. The nuclear translocation of NF-κB/p65 in each treatment group was assessed using the Image Xpress system. Non-stimulated THP-1 cells (NS) served as negative control. The percentage of NF-κB/p65 nuclear translocation in each treatment group was normalised and expressed relative to LPS-stimulated control group (contains DMSO 0.1% as diluent control). Data shown are the means ± S.E.M. of at least three independent experiments performed in triplicates, *p ≤ 0.05.</p

NF-κB/p65 nuclear localisation in differentiated THP-1 cells.

<p>Cells were fixed, permeabilised, stained with anti-NF-κB/p65 rabbit monoclonal antibody and visualised with Alexa Fluor^® 555 goat anti-rabbit IgG (green). The nuclei were counterstained with DAPI (blue). Microscopy images <b>A.</b> Inactive NF-κB/p65 proteins localisation in the cytoplasm of the non-stimulated THP-1 cells (top row) and <b>B.</b> Translocated NF-κB/p65 proteins into the nuclei of THP-1 cells following LPS stimulation (bottom row). Images were acquired for each fluorescence channel, using suitable TRITC and DAPI filters and a 63× objective. Scale bar: 10μm</p

Effect of IMD-0354 on the NF-κB/p65 nuclear translocation in LPS-stimulated THP-1 cells.

<p>The LPS-stimulated THP-1 cells were treated with IMD-0354 (10 μM) and DMSO (0.1% v/v, as diluent control). The treated cells were fixed with paraformaldehyde (3.7%) and immunolabelled with primary anti-NF-κB/p65 rabbit monoclonal antibody and visualized using Alexa Fluor 555^® secondary antibody. DAPI staining was used to identify the nuclei. The nuclear translocation of NF-κB/p65 in each treatment group was assessed using the Image Xpress system. Non-stimulated THP-1 cells (NS), receiving similar treatment served as negative control. The percentage of NF-κB/p65 nuclear translocation in each treatment group was normalised and expressed relative to LPS-stimulated control group. Data represents means ± S.E.M. of at least three independent experiments performed in triplicates, *p ≤ 0.05.</p

The expression of KOP receptor on LPS-stimulated THP-1 cells.

<p>Cells were fixed, permeabilised, immunolabelled with KOP receptor monoclonal antibody and visualised with Alexa Fluor 647^® goat anti-mouse IgG (red). The nuclei were counterstained with DAPI (blue). Images were acquired for each fluorescence channel, using suitable FITC and DAPI filters with 20 × objective. Scale bar: 25μm</p

The attenuation of NF-κB/p65 nuclear translocation by DYN 1–17 and the N-terminal fragments in LPS-stimulated THP-1 cells.

<p>The LPS-stimulated THP-1 cells were treated with the N-terminal fragments of DYN 1–17 and U50,488H at 1 μM and 10 nM for an hour. The treated cells were fixed with paraformaldehyde (3.7%) and immunolabelled with primary anti-NF-κB/p65 monoclonal antibody and visualized using Alexa Fluor 555^® secondary antibody. DAPI staining was used to identify the nuclei. The nuclear translocation of NF-κB/p65 in each treatment group was assessed using the Image Xpress screening system. Non-stimulated THP-1 cells (NS) served as negative control. The NF-κB/p65 translocation percentage in each treatment group was normalised and expressed relative to LPS-stimulated control group. Data shown are the means ± S.E.M. of at least three independent experiments performed in triplicates, *p ≤ 0.05.</p

The modulation of DYN 1–17 and the N-terminal fragments on the release of IL-1β and TNF-α in LPS-stimulated THP-1 cells.

<p>The LPS-stimulated THP-1 cells were treated with the N-terminal fragments of DYN 1–17 and U50,488H at 0.1 μM, 1 nM and 10 pM for 24 hr. The culture supernatants were collected and IL-1β and TNF-α release was measured using IL-1β and TNF-α AlphaLISA kit, respectively. The AlphaLISA signal was read using an Enspire-Alpha 2390 Multilabel Plate Reader. Non-stimulated THP-1 cells (NS) served as negative control. The release of IL-1β and TNF-α in each treatment group was normalised and expressed relative to LPS-stimulated control group. Data shown are the means ± S.E.M. of at least three independent experiments performed in triplicates. Statistical significance as denoted by * and # represent the IL-1β and TNF-α release between peptide-treated (solid-line) and LPS-stimulated control group or ML-190-treated group (dotted-line), respectively, p ≤ 0.05.</p

BE fragments IC50 for the inhibition of forskolin induced cAMP in HEK-MOP cells.

<p>BE fragments IC50 for the inhibition of forskolin induced cAMP in HEK-MOP cells.</p