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High Piezoelectric Performance in Lead-free BCHT Fine-grained Ceramics Synthesized by Mechanochemistry
(Elsevier, 2025) Santiago Andrades, L.; Romero Landa, Francisco Javier; Gotor, F. J.; Sayagués, M. J.; Moriche Tirado, Rocío; Universidad de Sevilla. Departamento de Física de la Materia Condensada; Ministerio de Ciencia, Innovación y Universidades (MICIU). España
Lead-free piezoelectric ceramics (Ba1-xCax) (Ti1-yHfy)O3 with stoichiometries close to the morphotropic phase boundary (MPB) were synthesized by high-energy ball milling. The influence of Hf and Ca contents and the sintering method (conventional and hot-press) on the piezoelectric, dielectric, and ferroelectric response was investigated. It was confirmed that the different phases stabilized at room temperature and the structural distortion are strongly dependent on the stoichiometry. The coexistence of tetragonal, orthorhombic and rhombohedral phases was observed in samples with the lowest Ca and Hf contents. These samples, which are in the MPB region, also showed the greatest structural distortion, resulting in higher values of d33. Samples with lower Hf content exhibited a higher coercive field, remnant polarization, and temperature in the ferroelectric to paraelectric transition. Despite the high sintering temperature leading to high densification, grain growth during sintering was limited because of the use of mechanochemically synthesized powders. Although Ba0.85Ca0.15Hf0.10Ti0.90O3 stoichiometry has been reported in the literature as the best for piezoelectric properties, in this work, BCHT solid solution with the lowest dopant content studied (Ba0.90Ca0.10Hf0.05Ti0.95O3) showed the best combination of functional properties. Ceramics of this composition with grain size <2 μm exhibited a d33 > 250 pC/N, with almost no relaxation after 24 h, and the highest permittivity. In the field of piezoelectric materials, there is considerable interest in reducing grain size while maintaining high piezoelectric performance, as this can lead to improvements in mechanical properties.
Impaired synaptic plasticity in behaving mice by inactivation of presenilin and accumulation of the neurexin gamma-secretase proteolytic substrate
(Academic Press, 2025-04-03) Arias-Aragón, Francisco; Sánchez-Hidalgo, Ana C.; Gruart, Agnès; Martinez-Mir, Amalia; Delgado-García, José M.; Gómez Scholl, Francisco Manuel; Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica; Junta de Andalucía; Ministerio de Ciencia e Innovación (MICIN). España; Ministerio de Economía y Competitividad (MINECO). España
Mutations in presenilin (PSEN1/2) genes are the main cause of familial Alzheimer's disease (fAD). Presenilin (PS) form the active component of the gamma-secretase complex, a protease that cleaves the C-terminal fragment (CTF) of multiple membrane proteins. The generation of mice lacking Psen1/2 genes in adult forebrain and of knockin mice expressing fAD-linked PSEN1 mutations favored a loss of function mechanism for PS/gamma-secretase in AD. In vitro, inactivation of PS impairs short- and long-term plasticity, but if PS regulates synaptic plasticity in vivo is not known, nor is it known the contribution of specific gamma-secretase substrates. In this study, we performed electrophysiological recordings at medial prefrontal cortex-basolateral (mPFC-BLA) synapse of behaving mice during fear conditioning, a type of associative memory. In controls, fear-conditioning decreases paired-pulse facilitation of the mPFC-BLA synapse, likely reflecting a memory-dependent increase in release probability. In contrast, PScKOtam mice lacking Psen1/2 genes in forebrain neurons in a tamoxifen-regulated manner show decreased paired-pulse facilitation at mPFC-BLA synapse along with impaired memory. Neurexins (Nrxns) are presynaptic membrane proteins processed by PS/gamma-secretase. Importantly, paired-pulse facilitation is further decreased in PScKOtam;NrxnCTF mice expressing increased NrxnCTF levels in PS-deficient neurons. Moreover, high-frequency stimulation induces long-term potentiation (LTP) at mPFC-BLA synapse of control mice, but LTP is impaired in PScKOtam mice and fully inhibited in PScKOtam;NrxnCTF mice. These findings suggest that PS enables learning-dependent adaptations in short and long-term synaptic plasticity by, at least in part, preventing the accumulation of NrxnCTF, pointing at NrxnCTF as a relevant factor downstream of PS dysfunction in AD
