Στάσεις και απόψεις εκπαιδευτικών για τη συνεκπαίδευση μαθητών με αυτισμό υψηλής λειτουργικότητας στο γενικό σχολείο

Στη σημερινή εποχή ο θεσμός της ενταξιακής εκπαίδευσης αποτελεί πραγματικότητα θέτοντας στους εκπαιδευτικούς την πρόκληση να ανταποκριθούν στα νέα δεδομένα της τάξης. Η παρούσα ερευνητική εργασία πραγματεύεται τις στάσεις και τις απόψεις των εκπαιδευτικών για τη συνεκπαίδευση των παιδιών με Υψηλής Λειτουργικότητας Αυτισμό (ΥΛΑ) στο πλαίσιο της γενικής τάξης. Στην έρευνα έλαβαν μέρος 150 εκπαιδευτικοί από διάφορες βαθμίδες της εκπαίδευσης. Ως εργαλείο χρησιμοποιήθηκε το γραπτό ερωτηματολόγιο που περιελάμβανε ερωτήσεις για τα δημογραφικά χαρακτηριστικά, καθώς και 20 ερωτήσεις κλειστού τύπου σχετικές με τις απόψεις και τις στάσεις των εκπαιδευτικών για τη συνεκπαίδευση των μαθητών με ΥΛΑ στη γενική τάξη. Τα αποτελέσματα της έρευνας έδειξαν ότι οι εκπαιδευτικοί είχαν θετική στάση απέναντι στο ζήτημα της συνεκπαίδευσης. Επίσης, βρέθηκε στατιστικά σημαντική σχέση ανάμεσα στους παράγοντες της ηλικίας και της εργασιακής εμπειρίας με μαθητές με ΔΑΦ και τις στάσεις των εκπαιδευτικών, σε αντίθεση με τους παράγοντες του φύλου και της επιμόρφωσης. Οι μικρότεροι ηλικιακά εκπαιδευτικοί και αυτοί που είχαν μεγαλύτερη εργασιακή εμπειρία με μαθητές με ΔΑΦ ήταν πιο θετικοί προς τη συνεκπαίδευση. Ακόμα, οι εκπαιδευτικοί θεωρούσαν ότι η συνεκπαίδευση είναι μια πρακτική που ωφελεί το σύνολο των μαθητών της τάξης και ότι ο βαθμός αναπηρίας του παιδιού είναι ο σημαντικότερος παράγοντας για την ουσιαστική ένταξή του στην τάξη του γενικού σχολείου.Nowadays, inclusive education is a reality and it challenges educators to cope with the new situation that occurs in the classroom. The present research paper is about the attitudes and the views of educators about the inclusive education of children with High Function Autism (HFA) in the mainstream classroom. The survey involved 150 educators from different levels of education. The tool was a written questionnaire that included demographic questions, as well as 20 close-ended questions related to teachers’ views and attitudes about inclusion of students with HFA in the classroom. The results of the research showed that teachers had a positive attitude towards the issue of inclusion. There was also a statistically significant relationship between the factors of age and work experience with students with ASD and teachers’ attitudes, in contrast with the factors of gender and post baccalaureate education. Younger educators and those who had more work experience with students with ASD were more positive about inclusion. Furthermore, educators considered inclusion as a practice that benefits all students in the classroom and the child’s degree of disability is the most important factor for its effective integration into the mainstream classroom

Activin-A limits Th17 pathogenicity and autoimmune neuroinflammation via CD39 and CD73 ectonucleotidases and Hif1-α–dependent pathways

In multiple sclerosis (MS), Th17 cells are critical drivers of autoimmune central nervous system (CNS) inflammation and demyelination. Th17 cells exhibit functional heterogeneity fostering both pathogenic and nonpathogenic, tissue-protective functions. Still, the factors that control Th17 pathogenicity remain incompletely defined. Here, using experimental autoimmune encephalomyelitis, an established mouse MS model, we report that therapeutic administration of activin-A ameliorates disease severity and alleviates CNS immunopathology and demyelination, associated with decreased activation of Th17 cells. In fact, activin-A signaling through activin-like kinase-4 receptor represses pathogenic transcriptional programs in Th17-polarized cells, while it enhances antiinflammatory gene modules. Whole-genome profiling and in vivo functional studies revealed that activation of the ATP-depleting CD39 and CD73 ectonucleotidases is essential for activin-A–induced suppression of the pathogenic signature and the encephalitogenic functions of Th17 cells. Mechanistically, the aryl hydrocarbon receptor, along with STAT3 and c-Maf, are recruited to promoter elements on Entpd1 and Nt5e (encoding CD39 and CD73, respectively) and other antiinflammatory genes, and control their expression in Th17 cells in response to activin-A. Notably, we show that activin-A negatively regulates the metabolic sensor, hypoxia-inducible factor-1α, and key inflammatory proteins linked to pathogenic Th17 cell states. Of translational relevance, we demonstrate that activin-A is induced in the CNS of individuals with MS and restrains human Th17 cell responses. These findings uncover activin-A as a critical controller of Th17 cell pathogenicity that can be targeted for the suppression of autoimmune CNS inflammation

