¿Integramos los modelos pedagógicos para trabajar el atletismo en los primeros cursos de educación primaria?: un diseño de proyectos de aprendizaje en educación física

La metodología en la iniciación deportiva en educación física ha ido evolucionando a lo largo del siglo XX, pasando de un modelo tradicional, centrado en la técnica y el resultado final, a nuevos modelos pedagógicos que dirigen su atención a la táctica y al desarrollo social, cognitivo y motor del alumnado. En este trabajo, se ha profundizado en los modelos, ludotécnico, jugando al atletismo y educación deportiva para trabajar el atletismo como contenido de las actividades físicas individuales. El principal objetivo es diseñar y desarrollar tres unidades didácticas de aprendizaje de atletismo, a través de dichos modelos pedagógicos. Los participantes son 63 alumnos de primer y segundo curso de primaria del colegio Torre Ramona de Zaragoza. El análisis de la variable, percepción del proceso por parte del alumnado y el profesorado, se realiza a través de una metodología cualitativa fundamentada en el análisis de contenido de los diarios de la maestra, dibujos elaborados por los alumnos y entrevistas individuales. De los resultados obtenidos, destacan: el alto nivel de entusiasmo, el elevado tiempo de compromiso motor y la implicación social entre alumnos. Se confirma que la aplicación de estos modelos pedagógicos presenta un efecto positivo en los primeros cursos de primaria.<br /

Nitric oxide from inflammatory origin impairs neural stem cell proliferation by inhibiting epidermal growth factor receptor signaling

Neuroinflammation is characterized by activation of microglial cells, followed by production of nitric oxide (NO), which may have different outcomes on neurogenesis, favoring or inhibiting this process. In the present study, we investigated how the inflammatory mediator NO can affect proliferation of neural stem cells (NSCs), and explored possible mechanisms underlying this effect. We investigated which mechanisms are involved in the regulation of NSC proliferation following treatment with an inflammatory stimulus (lipopolysaccharide plus IFN-gamma), using a culture system of subventricular zone (SVZ)-derived NSCs mixed with microglia cells obtained from wild-type mice (iNOS(+/+)) or from iNOS knockout mice (iNOS(-/-)). We found an impairment of NSC cell proliferation in iNOS(+/+) mixed cultures, which was not observed in iNOS(-/-) mixed cultures. Furthermore, the increased release of NO by activated iNOS(+/+) microglial cells decreased the activation of the ERK/MAPK signaling pathway, which was concomitant with an enhanced nitration of the EGF receptor. Preventing nitrogen reactive species formation with MnTBAP, a scavenger of peroxynitrite (ONOO-), or using the ONOO- degradation catalyst FeTMPyP cell proliferation and ERK signaling were restored to basal levels in iNOS(+/+) mixed cultures. Moreover, exposure to the NO donor NOC-18 (100 mu M), for 48 h, inhibited SVZ-derived NSC proliferation. Regarding the antiproliferative effect of NO, we found that NOC-18 caused the impairment of signaling through the ERK/MAPK pathway, which may be related to increased nitration of the EGF receptor in NSC. Using MnTBAP nitration was prevented, maintaining ERK signaling, rescuing NSC proliferation. We show that NO from inflammatory origin leads to a decreased function of the EGF receptor, which compromised proliferation of NSC. We also demonstrated that NO-mediated nitration of the EGF receptor caused a decrease in its phosphorylation, thus preventing regular proliferation signaling through the ERK/MAPK pathway.Foundation for Science and Technology, (FCT, Portugal); COMPETE; FEDER [PEst-C/SAU/LA0001/2013-2014, PEst-OE/EQB/LA0023/2013-2014, PTDC/SAU-NEU/102612/2008, PTDC/NEU-OSD/0473/2012]; FCT, Portugal [SERH/BPD/78901/2011, SERH/BD/38127/2007, SFRH/BD/77903/2011, SFRH/BD/79308/2011]info:eu-repo/semantics/publishedVersio

12-Deoxyphorbols Promote Adult Neurogenesis by Inducing Neural Progenitor Cell Proliferation via PKC Activation