La libertad de cátedra: Un limitado derecho constitucional
(Dykinson S.L., 2025) Álvarez Perea, Francisco Javier; Universidad de Sevilla. Departamento de Escultura e Historia de las Artes Plásticas; Universidad de Sevilla. HUM429: Museum
En el ordenamiento jurídico español la libertad de cátedra es un derecho indisociable e inherente al ejercicio docente, que parece dotar al enseñante y a su actividad profesional de un estatuto específico. Se trata de un derecho fundamental contemplado por la Constitución española de 1978 que dota de identidad a la actividad docente, si bien el texto constitucional no llega a aclarar el alcance y límites del ejercicio de esta libertad fundamental que, si bien está sometida a reserva de Ley al amparo del art. 53.1 de la CE, no está regulada expresamente por ninguna Ley Orgánica más allá de la mención a su reconocimiento en aquellas normas relativas a la enseñanza en la diversidad de niveles, por lo que es imprescindible recurrir a la justicia ordinaria pero, sobre todo, al Tribunal constitucional para conocer qué protege exactamente y cuáles son sus límites.
Luigi Ferrajoli. Una aproximación a su proyecto de constitucionalismo global
(Dykinson S.L., 2025) Álvarez Perea, Francisco Javier; Universidad de Sevilla. Departamento de Escultura e Historia de las Artes Plásticas; Universidad de Sevilla. HUM429: Museum
En este capítulo se pretende abordar y exponer la aportación de uno de los juristas italianos más prestigiosos en su ámbito, un académico que aborda en profundidad un amplísimo campo de estudio que abarca la filosofía del derecho, la teoría del derecho y el derecho constitucional. Se trata de Luigi Ferrajoli quien, en los últimos años, ha centrado su empeño en la tarea de promover un movimiento para la creación de una Constitución para la Tierra, es decir, pretende abordar la reforma del pacto social y político a nivel planetario.
Filamin A C-terminal fragment modulates Orai1 expression by inhibition of protein degradation
(American Physiological Society, 2025-01-07) Macias-DÍaz, Alvaro; Nieto-Felipe, Joel; Jardin, Isaac; Camello, Pedro J.; Martinez-Quintana, Eva M.; Salido, Gines M.; Smani Hajami, Tarik; Lopez, Jose J.; Rosado, Juan A.; Universidad de Sevilla. Departamento de Fisiología Médica y Biofísica; Junta de Extremadura; Ministerio de Ciencia e Innovación (MICIN). España
Filamin A (FLNA) is an actin-binding protein that has been reported to interact with STIM1 modulating the activation of Orai1 channels. Cleaving of FLNA by calpain leads to a C-terminal fragment that is involved in a variety of functional and pathological events, including pro-oncogenic activity in different types of cancer. Here, we show that full-length FLNA is downregulated in samples from patients with colon cancer as well as in the adenocarcinoma cell line HT-29. This is consistent with an increased calpain-dependent FLNA cleaving with enhanced expression of the C-terminal FLNA fragment accompanied by enhanced expression of Orai1 and STIM1, as well as store-operated Ca2+ entry (SOCE). To further explore the mechanism underlying the enhancement of SOCE by the C-terminal FLNA fragment, we expressed in HEK-293 cells the C-terminal FLNA region encompassing repeats 16–24 (FLNA16–24 fragment), which enhanced both Orai1 and STIM1 as well as SOCE. Transfection of the FLNA16–24 fragment attenuates Orai1 and STIM1 protein degradation, and, specifically, abrogates Orai1α lysosomal degradation and retains this channel in the plasma membrane. However, the C-terminal FLNA fragment did not induce a detectable modification in Orai1β degradation. Due to the relevance of SOCE in cell physiology, our results provide evidence of a novel mechanism for the regulation of Ca2+ influx with relevant pathophysiological implications
