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Amb l’auge de la IA en els darrers anys i en una societat on tot està de cada cop més connectat i digitalitzat, ha augmentat la demanda de l'eficàcia i velocitat de tot tipus de programes. Aquest augment, ha significat un impuls tecnològic molt gran, fent que de cada cop els programes siguin més eficients i sofisticats. Per intentar comprendre el funcionament de les IA, s’ha decidit crear un programa que recomana itineraris formatius personalitzats a usuaris. Per realitzar aquest projecte, s’ha fet una compilació de dades de cursos oferts per diferents entitats. Després es va crear una ontologia de cada conjunt de dades perquè el nostre programa pugui realitzar la recomanació. Un cop tinguem l’ontologia i les dades dels cursos carregats al programa, només faltaria introduir dades d’usuari i el programa podrà realitzar una recomanació. Més endavant la idea és que el programa creés les ontologies per ell mateix.

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[cat] El cinema és una eina fonamental per conèixer la història, i encara més en una societat en què l’audiovisual domina l’entreteniment i la comunicació. Les pel·lícules ens transporten a contexts anteriors, ens donen a conèixer fets històrics i ens transmeten idees clau del passat. Però també són una eina perillosa de desinformació i manipulació de la realitat, ja que no tenen compromisos amb la veracitat històrica. Per això, esdevé vital, per a l’aprenentatge i la conscienciació històrica sobre el nazisme i l’Holocaust, en el cas d’alumnes de 1r de batxillerat, i per això cal saber exercir una bona tasca docent, basada en el film El noi del pijama de ratlles., [eng] Cinema is a fundamental tool to uncover history, particularly in a society where audiovisual production dominates entertainment and communication. Films transport us to earlier contexts, introduce us to historical facts and transmit key ideas from the past. Nonetheless, they can also be a dangerous tool for misinformation and manipulation, as they make no commitment to historical truth. With regard to learning and historical awareness about Nazism and the Holocaust for first-year high school students, cinema becomes essential. In this vein, this paper offers an insight into utilising good teaching practice based on the film The Boy in the Striped Pyjamas.