Background: Neuropsychiatric and neurological disorders frequently occur after brain insults associated with neuronal loss. Strategies aimed to facilitate neuronal renewal by promoting neurogenesis constitute a promising therapeutic option to treat neuronal death-associated disorders. In the adult brain, generation of new neurons occurs physiologically throughout the entire life controlled by extracellular molecules coupled to intracellular signaling cascades. Proteins participating in these cascades within neurogenic regions constitute potential pharmacological targets to promote neuronal regeneration of injured areas of the central nervous system. Methodology: We have performed in vitro and in vivo approaches to determine neural progenitor cell proliferation to understand whether activation of kinases of the protein kinase C family facilitates neurogenesis in the adult brain. Results: We have demonstrated that protein kinase C activation by phorbol-12-myristate-13-acetate induces neural progenitor cell proliferation in vitro. We also show that the nontumorogenic protein kinase C activator prostratin exerts a proliferative effect on neural progenitor cells in vitro. This effect can be reverted by addition of the protein kinase C inhibitor G06850, demonstrating that the effect of prostratin is mediated by protein kinase C activation. Additionally, we show that prostratin treatment in vivo induces proliferation of neural progenitor cells within the dentate gyrus of the hippocampus and the subventricular zone. Finally, we describe a library of diterpenes with a 12-deoxyphorbol structure similar to that of prostratin that induces a stronger effect than prostratin on neural progenitor cell proliferation both in vitro and in vivo

A novel PKC activating molecule promotes neuroblast differentiation and delivery of newborn neurons in brain injuries

Neural stem cells are activated within neurogenic niches in response to brain injuries. This results in the production of neuroblasts, which unsuccessfully attempt to migrate toward the damaged tissue. Injuries constitute a gliogenic/non-neurogenic niche generated by the presence of anti-neurogenic signals, which impair neuronal differentiation and migration. Kinases of the protein kinase C (PKC) family mediate the release of growth factors that participate in different steps of the neurogenic process, particularly, novel PKC isozymes facilitate the release of the neurogenic growth factor neuregulin. We have demonstrated herein that a plant derived diterpene, (EOF2; CAS number 2230806-06-9), with the capacity to activate PKC facilitates the release of neuregulin 1, and promotes neuroblasts differentiation and survival in cultures of subventricular zone (SVZ) isolated cells in a novel PKC dependent manner. Local infusion of this compound in mechanical cortical injuries induces neuroblast enrichment within the perilesional area, and noninvasive intranasal administration of EOF2 promotes migration of neuroblasts from the SVZ towards the injury, allowing their survival and differentiation into mature neurons, being some of them cholinergic and GABAergic. Our results elucidate the mechanism of EOF2 promoting neurogenesis in injuries and highlight the role of novel PKC isozymes as targets in brain injury regeneration

Rapid β-amyloid deposition and cognitive impairment after cholinergic denervation in APP/PS1 mice

Although extensive evidence supports the role of amyloid-β (Aβ) in Alzheimer disease (AD), the neurotoxic mechanisms underlying AD pathogenesis are not understood. On the other hand, neuronal loss is the pathological feature that best correlates with cognitive impairment. We hypothesized that cholinergic neurodegeneration may lead to Aβ deposition and tested this by inducing selective cholinergic lesions in APPswe/PS1dE9 mice with murine p75(NTR) saporin (mu p75-SAP). Intracerebroventricular lesions that removed ~50% of cholinergic innervation to the cortex and hippocampus were induced in animals with incipient (~3 months) and marked (~7 months of age) Aβ deposition. Cranial windows were implanted and Aβ deposition was monitored in vivo using multiphoton microscopy. Aβ deposition was increased as soon as 7 days after the lesion and this effect was maintained up to 3 months later. Postmortem studies using immunohistochemistry with an anti-Aβ antibody corroborated these findings in both cerebral cortex and hippocampus. Tau phosphorylation was also significantly increased after the lesions. Cholinergic denervation resulted in early memory impairment at 3 months of age that worsened with age (~7 months); there was a synergistic effect between cholinergic denervation and the presence of APP/PS1 transgenes. Altogether, our data suggest that cholinergic denervation may trigger Aβ deposition and synergistically contribute to cognitive impairment in AD patients

Protein Kinase C: Targets to Regenerate Brain Injuries?

