Perceptions and academic and professional aspirations of teachers-in-training: Gender barriers or possibilities?

Purpose: This paper presents the results of the application of an adaptation of the "Perceived Barriers Questionnaire" (PBQ) (Rodríguez-Lajo, Vila & Freixa, 2008) to identify if there are gender roles and stereotypes that influence the perceptions and future expectations, both in academic and the professional spheres, of teachers-in-training at the University of Córdoba. Design/methodology: The sample of the study is composed of the students enrolled in the Social Education Degree and the Masters in Inclusive Education and Teaching Staff of Compulsory Secondary Education and Baccalaureate, Vocational Training and Language Teaching at the University of Córdoba. The questionnaire was administered to 157 students. The data were subjected to descriptive analysis, comparative means, correlational and regression analysis, study of internal consistency and factorial structure through exploratory and confirmatory factor analysis. Findings: The results show, among other issues, some professional aspirations related to training rather than leadership, a greater fear of negative evaluation in women than in men and an important relationship between the perception of the gender role attributed to men and women in the workplace and their own aspirations and educational and professional expectations. Research limitations/implications: The main limitation of the study s in its sample, as it is focused only on students of careers belonging to the field of Education Sciences and, specifically, at the University of Córdoba, so it would be interesting to carry out future studies with samples wider population. Originality/value: This study aims to highlight the importance of detecting possible gender barriers during the training of educators to implement the necessary measures to promote true equality between women and men. In this sense, this research can be extrapolated to any educational environment, as well as work.Peer Reviewe

Psychometric Study of “Questionnaire of Barriers Perceived” (QBP) in Higher Education

This article presents the process of adaptation and validation, and the resulting psychometric properties, of the “Questionnaire of Barriers Perceived” (QBP). The scale identifies whether a student’s perceptions and expectations are mediated by stereotypes or roles associated with gender through the study of their professional aspirations, fear of negative judgement, and perceptions/awareness of gender roles of men and women. Two descriptive studies were conducted via a cross-sectional poll. The questionnaire was administered first to 240 students and then to a total of 1044 student from all the degrees studied at the Faculty of Education at the university at which the study took place. The data were subjected to item content analysis, descriptive analysis, analysis of internal consistency, study of the relationship between variables, correlational analysis, and an exploratory and confirmatory factorial analysis. The results showed that the scale had a high goodness-of-fit index, as well as validity and reliability. The dimensions that the model comprised were found to be interrelated and coherent with the theoretical structure considered in the initial version of the instrument. The resulting questionnaire presented sufficient validity and reliability to be used in other contexts and studies of the same nature

Microglial response promotes neurodegeneration in the Ndufs4 KO mouse model of Leigh syndrome

Altres ajuts: Fundació "la Caixa" ID 100010434; PIF UABAcord transformatiu CRUE-CSICLeigh syndrome is a mitochondrial disease characterized by neurodegeneration, neuroinflammation, and early death. Mice lacking NDUFS4, a mitochondrial complex I subunit (Ndufs4 KO mice), have been established as a good animal model for studying human pathology associated with Leigh syndrome. As the disease progresses, there is an increase in neurodegeneration and neuroinflammation, thereby leading to deteriorating neurological symptoms, including motor deficits, breathing alterations, and eventually, death of the animal. However, despite the magnitude of neuroinflammation associated with brain lesions, the role of neuroinflammatory pathways and their main cellular components have not been addressed directly as relevant players in the disease pathology. Here, we investigate the role of microglial cells, the main immune cells of the CNS, in Leigh-like syndrome pathology, by pharmacologically depleting them using the colony-stimulating factor 1 receptor antagonist PLX3397. Microglial depletion extended lifespan and delayed motor symptoms in Ndufs4 KO mice, likely by preventing neuronal loss. Next, we investigated the role of the major cytokine interleukin-6 (IL-6) in the disease progression. IL-6 deficiency partially rescued breathing abnormalities and modulated gliosis but did not extend the lifespan or rescue motor decline in Ndufs4 KO mice. The present results show that microglial accumulation is pathogenic, in a process independent of IL-6, and hints toward a contributing role of neuroinflammation in the disease of Ndufs4 KO mice and potentially in patients with Leigh syndrome

Pleiotropic Effect of IL-6 Produced by B-Lymphocytes During Early Phases of Adaptive Immune Responses Against TB Infection

