Efecto del feedback, la percepción de competencia de los jugadores sobre su entrenador y la personalidad (optimismo/resiliencia) sobre variables psicológicas y de rendimiento en futbolistas con un nivel medio de experiencia

[ES] Una de las formas de intervención más utilizadas por los entrenadores es el feedback y, desde una perspectiva práctica, es habitual escuchar a los técnicos decir que el feedback positivo mejora más el rendimiento de sus deportistas que otros tipos de feedback. Sin embargo, no podemos dejar de tener en cuenta que los entrenadores trabajan con personas y, como todo trabajo que implica un trato humano, tiene una realidad compleja. Hay muchos factores que pueden influir en esta realidad, desde las características del entrenador hasta las de los propios jugadores. Así, en esta investigación hemos querido determinar cuál es el efecto del feedback sobre el valor dado a la tarea por los jugadores, la competencia percibida de los jugadores sobre sí mismos, la motivación autónoma, la vitalidad subjetiva y el bienestar tanto desde el punto de vista del afecto positivo como desde el afecto negativo (variables psicológicas) y también sobre la velocidad y la precisión de tiro a portería (variables de rendimiento). Para medir este efecto se ha tenido en cuenta cómo perciben los jugadores a su entrenador y las características personales de los jugadores (resiliencia y optimismo). Para la realización de esta investigación, hemos realizado un primer capítulo de fundamentación teórica previa, en el que tomamos como base del estudio la Teoría de la Autodeterminación (Deci y Ryan, 1985; Ryan y Deci, 2000, 2002), que muestra a los seres humanos como sujetos con tendencias innatas hacia el crecimiento personal que tratan de relacionarse de forma eficaz con su entorno (Ryan y Deci, 2000). En el segundo capítulo exponemos distintas definiciones de feedback, así como las múltiples clasificaciones encontradas en la literatura. Hemos dado especial énfasis al tipo de feedback que hemos utilizado, el feedback social comparativo falso, en dos versiones: positivo y negativo. Habiendo utilizado también la ausencia de feedback como parte del estudio. En el tercer capítulo exponemos los diferentes estudios que la literatura muestra en la relación entre el feedback y las variables objeto de estudio. Además, se presentan investigaciones sobre la competencia percibida del entrenador y las características personales estudiadas: resiliencia y optimismo. Para finalizar esta fundamentación teórica se presentan definiciones y estudios previos de las variables psicológicas y de rendimiento objeto de estudio. En el marco empírico del estudio, utilizamos una muestra de jugadores con un nivel medio de experiencia que, después de completar cuestionarios que nos diesen información de sus características personales y psicológicas, participaron en una prueba de rendimiento, en este caso de tiro a portería. En dicha prueba se les dividió en tres grupos sobre los que se realizó una intervención con dos tipos diferentes de feedback social comparativo falso (positivo y negativo) y un tercer grupo que no recibió feedback. Por último, se realizó una nueva toma de datos sobre las variables psicológicas objeto de estudio, para conocer las variaciones sucedidas durante la prueba de rendimiento. Finalmente, hemos podido discutir los resultados obtenidos y alcanzar algunas conclusiones en la relación entre las variables, apreciando así, que la realidad en las relaciones entrenador-jugador a través del feedback son complejas y precisan seguir siendo estudiadas. Por esto, hemos presentado unas limitaciones y unas futuras líneas de investigación que permitan continuar con el estudio del efecto del feedback, la percepción de competencia del entrenador y las características personales sobre las variables psicológicas y el rendimiento de los deportistas