Acute or chronic injury to the central nervous system (CNS), causes neuronal death and irreversible cognitive deficits or sensory-motor alteration. Despite the capacity of the adult CNS to generate new neurons from neural stem cells (NSC), neuronal replacement following an injury is a restricted process, which does not naturally result in functional regeneration. Therefore, potentiating endogenous neurogenesis is one of the strategies that are currently being under study to regenerate damaged brain tissue. The insignificant neurogenesis that occurs in CNS injuries is a consequence of the gliogenic/non-neurogenic environment that inflammatory signaling molecules create within the injured area. The modification of the extracellular signals to generate a neurogenic environment would facilitate neuronal replacement. However, in order to generate this environment, it is necessary to unearth which molecules promote or impair neurogenesis to introduce the first and/or eliminate the latter. Specific isozymes of the protein kinase C (PKC) family differentially contribute to generate a gliogenic or neurogenic environment in injuries by regulating the ADAM17 mediated release of growth factor receptor ligands. Recent reports describe several non-tumorigenic diterpenes isolated from plants of the Euphorbia genus, which specifically modulate the activity of PKC isozymes promoting neurogenesis. Diterpenes with 12-deoxyphorbol or lathyrane skeleton, increase NPC proliferation in neurogenic niches in the adult mouse brain in a PKCb dependent manner exerting their effects on transit amplifying cells, whereas PKC inhibition in injuries promotes neurogenesis. Thus, compounds that balance PKC activity in injuries might be of use in the development of new drugs and therapeutic strategies to regenerate brain injuries

Expression patterns of the aquaporin gene family during renal development: influence of genetic variability

High-throughput analyses have shown that aquaporins (AQPs) belong to a cluster of genes that are differentially expressed during kidney organogenesis. However, the spatiotemporal expression patterns of the AQP gene family during tubular maturation and the potential influence of genetic variation on these patterns and on water handling remain unknown. We investigated the expression patterns of all AQP isoforms in fetal (E13.5 to E18.5), postnatal (P1 to P28), and adult (9 weeks) kidneys of inbred (C57BL/6J) and outbred (CD-1) mice. Using quantitative polymerase chain reaction (PCR), we evidenced two mRNA patterns during tubular maturation in C57 mice. The AQPs 1-7-11 showed an early (from E14.5) and progressive increase to adult levels, similar to the mRNA pattern observed for proximal tubule markers (Megalin, NaPi-IIa, OAT1) and reflecting the continuous increase in renal cortical structures during development. By contrast, AQPs 2-3-4 showed a later (E15.5) and more abrupt increase, with transient postnatal overexpression. Most AQP genes were expressed earlier and/or stronger in maturing CD-1 kidneys. Furthermore, adult CD-1 kidneys expressed more AQP2 in the collecting ducts, which was reflected by a significant delay in excreting a water load. The expression patterns of proximal vs. distal AQPs and the earlier expression in the CD-1 strain were confirmed by immunoblotting and immunostaining. These data (1) substantiate the clustering of important genes during tubular maturation and (2) demonstrate that genetic variability influences the regulation of the AQP gene family during tubular maturation and water handling by the mature kidney

