Teaching Special Education to teachers as a cultural path

Recently the Italian Ministry of Education called the universities to a new training task. Paths through the Percorsi Abilitanti Speciali (PAS) and the Tirocini Formativi Attivi (TFA) for teachers became a part of universities educational task. In this frame this article describes the experience of teaching in two of these courses. Through the invitation of prominent guests and watching film clips, the course is characterized as a cultural program aimed to give future teachers a right based inclusion perspective.L’insegnamento della pedagogia speciale agli insegnanti in formazione come percorso culturaleDa alcuni anni il Ministero dell’Istruzione chiama le università ad un nuovo compito formativo. Attraverso i Percorsi Abilitanti Speciali (PAS) e la parte di didattica d’aula che accompagna i Tirocini Formativi Attivi (TFA), i percorsi di formazione degli insegnanti finalizzati all’abilitazione entrano a far parte dell’offerta didattica delle università. In questa cornice l’esperienza descritta nel presente articolo riguarda l’insegnamento della pedagogia speciale all’interno di Percorsi Abilitanti Speciali e Tirocini Formativi Attivi. Attraverso strumenti quali l’invito di ospiti autorevoli e visione di spezzoni di film, il corso si è connotato come un percorso culturale finalizzato ad offrire ai futuri docenti una prospettiva right based sull’inclusione scolastica

Inclusion processes for persons with intellectual disability through multiple negotiation networks

This article explores multiple aspects of the inclusion processes related to the CRPD (Convention on the Rights of persons with disabilities) implementation process carried out in Asti (NW Italy) between 2016 and 2020. For the purpose of this article, data have been collected regarding the work of social work professionals, who supported individuals and families following the methodology of "enabling co-design". The results show the necessity to allow interventions that create a support network to achieve full and equal citizenship, rethinking the transition to adult life through new epistemological categories that make it possible to overcome, both in theory and in practice, what is currently defined as a special adulthood. This goal may be achieved by adopting approaches that are more coherent with the scenario defined by the approval of the CRPD for the rights of persons with disabilities. Processi di inclusione per persone con disabilità intellettiva attraverso le reti negoziali multiple. Questo articolo esplora molteplici aspetti dei processi di inclusione relativi al percorso di attuazione della CRPD svolto ad Asti tra il 2016 e il 2020. Ai fini del presente articolo sono stati raccolti dati relativi al lavoro degli operatori che hanno sostenuto persone con disabilità e famiglie seguendo l'approccio della coprogettazione capacitante. I risultati mostrano la necessità di promuovere interventi che creino una rete di supporto per raggiungere una cittadinanza piena e paritaria, ripensando il passaggio alla vita adulta attraverso nuove categorie epistemologiche che permettano di superare, sia in teoria che in pratica, ciò che è attualmente definito come un adulto speciale. Questo obiettivo può essere raggiunto adottando approcci più coerenti con lo scenario definito dall'approvazione della CRPD per i diritti delle persone con disabilità

Identification of the zinc finger 216 (ZNF216) in human carcinoma cells. A potential regulator of EGFR activity

Epidermal Growth Factor Receptor (EGFR), a member of the ErbB family of receptor tyrosine kinase (RTK) proteins, is aberrantly expressed or deregulated in tumors and plays pivotal roles in cancer onset and metastatic progression. ZNF216 gene has been identified as one of Immediate Early Genes (IEGs) induced by RTKs. Overexpression of ZNF216 protein sensitizes 293 cell line to TNF-α induced apoptosis. However, ZNF216 overexpression has been reported in medulloblastomas and metastatic nasopharyngeal carcinomas. Thus, the role of this protein is still not clearly understood. In this study, the inverse correlation between EGFR and ZNF216 expression was confirmed in various human cancer cell lines differently expressing EGFR. EGF treatment of NIH3T3 cells overexpressing both EGFR and ZNF216 (NIH3T3-EGFR/ZNF216), induced a long lasting activation of EGFR in the cytosolic fraction and an accumulation of phosphorylated EGFR (pEGFR) more in the nuclear than in the cytosolic fraction compared to NIH3T3-EGFR cells. Moreover, EGF was able to stimulate an increased expression of ZNF216 in the cytosolic compartment and its nuclear translocation in a time-dependent manner in NIH3T3-EGFR/ZNF216. A similar trend was observed in A431 cells endogenously expressing the EGFR and transfected with Znf216. The increased levels of pEGFR and ZNF216 in the nuclear fraction of NIH3T3-EGFR/ZNF216 cells were paralleled by increased levels of phospho-MAPK and phospho-Akt. Surprisingly, EGF treatment of NIH3T3-EGFR/ZNF216 cells induced a significant increase of apoptosis thus indicating that ZNF216 could sensitize cells to EGF-induced apoptosis and suggesting that it may be involved in the regulation and effects of EGFR signaling