Differences Between Human and Murine Tau at the N-terminal End

Human tauopathies, such as Alzheimer’s disease (AD), have been widely studied in transgenic mice overexpressing human tau in the brain. The longest brain isoforms of Tau in mice and humans show 89% amino acid identity; however, the expression of the isoforms of this protein in the adult brain of the two species differs. Tau 3R isoforms are not present in adult mice. In contrast, the adult human brain contains Tau 3R and also Tau 4R isoforms. In addition, the N-terminal sequence of Tau protein in mice and humans differs, a Tau peptide (residues 17–28) being present in the latter but absent in the former. Here we review the main published data on this N-terminal sequence that suggests that human and mouse Tau proteins interact with different endogenous proteins and also show distinct secretion patternsThis study was funded by grants from Spanish Ministry of Economy and Competitiveness (Ministerio de Economía, Industria y Competitividad, Gobierno de España; BFU2016-77885-P), Structural Funds of the European Union from the Comunidad de Madrid [S2017/BMD-3700 (NEUROMETAB-CM)], institutional funding from the Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED, ISCIII), and an institutional grant from the Fundación R. Areces. JM-R has a fellowship from the Fundación La Caix

Pharmaceuticals and environmental risk assessment in municipal wastewater treatment plants and rivers from Peru

This is the first study dealing with removal of the pharmaceutical substances in municipal wastewater treatment plants (MWWTPs) from Peru and the impact of these compounds in surface waters receiving treated wastewater. To this aim, samples from MWWTP of Lima (Peruvian Coast), MWWTP of Cusco, Puno and Juliaca (Peruvian Highlands), as well surface water (confluence of Torococha and Coata rivers in Juliaca) were analyzed. A total of 38 target pharmaceuticals were included in this study and were determined by Liquid Chromatography coupled to tandem Mass Spectrometry (LC-MS/MS). Around 60% and 75% of the target pharmaceuticals could be quantified in surface water and MWWTPs, respectively. Acetaminophen was the drug found at the highest concentration, and it was present in all the treated wastewater samples reaching average values above 100 μg/L in the department of Puno. The gabapentin anti-epileptic drug (up to 11.85 μg/L in MWWTP Lima) and the antibiotics clarithromycin, trimethoprim, ciprofloxacin, sulfamethoxazole and azithromycin (1.86 to 4.47 μg/L in MWWTP Lima) were also found at moderate concentrations in the treated wastewater. In surface water, the highest concentration corresponded also to acetaminophen (28.70 μg/L) followed by sulfamethoxazole (4.36 μg/L). As regards the pharmaceuticals removal, data of this work showed that the MWWTP Cusco (aerobic biologic process by synthetic trickling filters as secondary treatment) was more efficient than the MWWTP Lima (a preliminary treatment that combines grilles, sand trap, degreaser-aerated and sieved of 1.0 mm). However, many pharmaceuticals (around 50% of the compounds investigated) presented concentrations in treated wastewater similar or even higher than in influent wastewater. The environmental ecological risk of pharmaceuticals was assessed based on calculated Risk Quotient (RQ) in the treated wastewater and surface water from the concentration data found in the samples. According to our data, three antibiotics (clarithromycin, ciprofloxacin, clindamycin) and the analgesic acetaminophen posed high environmental risk (RQ ≥ 1) on the aquatic environment. In the river, all antibiotics (except norfloxacin) as well as the analgesic-anti-inflammatory compounds acetaminophen, diclofenac posed a high environmental risk (RQ ≥ 1). Based on data reported in this work for the first time in water samples from Peru, it can be deduced that the treatment processes applied in important cities from Peru are not enough efficient to remove pharmaceuticals in wastewater. As a consequence, severe environmental risks associated to the presence of pharmaceuticals in treated wastewater and surface water are expected; so complementary treatment processes should be implemented in the MWWTPs for a more efficient elimination of these compounds

Alteration in the Synaptic and Extrasynaptic Organization of AMPA Receptors in the Hippocampus of P301S Tau Transgenic Mice