S-nitrosation and neuronal plasticity

Nitric oxide (NO) has long been recognized as a multifaceted participant in brain physiology. Despite the knowledge that was gathered over many years regarding the contribution of NO to neuronal plasticity, for example the ability of the brain to change in response to new stimuli, only in recent years have we begun to understand how NO acts on the molecular and cellular level to orchestrate such important phenomena as synaptic plasticity (modification of the strength of existing synapses) or the formation of new synapses (synaptogenesis) and new neurons (neurogenesis). Post-translational modification of proteins by NO derivatives or reactive nitrogen species is a non-classical mechanism for signalling by NO. S-nitrosation is a reversible post-translational modification of thiol groups (mainly on cysteines) that may result in a change of function of the modified protein. S-nitrosation of key target proteins has emerged as a main regulatory mechanism by which NO can influence several levels of brain plasticity, which are reviewed in this work. Understanding how S-nitrosation contributes to neural plasticity can help us to better understand the physiology of these processes, and to better address pathological changes in plasticity that are involved in the pathophysiology of several neurological diseases. Linked ArticlesThis article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visitFEDER funds via Programa Operacional Factores de Competitividade (COMPETE); COST action [BM1005]; Foundation for Science and Technology (FCT, Portugal) [PTDC/SAU-OSD/0473/2012, PEst-C/SAU/LA0001/2013-2014, PEst-OE/EQB/LA0023/2013-2014]; Spanish-Portuguese Integrated Action grant [PRI-AIBPT-2011-1015/E-10/12]; FCT [SFRH/BD/77903/2011]; I3SNS programme (ISCIII, Spanish Government

Instagram como herramienta de aprendizaje en Fisiología: @fisiofarma_us

Las redes sociales (RR.SS.) forman parte de nuestra vida diaria convirtiéndose en una de las principales vías de comunicación y búsqueda de información, especialmente entre los más jóvenes. Entre los usuarios que usan de las RR.SS., un gran número son estudiantes universitarios; y entre los temas más tratados se encuentran aquellos relativos a temáticas de ciencias de la salud. Es por ello por lo que desde el Departamento de Fisiología de la Facultad de Farmacia de la Universidad de Sevilla se desarrolló un proyecto de innovación docente durante el curso 2021-2022 cuyo objetivo era la utilización de las RR.SS. para el aprendizaje de las materias impartidas en nuestro departamento, analizando los posibles beneficios derivado del uso de esta por parte de nuestros estudiantes y profesores. Esta actividad consistió en el desarrollo de contenido divulgativo relativo a la Fisiología por parte de estudiantes del Grado en Farmacia, Grado en Óptica-optometría y Doble Grado en ambos, de nuestro Centro para posteriormente ser publicado en una cuenta de Instagram creada para tal fin (@fisiofarma_us). La opinión tanto de los estudiantes como del profesorado sobre el proyecto fue recogida a través de la encuesta al finalizar el proyecto, y se realizó un registro del impacto en la RR.SS. (seguidores, interacciones, etc). Nuestra cuenta Instagram tuvo un gran impacto en RR.SS. Entre los resultados a destacar, los estudiantes consideran que esta actividad ha favorecido su interés por la Fisiología y tanto estudiantes como profesores creen que esta actividad favoreció diferentes herramientas de aprendizaje. Estos resultados nos hacen concluir que el uso adecuado de las RR.SS. puede ser un método efectivo de aprendizaje e incentivo para fomentar una mejor compresión de las asignaturas de Fisiología en grados universitarios de ciencias de la salud, como Farmacia u Óptica-optometría.: Social networks (RR.SS.) have become an integral part of our daily lives and serve as one of the primary means of communication and information retrieval, particularly among younger. A significant proportion of RR.SS. users are university students, and health science topics are among the most frequently discussed subjects. Considering this, the Department of Physiology at the Facultyof Pharmacy at the University of Seville initiated a teaching innovation project during the 2021-2022 academic year. This project aimed to use RR.SS. as a tool for learning the subjects taught within our department and to analyse the potential benefits that could be derived from its use by our students and members of the physiology department. This initiative involved the creation of informative content related to Physiology by students enrolled in the Degree in Pharmacy, Degree in OpticsOptometry, and Double Degree programs at our faculty. This content was subsequently published on an Instagram account created explicitly for this purpose (@fisiofarma_us). At the end of the project, feedback was obtained from both students and professors of the physiology department via a survey, and data about the impact of our initiative on RR.SS. (e.g., number of followers, interactions, and others) was recorded. Our Instagram account generated considerable interest on RR.SS. Notably, students reported that this activity increased their stake in Physiology, and both students and faculty members indicated that it facilitated the use of various learning tools. Based on these findings, we conclude that the use of RR.SS. can effectively enhance learning and promote a deeper understanding of Physiology-related subjects among students enrolled in university-level health science programs such as Pharmacy or Optics-Optometr