The role of B cells migrating to the lung and forming follicles during tuberculosis (TB) inflammation is still the subject of debate. In addition to their antibody production and antigen-presenting functions, B cells secrete different cytokines and chemokines, thus participating in complex networks of innate and adaptive immunity. Importantly, lung B-cells produce high amounts of the pleiotropic gp130 cytokine IL-6. Its role during TB infection remains controversial, partly due to the fact that IL-6 is produced by different cell types. To investigate the impact of IL-6 produced by B cells on TB susceptibility and immune responses, we established a mouse strain with specific IL-6 deficiency in B cells (CD19cre-IL-6fl/fl, B-IL-6KO) on the B6 genetic background. Selective abrogation of IL-6 in B cells resulted in shortening the lifespan of TB-infected B-IL-6KO mice compare to the wild-type controls. We provide evidence that at the initial TB stages B cells serve as a critical source of IL-6. In the lung, the effect of IL-6 deficiency in B cells is associated rather with B and T cell functioning, than with macrophage polarization. TB-infected B-IL-6KO mice displayed diminished sizes of B cells themselves, CD4 + IFN-γ +, Th17 +, and CD4 + CXCR5 + follicular T cell populations. The pleiotropic effect of B-cell-derived IL-6 on T-cells demonstrated in our study bridges two major lymphocyte populations and sheds some light on B- and T-cells interactions during the stage of anti-TB response when the host switches on a plethora of acquired immune reactions

Astrocytic IL-6 Influences the Clinical Symptoms of EAE in Mice

Interleukin-6 (IL-6) is a multifunctional cytokine that not only plays major roles in the immune system, but also serves as a coordinator between the nervous and endocrine systems. IL-6 is produced in multiple cell types in the CNS, and in turn, many cells respond to it. It is therefore important to ascertain which cell type is the key responder to IL-6 during both physiological and pathological conditions. In order to test the role of astrocytic IL-6 in neuroinflammation, we studied an extensively-used animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), in mice with an IL-6 deficiency in astrocytes (Ast-IL-6 KO). Results indicate that lack of astrocytic IL-6 did not cause major changes in EAE symptomatology. However, a delay in the onset of clinical signs was observed in Ast-IL-6 KO females, with fewer inflammatory infiltrates and decreased demyelination and some alterations in gliosis and vasogenesis, compared to floxed mice. These results suggest that astrocyte-secreted IL-6 has some roles in EAE pathogenesis, at least in females

Investiguen el paper de les metal·lotioneïnes en les Encefalopaties Enpongiformes Transmissibles

Les metal·lotioneïnes (MT) formen part dels mecanismes encefàlics de defensa que actuen en cas d'un procés patològic que afecti el sistema nerviós central. Per això, i per les seves propietats antioxidants, investigadors del CReSA i de la UAB han inoculat, per via intracerebral, una soca d'EETs a ratolins transgènics per intentar comprendre millor la relació que existeix entre les MTs i la patogènia de la tremolor ovina

A new mouse model to study restoration of interleukin-6 (IL-6) expression in a Cre-dependent manner : microglial IL-6 regulation of experimental autoimmune encephalomyelitis

Altres ajuts: "La Marató TV3" 20142210Interleukin-6 (IL-6) is a pleiotropic cytokine that controls numerous physiological processes both in basal and neuroinflammatory conditions, including the inflammatory response to experimental autoimmune encephalomyelitis (EAE). IL-6 is produced by multiple peripheral and central cells, and until now, the putative roles of IL-6 from different cell types have been evaluated through conditional cell-specific IL-6 knockout mice. Nevertheless, these mice probably undergo compensatory responses of IL-6 from other cells, which makes it difficult to assess the role of each source of IL-6. To give some insight into this problem, we have produced a novel mouse model: a conditional reversible IL-6 KO mouse (IL6-DIO-KO). By using double-inverted, open-reading-frame (DIO) technology, we created a mouse line with the loss of Il6 expression in all cells that can be restored by the action of Cre recombinase. Since microglia are one of the most important sources and targets of IL-6 into the central nervous system, we have recovered microglial Il6 expression in IL6-DIO-KO mice through breeding to Cx3cr1 -CreER mice and subsequent injection of tamoxifen (TAM) when mice were 10-16 weeks old. Then, they were immunized with myelin oligodendrocyte glycoprotein 35-55 peptide (MOG) 7 weeks after TAM treatment to induce EAE. Clinical symptoms and demyelination, CD3 infiltration, and gliosis in the spinal cord were evaluated. IL6-DIO-KO mice were resistant to EAE, validating the new model. Restoration of microglial Il6 was sufficient to develop a mild version of EAE-related clinical symptoms and neuropathology. IL6-DIO-KO mouse is an excellent model to understand in detail the role of specific cellular sources of IL-6 within a recovery-of-function paradigm in EAE

Copper Modulation as a Therapy for Alzheimer's Disease?

