El Prácticum como enseñanza reflexiva: una propuesta de innovación didáctica realizada en la Escuela de Magisterio de la UAH

En este artículo presentamos una experiencia piloto de innovación referida al Prácticum, realizada en la E. de Magisterio de la UAH., durante los cursos 2006-07 y 2007-08. La experiencia, que parte de la premisa de formar un profesor crítico y con criterio, nos ha llevado a situarnos en el modelo del profesor refl exivo. Empezamos indicando el origen de la propuesta, y más tarde justifi camos las bases del modelo, explicamos la metodología que hemos empleado e indicamos las conclusiones que se derivan de la experiencia.                                                                                                                                  This article presents a pilot and innovative experience dealing with the Teaching Practice that has been carried out at the Teacher Training School of the University of Alcalá during the academic years 2006/07 and 2007/08. This experience is based on the premise of educating a teacher so that s/he can become a person of sound judgement and constructive criticism and it has made us choose the refl exive teacher model. Our study begins by indicating the background of our proposal and continues by reasoning the basis of that model. Then we explain the methodology we have used and we fi nally point out the conclusions we have reached from this innovative experience

El Prácticum como enseñanza reflexiva: una propuesta de innovación didáctica realizada en la Escuela de Magisterio de la UAH

En este artículo presentamos una experiencia piloto de innovación referida al Prácticum, realizada en la E. de Magisterio de la UAH., durante los cursos 2006-07 y 2007-08. La experiencia, que parte de la premisa de formar un profesor crítico y con criterio, nos ha llevado a situarnos en el modelo del profesor refl exivo. Empezamos indicando el origen de la propuesta, y más tarde justifi camos las bases del modelo, explicamos la metodología que hemos empleado e indicamos las conclusiones que se derivan de la experiencia.This article presents a pilot and innovative experience dealing with the Teaching Practice that has been carried out at the Teacher Training School of the University of Alcalá during the academic years 2006/07 and 2007/08. This experience is based on the premise of educating a teacher so that s/he can become a person of sound judgement and constructive criticism and it has made us choose the refl exive teacher model. Our study begins by indicating the background of our proposal and continues by reasoning the basis of that model. Then we explain the methodology we have used and we finally point out the conclusions we have reached from this innovative experience

El Prácticum como enseñanza reflexiva: una propuesta de innovación didáctica realizada en la Escuela de Magisterio de la UAH

En este artículo presentamos una experiencia piloto de innovación referida al Prácticum, realizada en la E. de Magisterio de la UAH., durante los cursos 2006-07 y 2007-08. La experiencia, que parte de la premisa de formar un profesor crítico y con criterio, nos ha llevado a situarnos en el modelo del profesor refl exivo. Empezamos indicando el origen de la propuesta, y más tarde justifi camos las bases del modelo, explicamos la metodología que hemos empleado e indicamos las conclusiones que se derivan de la experiencia.This article presents a pilot and innovative experience dealing with the Teaching Practice that has been carried out at the Teacher Training School of the University of Alcalá during the academic years 2006/07 and 2007/08. This experience is based on the premise of educating a teacher so that s/he can become a person of sound judgement and constructive criticism and it has made us choose the refl exive teacher model. Our study begins by indicating the background of our proposal and continues by reasoning the basis of that model. Then we explain the methodology we have used and we finally point out the conclusions we have reached from this innovative experience

Laforin, a dual specificity protein phosphatase involved in Lafora disease, is phosphorylated at Ser25 by AMP-activated protein kinase

Carlos Romá-Mateo et alt.Lafora progressive myoclonus epilepsy [LD (Lafora disease)] is a fatal autosomal recessive neurodegenerative disorder caused by loss-of-function mutations in either the EPM2A gene, encoding the dual-specificity phosphatase laforin, or the EPM2B gene, encoding the E3-ubiquitin ligase malin. Previously, we and others showed that laforin and malin form a functional complex that regulates multiple aspects of glycogen metabolism, and that the interaction between laforin and malin is enhanced by conditions activating AMPK (AMP-activated protein kinase). In the present study, we demonstrate that laforin is a phosphoprotein, as indicated by two-dimensional electrophoresis, and we identify Ser25 as the residue involved in this modification. We also show that Ser25 is phosphorylated both in vitro and in vivo by AMPK. Lastly, we demonstrate that this residue plays a critical role for both the phosphatase activity and the ability of laforin to interact with itself and with previously established binding partners. The results of the present study suggest that phosphorylation of laforin-Ser25 by AMPK provides a mechanism to modulate the interaction between laforin and malin. Regulation of this complex is necessary to maintain normal glycogen metabolism. Importantly, Ser25 is mutated in some LD patients (S25P), and our results begin to elucidate the mechanism of disease in these patientsThis work was supported the Spanish Ministry of Education and Science [grant number SAF2008-01907 (to P.S.)]; the Generalitat Valenciana [grant number Prometeo 2009/051 (to P.S.)]; the National Institutes of Health [grant numbers R00NS061803, P20RR020171, R01NS070899 (to M.S.G.)]; and the University of Kentucky College of Medicine startup funds (to M.S.G.)Peer reviewe

