Convivencia escolar e inclusión: un estudio en aulas con alumnado afectado por enfermedades raras / Convivência escolar e inclusão: um estudo em classes com estudantes afetados por doenças raras / School coexistence and inclusion: a study in classes with students affected by rare diseases

Este artículo presenta la herramienta metodológica utilizada en una investigación sobre convivencia, inclusión y enfermedades raras realizada en la Universidad Pública de Navarra (UPNA), detallando el marco teórico del estudio y cómo se han diseñado e implementado algunos cuestionarios (dirigidos al alumnado de educación primaria y profesorado); para estudiar las relaciones entre iguales en las aulas en las que convive el alumnado con enfermedades raras o poco frecuentes (ER-EPF). Los cuestionarios se centran en la percepción y experiencia del buen trato y del maltrato por parte del alumnado, así como en la convivencia con su grupo de iguales y en las intervenciones del profesorado en este ámbito, desde los parámetros de la inclusión educativa y la convivencia positiva.

Este artigo apresenta a ferramenta metodológica utilizada em uma pesquisa sobre convivência, inclusão e doenças raras, que está sendo realizada na Universidade Pública de Navarra (UPNA), detalhando o marco teórico do estudo e como alguns questionários (destinados a alunos do ensino primário e professores) foram concebidos e conduzidos para estudar as relações entre pares em salas de aula onde estudantes com doenças raras ou pouco frequentes coexistem (RD). Os questionários estão focados principalmente na percepção e na experiência de bons tratamentos e de abusos por parte dos estudantes, bem como na convivência com o grupo de pares e nas intervenções dos professores, a partir dos parâmetros de inclusão educacional e da convivência positiva.

This article presents the methodological tool used in a research on coexistence, inclusion and rare diseases that is being carried out at the Public University of Navarra (UPNA). It details the theoretical framework and how some questionnaires have been designed and conducted (aimed at primary school students and teachers) to study peer relationships in classrooms where students with rare diseases coexist (RD). The questionnaires are mainly focused on the perception and experience of good and bad treatment by students, as well as coexistence with their peer group and teacher interventions, from the parameters of educational inclusion and positive coexistence.

Toxic (Al, Cd, and Pb) and trace metal (B, Ba, Cu, Fe, Mn, Sr, and Zn) levels in tissues of slaughtered steers: risk assessment for the consumers.

The levels of toxic metals (Al, Cd, Pb) and trace metals (B, Ba, Cu, Fe, Mn, Sr, Zn) were analyzed by inductively coupled plasma optical emission spectrometry (ICP-OES) in the muscle (sirloin and chuck) and liver from a total of 180 samples of steers (less than 2 years old) (Bos taurus) of foreign and local origin slaughtered on the island of La Palma (Canary Islands, Spain). As regards toxic metals, Al was the metal with the highest contents in both tissues of the foreign steers (3.75 mg/kg in the muscle and 55.3 mg/kg in the liver) and the local steers (5.60 mg/kg in the muscle and 8.65 mg/kg in the liver). In conclusion, the present study confirmed that beef is a source of trace elements, mainly Fe and Zn. In addition, the consumption of this type of beef did not show significant intakes of toxic metals (Al, Cd, and Pb) and, therefore, the consumption of the steer muscle and liver does not pose a toxicological risk for Spanish consumers.

Regulatory lymphocytes are key factors in MHC-independent resistance to EAE.