Tau pathology is a hallmark of Alzheimer's disease (AD) and other tauopathies, but how pathological tau accumulation alters the glutamate receptor dynamics driving synaptic dysfunction is unclear. Here, we determined the impact of tau pathology on AMPAR expression, density, and subcellular distribution in the hippocampus of P301S mice using immunoblot, histoblot, and quantitative SDS-digested freeze-fracture replica labeling (SDS-FRL). Histoblot and immunoblot showed differential regulation of GluA1 and GluA2 in the hippocampus of P301S mice. The GluA2 subunit was downregulated in the hippocampus at 3 months while both GluA1 and GluA2 subunits were downregulated at 10 months. However, the total amount of GluA1-4 was similar in P301S mice and in age-matched wild-type mice. Using quantitative SDS-FRL, we unraveled the molecular organization of GluA1-4 in various synaptic connections at a high spatial resolution on pyramidal cell spines and interneuron dendrites in the CA1 field of the hippocampus in 10-month-old P301S mice. The labeling density for GluA1-4 in the excitatory synapses established on spines was significantly reduced in P301S mice, compared to age-matched wild-type mice, in the strata radiatum and lacunosum-moleculare but unaltered in the stratum oriens. The density of synaptic GluA1-4 established on interneuron dendrites was significantly reduced in P301S mice in the three strata. The labeling density for GluA1-4 at extrasynaptic sites was significantly reduced in several postsynaptic compartments of CA1 pyramidal cells and interneurons in the three dendritic layers in P301S mice. Our data demonstrate that the progressive accumulation of phospho-tau is associated with alteration of AMPARs on the surface of different neuron types, including synaptic and extrasynaptic membranes, leading to a decline in the trafficking and synaptic transmission, thereby likely contributing to the pathological events taking place in AD

Different modes of synaptic and extrasynaptic NMDA receptor alteration in the hippocampus of P301S tau transgenic mice

N-methyl-d-aspartate receptors (NMDARs) are pivotal players in the synaptic transmission and synaptic plasticity underlying learning and memory. Accordingly, dysfunction of NMDARs has been implicated in the pathophysiology of Alzheimer disease (AD). Here, we used histoblot and sodium dodecylsulphate-digested freeze-fracture replica labelling (SDS-FRL) techniques to investigate the expression and subcellular localisation of GluN1, the obligatory subunit of NMDARs, in the hippocampus of P301S mice. Histoblots showed that GluN1 expression was significantly reduced in the hippocampus of P301S mice in a laminar-specific manner at 10 months of age but was unaltered at 3 months. Using the SDS-FRL technique, excitatory synapses and extrasynaptic sites on spines of pyramidal cells and interneuron dendrites were analysed throughout all dendritic layers in the CA1 field. Our ultrastructural approach revealed a high density of GluN1 in synaptic sites and a substantially lower density at extrasynaptic sites. Labelling density for GluN1 in excitatory synapses established on spines was significantly reduced in P301S mice, compared with age-matched wild-type mice, in the stratum oriens (so), stratum radiatum (sr) and stratum lacunosum-moleculare (slm). Density for synaptic GluN1 on interneuron dendrites was significantly reduced in P301S mice in the so and sr but unaltered in the slm. Labelling density for GluN1 at extrasynaptic sites showed no significant differences in pyramidal cells, and only increased density in the interneuron dendrites of the sr. This differential alteration of synaptic versus extrasynaptic NMDARs supports the notion that the progressive accumulation of phospho-tau is associated with changes in NMDARs, in the absence of amyloid-β pathology, and may be involved in the mechanisms causing abnormal network activity of the hippocampal circui

TNAP upregulation is a critical factor in Tauopathies and its blockade ameliorates neurotoxicity and increases life-expectancy