CoNLoCNN: Exploiting Correlation and Non-Uniform Quantization for Energy-Efficient Low-precision Deep Convolutional Neural Networks

In today's era of smart cyber-physical systems, Deep Neural Networks (DNNs) have become ubiquitous due to their state-of-the-art performance in complex real-world applications. The high computational complexity of these networks, which translates to increased energy consumption, is the foremost obstacle towards deploying large DNNs in resource-constrained systems. Fixed-Point (FP) implementations achieved through post-training quantization are commonly used to curtail the energy consumption of these networks. However, the uniform quantization intervals in FP restrict the bit-width of data structures to large values due to the need to represent most of the numbers with sufficient resolution and avoid high quantization errors. In this paper, we leverage the key insight that (in most of the scenarios) DNN weights and activations are mostly concentrated near zero and only a few of them have large magnitudes. We propose CoNLoCNN, a framework to enable energy-efficient low-precision deep convolutional neural network inference by exploiting: (1) non-uniform quantization of weights enabling simplification of complex multiplication operations; and (2) correlation between activation values enabling partial compensation of quantization errors at low cost without any run-time overheads. To significantly benefit from non-uniform quantization, we also propose a novel data representation format, Encoded Low-Precision Binary Signed Digit, to compress the bit-width of weights while ensuring direct use of the encoded weight for processing using a novel multiply-and-accumulate (MAC) unit design

Extracellular GTP is a Potent Water- Transport Regulator via Aquaporin 5 Plasma-Membrane Insertion in M1-CCD Epithelial Cortical Collecting Duct Cells

Background/Aims: Extracellular GTP is able to modulate some specific functions in neuron, glia and muscle cell models as it has been demonstrated over the last two decades. In fact, extracellular GTP binds its specific plasma membrane binding sites and induces signal transduction via [Ca(2+)]i increase. We demonstrate, for the first time, that extracellular GTP is able to modulate cell swelling in M1-CCD cortical collecting duct epithelial cells via upregulation of aquaporin 5 (AQP5) expression. Methods: We used videoimaging, immunocitochemistry, flow cytometry, confocal techniques, Western blotting and RT-PCR for protein and gene expression analysis, respectively. Results: We demonstrate that AQP5 mRNA is up-regulated 7 h after the GTP exposure in the cell culture medium, and its protein level is increased after 12-24 h. We show that AQP5 is targeted to the plasma membrane of M1-CCD cells, where it facilitates cell swelling, and that the GTP-dependent AQP5 up-regulation occurs via [Ca(2+)]i increase. Indeed, GTP induces both oscillating and transient [Ca(2+)]i increase, and specifically the oscillating kinetic appears to be responsible for blocking cell cycle in the S-phase while the [Ca(2+)]i influx, with whatever kinetic, seems to be responsible for inducing AQP5 expression. Conclusion: The role of GTP as a regulator of AQP5-mediated water transport in renal cells is of great importance in the physiology of renal epithelia, due to its possible physiopathological implications. GTP-dependent AQP5 expression could act as osmosensor. In addition, the data presented here suggest that GTP might play the same role in other tissues where rapid water transport is required for cell volume regulation and maintenance of the homeostasis. © 2014 S. Karger AG, Basel. ispartof: Cellular Physiology and Biochemistry vol:33 issue:3 pages:731-46 ispartof: location:Germany status: publishe

Adhesion of Immature and Mature T Cells Induces in Human Thymic Epithelial Cells (TEC) Activation of IL-6 Gene Trascription Factors (NF-κB And NF-IL6) and IL-6 Gene Expression : Role of αtβ1 and α6β4 Integrins