Laforin, the most common protein mutated in Lafora disease, regulates autophagy

Lafora disease (LD) is an autosomal recessive, progressive myoclonus epilepsy, which is characterized by the accumulation of polyglucosan inclusion bodies, called Lafora bodies, in the cytoplasm of cells in the central nervous system and in many other organs. However, it is unclear at the moment whether Lafora bodies are the cause of the disease, or whether they are secondary consequences of a primary metabolic alteration. Here we describe that the major genetic lesion that causes LD, loss-of-function of the protein laforin, impairs autophagy. This phenomenon is confirmed in cell lines from human patients, mouse embryonic fibroblasts from laforin knockout mice and in tissues from such mice. Conversely, laforin expression stimulates autophagy. Laforin regulates autophagy via the mammalian target of rapamycin kinase-dependent pathway. The changes in autophagy mediated by laforin regulate the accumulation of diverse autophagy substrates and would be predicted to impact on the Lafora body accumulation and the cell stress seen in this disease that may eventually contribute to cell death

Association Between Preexisting Versus Newly Identified Atrial Fibrillation and Outcomes of Patients With Acute Pulmonary Embolism

Background Atrial fibrillation (AF) may exist before or occur early in the course of pulmonary embolism (PE). We determined the PE outcomes based on the presence and timing of AF. Methods and Results Using the data from a multicenter PE registry, we identified 3 groups: (1) those with preexisting AF, (2) patients with new AF within 2 days from acute PE (incident AF), and (3) patients without AF. We assessed the 90-day and 1-year risk of mortality and stroke in patients with AF, compared with those without AF (reference group). Among 16 497 patients with PE, 792 had preexisting AF. These patients had increased odds of 90-day all-cause (odds ratio [OR], 2.81; 95% CI, 2.33-3.38) and PE-related mortality (OR, 2.38; 95% CI, 1.37-4.14) and increased 1-year hazard for ischemic stroke (hazard ratio, 5.48; 95% CI, 3.10-9.69) compared with those without AF. After multivariable adjustment, preexisting AF was associated with significantly increased odds of all-cause mortality (OR, 1.91; 95% CI, 1.57-2.32) but not PE-related mortality (OR, 1.50; 95% CI, 0.85-2.66). Among 16 497 patients with PE, 445 developed new incident AF within 2 days of acute PE. Incident AF was associated with increased odds of 90-day all-cause (OR, 2.28; 95% CI, 1.75-2.97) and PE-related (OR, 3.64; 95% CI, 2.01-6.59) mortality but not stroke. Findings were similar in multivariable analyses. Conclusions In patients with acute symptomatic PE, both preexisting AF and incident AF predict adverse clinical outcomes. The type of adverse outcomes may differ depending on the timing of AF onset.info:eu-repo/semantics/publishedVersio

Significado biológico de las isoformas de C4b-binding protein (C4BP)

Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de lectura: 10-11-199

A meta-analysis indicates that the regulation of cell motility is a non-intrinsic function of chemoattractant receptors that is governed independently of directional sensing