A main challenge in biology is to understand the development of the human body, namely how cell and tissue shape transitions occur. Our organism is riddled with curved cell layers that withstand stress and react to it depending on their function, and this is where physics plays an important role, trying to unveil the forces and mechanical properties of these tissues. Thus, the study hereby presented aims to characterize human pluripotent stem cell monolayer curling transitions, and tries to set the fine line that separates them from the dewetting transitions. For controlling these changes in form, we apply different geometrical constraints by varying the size and shape of the islands using photopatterning of extracellular matrix (ECM) proteins on dishes, and apart from that, we subject the cell monolayers to different external chemical and physical stimuli: we inhibit or activate contractility of the cells by using Y27 drug, we control apical constriction optogenetically, or we vary the cell-substrate adhesion by either using dispase or creating ECM protein gradients. In order to gain control over the curling and dewetting transitions, the role of the different geometrical constraints and external stimuli is assessed. This work shows the contribution of each variable by measuring some mechanical and physical properties of the monolayers, such as curvatures, velocities and traction forces exerted by the tissues. These magnitudes, which change with the stimuli, hold the key that governs the transition, and after assessing the relations between them, we are able of programming the dewetting and curling transitions at will. Finally, the potential of this system as a biological actuator is evaluated, by trying to make a hand-like monolayer curl and grab a bead or a cell spheroid., Uno de los principales desafíos en biología es comprender el desarrollo del cuerpo humano, en particular cómo ocurren las transiciones en la forma de las células y los tejidos. Nuestro organismo está lleno de capas de células curvas que resisten el estrés y reaccionan ante él según su función, y aquí es donde la física desempeña un papel importante, tratando de analizar las fuerzas y propiedades mecánicas de estos tejidos. Por lo tanto, el estudio que se presenta aquí tiene como objetivo caracterizar las transiciones de monocapas de células madre pluripotentes humanas que se curvan y trata de establecer la línea que las separa de las transiciones de ''dewetting''. Para controlar estos cambios en la forma, aplicamos diferentes restricciones geométricas al variar el tamaño y la forma de las islas. Además de eso, sometemos las monocapas celulares a diferentes estímulos químicos y físicos externos: inhibimos o activamos la contractilidad de las células utilizando el fármaco Y27, controlamos la constricción apical de forma optogenética o variamos la adhesión célula-sustrato mediante el uso de dispasa o la creación de gradientes de proteínas de la matriz extracelular. Para obtener el control sobre las transiciones de ''curling'' y ''dewetting'', evaluamos el papel de las diferentes restricciones geométricas y estímulos externos. Este trabajo muestra la contribución de cada variable al medir algunas propiedades mecánicas y físicas de las monocapas, como curvaturas, velocidades y fuerzas de tracción ejercidas por los tejidos. Estas magnitudes, que cambian con los estímulos, son la clave para gobernar la transición, y después de evaluar las relaciones entre ellas, somos capaces de programar las transiciones de "dewetting" y "curling" a voluntad. Finalmente, se evalúa el potencial de este sistema como actuador biológico, tratando de hacer que una monocapa con forma de asterisco se pliegue y agarre un esferoide celular. User traduce also to catalan ChatGPT Un dels reptes princ, Un dels reptes principals en biologia és entendre el desenvolupament del cos humà, concretament com ocorren les transicions en la forma de les cèl·lules i els teixits. El nostre organisme està ple de capes de cèl·lules corbades que resisteixen l'estrès i hi reaccionen segons la seva funció, i aquí és on la física juga un paper important, tractant de desxifrar les forces i les propietats mecàniques d'aquests teixits. Per tant, l'estudi que es presenta aquí té com a objectiu caracteritzar les transicions d'enrollament de monocapes de cèl·lules mare pluripotents humanes i tracta d'establir la línia que les separa de les transicions de "dewetting". Per controlar aquests canvis en la forma, apliquem diferents restriccions geomètriques variant la mida i la forma de les illes. A més a més, sotmetem les monocapes cel·lulars a diferents estímuls químics i físics externs: inhibim o activem la contractilitat de les cèl·lules mitjançant l'ús del fàrmac Y27, controlem la constricció apical de forma optogenètica o variem la adhesió cèl·lula-substrat utilitzant dispasa o creant gradients de proteïnes de la matriu extracel·lular. Per obtenir el control sobre les transicions de "curling" i "dewetting", avaluem el paper de les diferents restriccions geomètriques i estímuls externs. Aquest treball mostra la contribució de cada variable mitjançant la mesura de diverses propietats mecàniques i físiques de les monocapes, com ara la curvatura, velocitats i forces de tracció exercides pels teixits. Aquestes magnituds, que canvien amb els estímuls, són clau per a governar la transició, i després d'avaluar les relacions entre elles, som capaços de programar les transicions de "dewetting" i "curling" a voluntat. Finalment, s'avalua el potencial d'aquest sistema com a actuador biològic, tractant de fer que una monocapa amb forma de asterisc s'enrotlli i agafi un esferoide cel·lular.

© 2020, The Author(s). Many neurodevelopmental disorders are characterized by impaired functional synaptic plasticity and abnormal dendritic spine morphology, but little is known about how these are related. Previous work in the Fmr1-/y mouse model of fragile X (FX) suggests that increased constitutive dendritic protein synthesis yields exaggerated mGluR5-dependent long-term synaptic depression (LTD) in area CA1 of the hippocampus, but an effect on spine structural plasticity remains to be determined. In the current study, we used simultaneous electrophysiology and time-lapse two photon imaging to examine how spines change their structure during LTD induced by activation of mGluRs or NMDA receptors (NMDARs), and how this plasticity is altered in Fmr1-/y mice. We were surprised to find that mGluR activation causes LTD and AMPA receptor internalization, but no spine shrinkage in either wildtype or Fmr1-/y mice. In contrast, NMDAR activation caused spine shrinkage as well as LTD in both genotypes. Spine shrinkage was initiated by non-ionotropic (metabotropic) signaling through NMDARs, and in wild-type mice this structural plasticity required activation of mTORC1 and new protein synthesis. In striking contrast, NMDA-induced spine plasticity in Fmr1-/y mice was no longer dependent on acute activation of mTORC1 or de novo protein synthesis. These findings reveal that the structural consequences of mGluR and metabotropic NMDAR activation differ, and that a brake on spine structural plasticity, normally provided by mTORC1 regulation of protein synthesis, is absent in FX. Increased constitutive protein synthesis in FX appears to modify functional and structural plasticity induced through different glutamate receptors.