T cell precursors homed to thymus develop in close contact with stromal cells. Among them, thymic epithelial cells (TEC) are known to exert dominant roles in their survival and functional shaping. Key molecules mediating TEC/thymocytes interactions include cytokines and growth factors secreted by the two cell types and adhesion receptors mediating cell contact. Signaling events triggered in thymocytes by adhesion to epithelial cells have been extensively investigated, whereas little is known on the opposite phenomenon. We have previously investigated this issue in a co-culture system composed of TEC cultures derived from human normal thymus and heterologous thymocytes. We demonstrated that thymocytes adhere to TEC involving β1 and β4 integrins and induce the clustering of (α3β1 and α6β4 heterodimers at the TEC surface. In addition thymocyte adhesion was followed by activation of NF-κB and NF-IL6 gene transciption factors and enhanced IL-6 production. The two latter phenomena were reproduced by the cross-linking of the α3, α6, β1 and β4 integrins, thus implying that the α3β1 and α6β4 heterodimers can signal during thymocyte adhesion. We have extended our previous work investigating in the same experimental setting the inducing activity of non stimulated or activated policlonal or clonal mature T cells as representative of the more mature thymocyte subset. We found that adhesion of unstimulated T cell i) involved β1, but not β4 integrin functions at the surface ii) induced the clustering of α3β1 , but not α2β1 heterodimers at the TEC surface and iii) up-regulated the nuclear binding activity of NF-κB transcription factor and the IL-6 secretion. We propose that α3β1 and α6β4 heterodimers are induced to cluster at the TEC surface recognizing yet unknown cellular ligands differentially expressed during T cell development

Mechanisms of endothelial cell dysfunction in cystic fibrosis

Although cystic fibrosis (CF) patients exhibit signs of endothelial perturbation, the functions of the cystic fibrosis conductance regulator (CFTR) in vascular endothelial cells (EC) are poorly defined. We sought to uncover biological activities of endothelial CFTR, relevant for vascular homeostasis and inflammation. We examined cells from human umbilical cords (HUVEC) and pulmonary artery isolated from non-cystic fibrosis (PAEC) and CF human lungs (CF-PAEC), under static conditions or physiological shear. CFTR activity, clearly detected in HUVEC and PAEC, was markedly reduced in CF-PAEC. CFTR blockade increased endothelial permeability to macromolecules and reduced trans‑endothelial electrical resistance (TEER). Consistent with this, CF-PAEC displayed lower TEER compared to PAEC. Under shear, CFTR blockade reduced VE-cadherin and p120 catenin membrane expression and triggered the formation of paxillin- and vinculin-enriched membrane blebs that evolved in shrinking of the cell body and disruption of cell-cell contacts. These changes were accompanied by enhanced release of microvesicles, which displayed reduced capability to stimulate proliferation in recipient EC. CFTR blockade also suppressed insulin-induced NO generation by EC, likely by inhibiting eNOS and AKT phosphorylation, whereas it enhanced IL-8 release. Remarkably, phosphodiesterase inhibitors in combination with a β2 adrenergic receptor agonist corrected functional and morphological changes triggered by CFTR dysfunction in EC. Our results uncover regulatory functions of CFTR in EC, suggesting a physiological role of CFTR in the maintenance EC homeostasis and its involvement in pathogenetic aspects of CF. Moreover, our findings open avenues for novel pharmacology to control endothelial dysfunction and its consequences in CF

Calcitonin-Induced Effects on Amniotic Fluid-Derived Mesenchymal Stem Cells

Background/Aims: Mesenchymal stem cells from human amniotic fluid (huAFMSCs) can differentiate into multiple lineages and are not tumorigenic after transplantation, making them good candidates for therapeutic purposes. The aim was to determine the effects of calcitonin on these huAFMSCs during osteogenic differentiation, in terms of the physiological role of calcitonin in bone homeostasis. Methods: For huAFMSCs cultured under different conditions, we assayed: expression of the calcitonin receptor, using immunolabelling techniques; proliferation and osteogenesis, using colorimetric and enzymatic assays; intracellular Ca2+ and cAMP levels, using videomicroscopy and spectrophotometry. Results: The calcitonin receptor was expressed in proliferating and osteo-differentiated huAFMSCs. Calcitonin triggered intracellular Ca2+ increases and cAMP production. Its presence in cell medium also induced dose-dependent inhibitory effects on proliferation and increased osteogenic differentiation of huAFMSCs, as also indicated by enhancement of specific markers and alkaline phosphatase activity. Conclusions: These data show that huAFMSCs represent a potential osteogenic model to study in-vitro cell responses to calcitonin (and other members of the calcitonin family). This leads the way to the opening of new lines of research that will add new insight both in cell therapies and in the pharmacological use of these molecules