BACKGROUND AND OBJECTIVES: Resistant and susceptible mouse strains to experimental autoimmune encephalomyelitis (EAE), an inducible demyelinating experimental disease serving as animal model for multiple sclerosis, have been described. We aimed to explore MHC-independent mechanisms inducing resistance to EAE. METHODS: For EAE induction, female C57BL/6 (susceptible strain) and CD1 (resistant outbred strain showing heterogeneous MHC antigens) mice were immunized with the 35-55 peptide of myelin oligodendrocyte glycoprotein (MOG35-55). We studied T cell proliferation, regulatory and effector cell subpopulations, intracellular and serum cytokine patterns, and titers of anti-MOG serum antibodies. RESULTS: Upon immunization with MOG35-55, T lymphocytes from susceptible mice but not that of resistant strain were capable of proliferating when stimulated with MOG35-55. Accordingly, resistant mice experienced a rise in regulatory B cells (P=0.001) and, to a lower extent, in regulatory T cells (P=0.02) compared with C57BL/6 susceptible mice. As a consequence, MOG35-55-immunized C57BL/6 mice showed higher percentages of CD4+ T cells producing both IFN-gamma (P=0.02) and IL-17 (P=0.009) and higher serum levels of IL-17 (P=0.04) than resistant mice. CONCLUSIONS: Expansion of regulatory B and T cells contributes to the induction of resistance to EAE by an MHC-independent mechanism.

A novel molecular mechanism involved in multiple myeloma development revealed by targeting MafB to haematopoietic progenitors.

Understanding the cellular origin of cancer can help to improve disease prevention and therapeutics. Human plasma cell neoplasias are thought to develop from either differentiated B cells or plasma cells. However, when the expression of Maf oncogenes (associated to human plasma cell neoplasias) is targeted to mouse B cells, the resulting animals fail to reproduce the human disease. Here, to explore early cellular changes that might take place in the development of plasma cell neoplasias, we engineered transgenic mice to express MafB in haematopoietic stem/progenitor cells (HS/PCs). Unexpectedly, we show that plasma cell neoplasias arise in the MafB-transgenic mice. Beyond their clinical resemblance to human disease, these neoplasias highly express genes that are known to be upregulated in human multiple myeloma. Moreover, gene expression profiling revealed that MafB-expressing HS/PCs were more similar to B cells and tumour plasma cells than to any other subset, including wild-type HS/PCs. Consistent with this, genome-scale DNA methylation profiling revealed that MafB imposes an epigenetic program in HS/PCs, and that this program is preserved in mature B cells of MafB-transgenic mice, demonstrating a novel molecular mechanism involved in tumour initiation. Our findings suggest that, mechanistically, the haematopoietic progenitor population can be the target for transformation in MafB-associated plasma cell neoplasias.

Increased peripheral blood CD5+ B cells predict earlier conversion to MS in high-risk clinically isolated syndromes.

Clinically isolated syndrome patients (CIS) with oligoclonal IgG bands (OCGB) are at high risk for clinically definite multiple sclerosis (MS). However, the outcome for individual patients is unpredictable and the search for reliable blood markers predicting early conversion to multiple sclerosis (MS) has clinical relevance. CD5+ B cells (CD5+Bc) are involved in some autoimmune diseases. This study investigated whether high blood CD5+Bc percentage can predict CIS conversion to MS. Fifty-five consecutive CIS showing OCGB were prospectively studied. Every patient underwent a brain MRI study and a flow cytometry analysis of CD5+Bc percentage. Conversion to MS was studied during follow-up. The CD5+Bc percentage was assessed in 40 controls and a cut-off value of 3.5% (mean+2 SD) was calculated. A blood CD5+Bc percentage above this value predicted earlier conversion to MS in the whole group (hazard ratio [HR]: 3.40; 95% confidence interval [CI]: 1.69-6.68; p=0.0005) and in CIS patients fulfilling three or more Barkhof-Tintoré criteria plus OCGB, who showed higher risk for MS (HR: 3.79; 95% CI: 1.86-15.32; p=0.0018). Multivariate analysis also showed a predictive value for high blood CD5+Bc count (HR: 4.3; 95% CI: 1.9-9.5; p<0.0001). It was concluded that high percentages of CD5+Bc independently associate with increased risk of early conversion to MS in CIS patients with OCGB and Barkhof-Tintoré criteria.