28 p.-4 fig.-4 tab.Chemoattraction, defined as the migration of a cell toward a source of a chemical gradient, is controlled by chemoattractant receptors. Chemoattraction involves two basic activities, namely, directional sensing, a molecular mechanism that detects the direction of a source of chemoattractant, and actin-based motility, which allows the migration of a cell towards it. Current models assume first, that chemoattractant receptors govern both directional sensing and motility (most commonly inducing an increase in the migratory speed of the cells, i.e. chemokinesis), and, second, that the signaling pathways controlling both activities are intertwined. We performed a meta-analysis to reassess these two points. From this study emerge two main findings. First, although many chemoattractant receptors govern directional sensing, there are also receptors that do not regulate cell motility, suggesting that is the ability to control directional sensing, not motility, that best defines a chemoattractant receptor. Second, multiple experimental data suggest that receptor-controlled directional sensing and motility can be controlled independently. We hypothesize that this independence may be based on the existence of separated signalling modules that selectively govern directional sensing and motility in chemotactic cells. Together, the information gathered can be useful to update current models representing the signalling from chemoattractant receptors. The new models may facilitate the development of strategies for a more effective pharmacological modulation of chemoattractant receptor-controlled chemoattraction in health and disease. “We shall not cease from exploration And the end of all our exploring Will be to arrive where we started And know the place for the first time” from “Little Gidding” by T.S. ElliotThis work was supported by grants SAF-2014-53151-R (Ministerio de Economía y Competitividad), SAF2017-83306-R (Ministerio de Ciencia, Innovación y Universidades), RIER (RETICS Program/Instituto de Salud Carlos III) (RD08/0075, RD16/0012/0007) and PID2020-114147RB-100 (Ministerio de Ciencia e Innovación).Peer reviewe

The chemokine receptor CCR7 uses distinct signaling modules with biased functionality to regulate dendritic cells

10 p.-1 fig.-1 tab.Chemotaxis is a molecular mechanism that confers leukocytes the ability to detect gradients of chemoattractants. Chemokine receptors are well-known regulators of chemotaxis in leukocytes; however, they can regulate several other activities in these cells. This information has been often neglected, probably due to the paramount role of chemotaxis in the immune system and in biology. Therefore, the experimental data available on the mechanisms used by chemokine receptors to regulate other functions of leukocytes is sparse. The results obtained in the study of the chemokine receptor CCR7 in dendritic cells (DCs) provide interesting information on this issue. CCR7 guides the DCs from the peripheral tissues to the lymph nodes, where these cells control T cell activation. CCR7 can regulate DC chemotaxis, survival, migratory speed, cytoarchitecture, and endocytosis. Biochemical and functional analyses show: first, that CCR7 uses in DCs the PI3K/Akt pathway to control survival, the MAPK pathway to control chemotaxis, and the RhoA pathways to regulate actin dynamics, which in turn controls migratory speed, cytoarchitecture, and endocytosis; second, that these three signaling pathways behave as modules with a high degree of independence; and third, that although each one of these routes can regulate several functions in different settings, CCR7 promotes in DCs a functional bias in each pathway. The data uncover an interesting mechanism used by CCR7 to regulate the DCs, entailing multifunctional signaling pathways organized in modules with biased functionality. A similar mechanism could be used by other chemoattractant receptors to regulate the functions of leukocytes.This work was supported by grants SAF-2014-53151-R(Ministerio de Economía y Competitividad), SAF2017-83306-R (Ministerio de Ciencia, Innovación y Universidades),and RETICSProgram/InstitutodeSaludCarlosIII(RIER) (RD08/0075).Peer reviewe

The actin cytoskeleton at the immunological synapse of dendritic cells

10 p.-1 fig.-1 tab.Dendritic cells (DCs) are considered the most potent antigen-presenting cells. DCs control the activation of T cells (TCs) in the lymph nodes. This process involves forming a specialized superstructure at the DC-TC contact zone called the immunological synapse (IS). For the sake of clarity, we call IS(DC) and IS(TC) the DC and TC sides of the IS, respectively. The IS(DC) and IS(TC) seem to organize as multicentric signaling hubs consisting of surface proteins, including adhesion and costimulatory molecules, associated with cytoplasmic components, which comprise cytoskeletal proteins and signaling molecules. Most of the studies on the IS have focused on the IS(TC), and the information on the IS(DC) is still sparse. However, the data available suggest that both IS sides are involved in the control of TC activation. The IS(DC) may govern activities of DCs that confer them the ability to activate the TCs. One key component of the IS(DC) is the actin cytoskeleton. Herein, we discuss experimental data that support the concept that actin polarized at the IS(DC) is essential to maintaining IS stability necessary to induce TC activation.JR-F was supported by grants awarded by Ministerio de Economía y Competitividad (SAF2014-53151-R, SAF2017-83306-R, and 2020AEP158 Ayuda Extra.2020 TEC2017-85059-C3-3-R), RIER (RETICS Program/Instituto de Salud Carlos III) (RD08/0075), and Consejería de Educación y Empleo from Comunidad de Madrid (Raphyme, S2010/BMD-2350).Peer reviewe