© 2020, The Author(s). Many neurodevelopmental disorders are characterized by impaired functional synaptic plasticity and abnormal dendritic spine morphology, but little is known about how these are related. Previous work in the Fmr1-/y mouse model of fragile X (FX) suggests that increased constitutive dendritic protein synthesis yields exaggerated mGluR5-dependent long-term synaptic depression (LTD) in area CA1 of the hippocampus, but an effect on spine structural plasticity remains to be determined. In the current study, we used simultaneous electrophysiology and time-lapse two photon imaging to examine how spines change their structure during LTD induced by activation of mGluRs or NMDA receptors (NMDARs), and how this plasticity is altered in Fmr1-/y mice. We were surprised to find that mGluR activation causes LTD and AMPA receptor internalization, but no spine shrinkage in either wildtype or Fmr1-/y mice. In contrast, NMDAR activation caused spine shrinkage as well as LTD in both genotypes. Spine shrinkage was initiated by non-ionotropic (metabotropic) signaling through NMDARs, and in wild-type mice this structural plasticity required activation of mTORC1 and new protein synthesis. In striking contrast, NMDA-induced spine plasticity in Fmr1-/y mice was no longer dependent on acute activation of mTORC1 or de novo protein synthesis. These findings reveal that the structural consequences of mGluR and metabotropic NMDAR activation differ, and that a brake on spine structural plasticity, normally provided by mTORC1 regulation of protein synthesis, is absent in FX. Increased constitutive protein synthesis in FX appears to modify functional and structural plasticity induced through different glutamate receptors.

Synaptic plasticity involves structural modifications in dendritic spines that are modulated by local protein syn-thesis and actin remodeling. Here, we investigated the molecular mechanisms that connect synaptic stimulation to these processes. We found that the phosphorylation of isoform-specific sites in eEF1A2—an essential transla-tion elongation factor in neurons—is a key modulator of structural plasticity in dendritic spines. Expression of a nonphosphorylatable eEF1A2 mutant stimulated mRNA translation but reduced actin dynamics and spine density. By contrast, a phosphomimetic eEF1A2 mutant exhibited decreased association with F-actin and was inactive as a translation elongation factor. Activation of metabotropic glutamate receptor signaling triggered transient dissociation of eEF1A2 from its regulatory guanine exchange factor (GEF) protein in dendritic spines in a phosphorylation-dependent manner. We propose that eEF1A2 establishes a cross-talk mechanism that coordinates translation and actin dynamics during spine remodeling

En el presente trabajo se presenta la implementación de un modelo de consumo y emisiones respecto a la potencia específica demandada, aplicado a vehículos con motores de combustión interna. Además de esta implementación, se realiza la validación de los datos necesarios para la construcción del modelo, obtenidos con un método de simulación y con uno experimental. La simulación para la obtención de los datos se realiza con el programa Advisor, el cual se parametriza para adaptarse a las condiciones deseadas. La obtención de datos de forma experimental se realiza a través de un dispositivo bluetooth conectado al vehículo y la aplicación móvil Torque PRO. La comparación de ambos métodos permite ver sus diferencias, así como sus puntos fuertes y débiles. La implementación del modelo se realiza a través de un programa en Matlab. Esta implementación permite definir los parámetros necesarios para la construcción de dicho modelo, ajustándolo a los datos proporcionados. Se comprueba la bondad del ajuste del modelo en cuanto al consumo y, en menor medida, en cuanto a las emisiones. La implementación realizada permite, a partir de unos datos iniciales que se pueden obtener de distintas fuentes, la definición del modelo. Una vez obtenido este modelo, se pueden realizar predicciones de consumo y emisiones en base a él, en función de la potencia requerida al motor.

La realitat virtual és una tecnologia emergent i cada cop té més rellevància en la industria de la informàtica. Degut a aquest creixement, cada vegada hi ha més empreses i més desenvolupadors que treballen amb realitat virtual. El problema és que hi ha diferents dispositius amb diferents capacitats i costos y, per tant, diferents maneres de desenvolupar per a aquest ampli ventall de possibilitats. Això suposa un problema ja que provoca que les aplicacions tinguin dificultats alhora de suportarmultiplataforma. És per això que l’objectiu d’aquest projecte és crear una API o “Asset” que permet a les aplicacions tenir multiplataforma aplicant els mínims canvis. Consisteix en crear un seguit d’eines considerant diferents dispositius per tal de que el desenvolupament d’una aplicació no experimenti canvis o n’experimenti els mínims canvis per tal de ser usada en un dispositiu o en un altre. Sempre tenint en compte les capacitats dels diferents dispositius.

