RESUMO
Nowadays, several books published in different fonts advertised as being particularly suitable for dyslexics are available on the market. Our research aimed to assess the significance of a specific reading font especially designed for dyslexia, called EasyReading™. The performances of good readers and dyslexics were compared. Fourth grade primary school students (533 students in total) were assessed based on reading tasks presented with two different layouts: the popular Times New Roman and EasyReading™, in order to investigate whether children's performances were influenced by the fonts used. The results of the study were both statistically and clinically significant, proving that EasyReading™ can be considered a compensating tool for readers with dyslexia, and a simplifying font for all categories of readers.
RESUMO
Neurogenesis is a key developmental event through which neurons are generated from neural stem/progenitor cells. Chromatin remodeling BAF (mSWI/SNF) complexes have been reported to play essential roles in the neurogenesis of the central nervous system. However, whether BAF complexes are required for neuron generation in the olfactory system is unknown. Here, we identified onscBAF and ornBAF complexes, which are specifically present in olfactory neural stem cells (oNSCs) and olfactory receptor neurons (ORNs), respectively. We demonstrated that BAF155 subunit is highly expressed in both oNSCs and ORNs, whereas high expression of BAF170 subunit is observed only in ORNs. We report that conditional deletion of BAF155, a core subunit in both onscBAF and ornBAF complexes, causes impaired proliferation of oNSCs as well as defective maturation and axonogenesis of ORNs in the developing olfactory epithelium (OE), while the high expression of BAF170 is important for maturation of ORNs. Interestingly, in the absence of BAF complexes in BAF155/BAF170 double-conditional knockout mice (dcKO), OE is not specified. Mechanistically, BAF complex is required for normal activation of Pax6-dependent transcriptional activity in stem cells/progenitors of the OE. Our findings unveil a novel mechanism mediated by the mSWI/SNF complex in OE neurogenesis and development.