Activin-A induces regulatory T cells that suppress T helper cell immune responses and protect from allergic airway disease

Activin-A is a pleiotropic cytokine that participates in developmental, inflammatory, and tissue repair processes. Still, its effects on T helper (Th) cell–mediated immunity, critical for allergic and autoimmune diseases, are elusive. We provide evidence that endogenously produced activin-A suppresses antigen-specific Th2 responses and protects against airway hyperresponsiveness and allergic airway disease in mice. Importantly, we reveal that activin-A exerts suppressive function through induction of antigen-specific regulatory T cells that suppress Th2 responses in vitro and upon transfer in vivo. In fact, activin-A also suppresses Th1-driven responses, pointing to a broader immunoregulatory function. Blockade of interleukin 10 and transforming growth factor β1 reverses activin-A–induced suppression. Remarkably, transfer of activin-A–induced antigen-specific regulatory T cells confers protection against allergic airway disease. This beneficial effect is associated with dramatically decreased maturation of draining lymph node dendritic cells. Therapeutic administration of recombinant activin-A during pulmonary allergen challenge suppresses Th2 responses and protects from allergic disease. Finally, we demonstrate that immune cells infiltrating the lungs from individuals with active allergic asthma, and thus nonregulated inflammatory response, exhibit significantly decreased expression of activin-A's responsive elements. Our results uncover activin-A as a novel suppressive factor for Th immunity and a critical controller of allergic airway disease

Genetic Variants of Surfactant Proteins A, B, C, and D in Bronchopulmonary Dysplasia

BPD_28D (O2 dependency at 28 days of life) and BPD_36W (O2 dependency at 36 wks post-menstrual age) are diseases of prematurely born infants exposed to mechanical ventilation and/or oxygen supplementation. In order to determine whether genetic variants of surfactant proteins (SPs-A, B, C, and D) and SP-B-linked microsatellite markers are risk factors in BPD, we performed a family based association study using a Greek study group of 71 neonates (<30 wks gestational age) from 60 families with, 52 BPD_28D and 19 BPD_36W, affected infants. Genotyping was performed using newly designed pyrosequencing assays and previously published methods. Associations between genetic variants of SPs and BPD subgroups were determined using Transmission Disequilibrium Test (TDT) and Family Based Association Test (FBAT). Significant associations (p ≤ 0.01) were observed for alleles of SP-B and SP-B-linked microsatellite markers, and haplotypes of SP-A, SP-D, and SP-B. Specifically, allele B-18_C associated with susceptibility in BPD_36W. Microsatellite marker AAGG_6 associated with susceptibility in BPD_28D/36W group. Haplotype analysis revealed ten susceptibility and one protective haplotypes for SP-B and SP-B-linked microsatellite markers and two SP-A-SP-D protective haplotypes. The data indicate that SP loci are linked to BPD. Studies in different study groups and/or of larger sample size are warranted to confirm these observations and delineate genetic background of BPD subgroups

Quantitative expression of osteopontin in nasal mucosa of patients with allergic rhinitis: effects of pollen exposure and nasal glucocorticoid treatment

<p>Abstract</p> <p>Background</p> <p>Osteopontin (OPN) is a multifunctional cytokine that has been primarily investigated in Th1 diseases. Recently, it has also been implicated in Th2-mediated allergic diseases, such as asthma. The expression of OPN in allergic rhinitis (AR) is currently unknown, as is the effect of intranasal glucocorticosteroids (GCs) on that expression.</p> <p>Methods</p> <p>Subjects with AR were randomised to receive treatment with fluticasone propionate (FP) (n = 12) or a placebo (n = 16) over the grass pollen season and nasal biopsies were taken prior to, and during the season. OPN expression in the nasal mucosa was examined with immunohistochemistry. Healthy non-AR controls (n = 5) were used as a comparator.</p> <p>Results</p> <p>OPN expression was detected in epithelial cells, subepithelial infiltrating/inflammatory cells and cells lining the vessels and glands of all subjects. Comparison of the pre- and peak-pollen season biopsy sections in placebo treated patients revealed no increase in OPN expression during the grass pollen season (5.7% vs 6.4%). Treatment with a local glucocorticosteroid did not alter the expression of OPN during pollen exposure (6.2% vs 6.7%).</p> <p>Conclusion</p> <p>OPN has been increasingly associated with the pathogenesis of various Th2-mediated diseases. However, our finding that the OPN expression in the nasal mucosa of AR patients is not significantly affected by allergen exposure and is comparable to that of the healthy controls, suggests that intracellular OPN is not directly involved in the pathogenesis of allergic rhinitis.</p