Tauopathies are a family of neurodegenerative diseases characterized by the presence of abnormally hyperphosphorylated Tau protein. Several studies have proposed that increased extracellular Tau (eTau) leads to the spread of cerebral tauopathy. However, the molecular mechanisms underlying eTau-induced neurotoxicity remain unclear. Previous in vitro studies reported that the ecto-enzyme tissue-nonspecific alkaline phosphatase (TNAP) dephosphorylate eTau at different sites increasing its neurotoxicity. Here, we confirm TNAP protein upregulation in the brains of Alzheimer's patients and found a similar TNAP increase in Pick's disease patients and P301S mice, a well-characterized mouse model of tauopathies. Interestingly, the conditional overexpression of TNAP causes intracellular Tau hyperphosphorylation and aggregation in cells neighbouring those overexpressing the ectoenzyme. Conversely, the genetic disruption of TNAP reduced the dephosphorylation of eTau and decreased neuronal hyperactivity, brain atrophy, and hippocampal neuronal death in P301S mice. TNAP haploinsufficiency in P301S mice prevents the decreased anxiety-like behaviour, motor deficiency, and increased memory capacity and life expectancy. Similar results were observed by the in vivo pharmacological blunting of TNAP activity. This study provides the first in vivo evidence demonstrating that raised TNAP activity is critical for Tau-induced neurotoxicity and suggest that TNAP blockade may be a novel and efficient therapy to treat tauopathiesThis work was supported by funding from the following: Spanish Ministry of Economy and Competitiveness RTI2018-095753-B-I00 (to M.D.-H.), BFU2016-77885-P (to F.H.) and PGC2018-096177-B-I00 (to J.A.); European Union H2020 program H2020-MSCA-ITN-2017 number 766124 (to M.D-H); European Regional Development Funds from the Comunidad de Madrid S2017/BMD-3700 (NEUROMETAB-CM) (to F.H.); UCM-Santander Central Hispano Bank PR41/17–21,014 (to M.D-H); CIBERNED-ISCIII; and the Fundación R. Areces (to F.H.). A.S-S was hired by RTI2018-095753-B-I00 grant and as postdoctoral researcher by UCM (CT48/19), C.dL. and C.B. were hired by H2020-MSCA-ITN-2017 (grant number 766124), and J M-R had a fellowship from the Fundación La Caixa. This work was supported in part by ERD

Tau-positive nuclear indentations in P301S tauopathy mice

Increased incidence of neuronal nuclear indentations is a well-known feature of the striatum of Huntington's disease (HD) brains and, in Alzheimer's disease (AD), neuronal nuclear indentations have recently been reported to correlate with neurotoxicity caused by improper cytoskeletal/nucleoskeletal coupling. Initial detection of rod-shaped tau immunostaining in nuclei of cortical and striatal neurons of HD brains and in hippocampal neurons of early Braak stage AD led us to coin the term 'tau nuclear rods (TNRs).' Although TNRs traverse nuclear space, they in fact occupy narrow cytoplasmic extensions that fill indentations of the nuclear envelope and we will here refer to this histological hallmark as Tau-immunopositive nuclear indentations (TNIs). We reasoned that TNI formation is likely secondary to tau alterations as TNI detection in HD correlates with an increase in total tau, particularly of the isoforms with four tubulin binding repeats (4R-tau). Here we analyze transgenic mice that overexpress human 4R-tau with a frontotemporal lobar degeneration-tau point mutation (P301S mice) to explore whether tau alteration is sufficient for TNI formation. Immunohistochemistry with various tau antibodies, immunoelectron microscopy and double tau-immunofluorescence/DAPI-nuclear counterstaining confirmed that excess 4R-tau in P301S mice is sufficient for the detection of abundant TNIs that fill nuclear indentations. Interestingly, this does not correlate with an increase in the number of nuclear indentations, thus suggesting that excess total tau or an isoform imbalance in favor of 4R-tau facilitates tau detection inside preexisting nuclear indentations but does not induce formation of the latter. In summary, here we demonstrate that tau alteration is sufficient for TNI detection and our results suggest that the neuropathological finding of TNIs becomes a possible indicator of increased total tau and/or increased 4R/3R-tau ratio in the affected neurons apart from being an efficient way to monitor pathology-associated nuclear indentations

El reto de la inclusión de los Objetivos de Desarrollo Sostenible en la formación inicial de profesores de secundaria: creación del MOOC curso cero sobre educación y ODS, inclusión en asignaturas y en trabajos fin de máster

Memoria ID-041. Ayudas de la Universidad de Salamanca para la innovación docente, curso 2021-2022