The role of metals in the pathophysiology of Alzheimer's disease (AD) has gained considerable support in recent years, with both in vitro and in vivo data demonstrating that a mis-metabolism of metal ions, such as copper and zinc, may affect various cellular cascades that ultimately leads to the development and/or potentiation of AD. In this paper, we will provide an overview of the preclinical and clinical literature that specifically relates to attempts to affect the AD cascade by the modulation of brain copper levels. We will also detail our own novel animal data, where we treated APP/PS1 (7-8 months old) mice with either high copper (20 ppm in the drinking water), high cholesterol (2% supplement in the food) or a combination of both and then assessed β-amyloid (Aβ) burden (soluble and insoluble Aβ), APP levels and behavioural performance in the Morris water maze. These data support an interaction between copper/cholesterol and both Aβ and APP and further highlight the potential role of metal ion dyshomeostasis in AD

IL-6 Trans-Signaling in the Brain Influences the Metabolic Phenotype of the 3xTg-AD Mouse Model of Alzheimer's Disease

Altres ajuts: Fundació La Marató de TV3 (20142210)Alzheimer's disease (AD) is a neurodegenerative disorder that causes the most prevalent dementia in the elderly people. Obesity and insulin resistance, which may cause major health problems per se, are risk factors for AD, and cytokines such as interleukin-6 (IL-6) have a role in these conditions. IL-6 can signal either through a membrane receptor or by trans-signaling, which can be inhibited by the soluble form of the co-receptor gp130 (sgp130). We have addressed the possibility that blocking IL-6 trans-signaling in the brain could have an effect in the triple transgenic 3xTg-AD mouse model of AD and/or in obesity progression, by crossing 3xTg-AD mice with GFAP-sgp130Fc mice. To serve as control groups, GFAP-sgp130Fc mice were also crossed with C57BL/6JOlaHsd mice. Seventeen-month-old mice were fed a control diet (18% kcal from fat) and a high-fat diet (HFD; 58.4% kcal from fat). In our experimental conditions, the 3xTg-AD model showed a mild amyloid phenotype, which nevertheless altered the control of body weight and related endocrine and metabolic factors, suggestive of a hypermetabolic state. The inhibition of IL-6 trans-signaling modulated some of these traits in both 3xTg-AD and control mice, particularly during HFD, and in a sex-dependent manner. These experiments provide evidence of IL-6 trans-signaling playing a role in the CNS of a mouse model of AD

Aberrant perineuronal nets alter spinal circuits, impair motor function, and increase plasticity

Altres ajuts: acords transformatius de la UABPerineuronal nets (PNNs) are a specialized extracellular matrix that have been extensively studied in the brain. Cortical PNNs are implicated in synaptic stabilization, plasticity inhibition, neuroprotection, and ionic buffering. However, the role of spinal PNNs, mainly found around motoneurons, is still unclear. Thus, the goal of this study is to elucidate the role of spinal PNNs on motor function and plasticity in both intact and spinal cord injured mice. We used transgenic mice lacking the cartilage link protein 1 (Crtl1 KO mice), which is implicated in PNN assembly. Crtl1 KO mice showed disorganized PNNs with an altered proportion of their components in both motor cortex and spinal cord. Behavioral and electrophysiological tests revealed motor impairments and hyperexcitability of spinal reflexes in Crtl1 KO compared to WT mice. These functional outcomes were accompanied by an increase in excitatory synapses around spinal motoneurons. Moreover, following spinal lesions of the corticospinal tract, Crtl1 KO mice showed increased contralateral sprouting compared to WT mice. Altogether, the lack of Crtl1 generates aberrant PNNs that alter excitatory synapses and change the physiological properties of motoneurons, overall altering spinal circuits and producing motor impairment. This disorganization generates a permissive scenario for contralateral axons to sprout after injury