El present projecte s’entén com el primer d’una sèrie d’estudis destinats a la caracterització i optimització d’un motor Stirling. Aquest motor de combustió externa té un gran potencial d’aprofitament eficient de l’energia. De fet, el cicle Stirling ideal presenta el mateix rendiment que una màquina de Carnot. Per aconseguir-ho, però, cal afegir i optimitzar un regenerador al motor. El regenerador és un bescanviador de calor on s’aprofita la inèrcia tèrmica del propi fluid de treball. Per a optimitzar un motor Stirling cal una simulació detallada del regenerador, típicament mitjançant eines de fluidodinàmica computacional (CFD). Per a fer-ho es requereix tenir ben caracteritzat el cicle complet i poder definir adequadament les condicions de treball i de contorn de la simulació CFD. Per tant, és imprescindible tenir un model simplificat del cicle complet. El present projecte té com a objectiu principal la definició, implementació i verificació d’aquest modelatge del cicle complet. En aquest document, després d’una introducció definint la motivació, objectius i abast del projecte, s’inclou la descripció del cicle Stirling i les seves diferents configuracions. Seguidament, es comenten i justifiquen les hipòtesis emprades per la modelització matemàtica del cicle complet. Després de la descripció de la obtenció de les equacions de conservació es presenta l’algoritme implementat emprant l’eina MATLAB. Es dedica un capítol a mostrar el procés de verificació de l’eina desenvolupada, incloent-hi les diferents estratègies provades i les fortaleses i les debilitats del codi. Finalment, s’inclou una primera proposta de l’estratègia a seguir en les següents fases del projecte global de caracterització i optimització del motor Stirling. L’eina resultant del present estudi es facilitarà als docents de l’assignatura d’Ampliació de Màquines Tèrmiques (assignatura optativa del Màster Universitari en Enginyeria de l’Automoció i del Màster Universitari en Enginyeria Industrial) per ser

Quantum Mechanics is considered as one of the most weird branches in physics with the most, although accurate, counter intuitive predictions. The problem lies not on the theory but on what it is trying to explain: the microscopic world. Moreover, due to the complicated form of the Schrödinger equation, there are only few examples where an analytical solution to the problem exists. Therefore, the motivation of this paper is to explore the effects of Quantum Mechanics solving the Schrödinger equation numerically for different potentials. Firstly, the algorithms and the numerical methods used to calculate the eigenvalues and the eigenstates are explained. Subsequently, on the results section, the numerical system is stressed to find out its precision and the method is used for two real models: the ammonia molecule and the hydrogen atom. Finally, an applet that uses the numerical system of this paper is discussed., 2017/2018

Synapses store information by long-lasting modifications of their structure and molecular composition, but the precise chronology of these changes has not been studied at single-synapse resolution in real time. Here we describe the spatiotemporal reorganization of postsynaptic substructures during long-term potentiation (LTP) at individual dendritic spines. Proteins translocated to the spine in four distinct patterns through three sequential phases. In the initial phase, the actin cytoskeleton was rapidly remodeled while active cofilin was massively transported to the spine. In the stabilization phase, cofilin formed a stable complex with F-actin, was persistently retained at the spine, and consolidated spine expansion. In contrast, the postsynaptic density (PSD) was independently remodeled, as PSD scaffolding proteins did not change their amount and localization until a late protein synthesis-dependent third phase. Our findings show how and when spine substructures are remodeled during LTP and explain why synaptic plasticity rules change over time., RIKEN Brain Science Institute, National Institutes of Health (U.S.) (Grant R01DA17310), Human Frontier Science Program (Strasbourg, France), Paul and Anne Punzak Marcus Fund

We report the characterization of tris(2-pyridylmethyl)amine (TPA) as a membrane-permeable zinc chelator for intercepting biological mobile zinc. Compared to N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), TPA chelates zinc with faster kinetics in cuvettes, live cells, and brain slices. TPA also is generally less toxic than TPEN in cell culture. Mechanistic analysis indicates that these improvements arise from both the electronic and steric properties of TPA including weaker metal-binding affinity, lower pK[subscript a], and smaller size. These results demonstrate that TPA chelation is a valuable addition to the methodologies available for investigating mobile zinc in biology., National Institute of General Medical Sciences (U.S.) (Grant GM065519), FRAXA Research Foundation (Fellowship)

Animals can make faster behavioral responses to multisensory stimuli than to unisensory stimuli. The superior colliculus (SC), which receives multiple inputs from different sensory modalities, is considered to be involved in the initiation of motor responses. However, the mechanism by which multisensory information facilitates motor responses is not yet understood. Here, we demonstrate that multisensory information modulates competition among SC neurons to elicit faster responses. We conducted multiunit recordings from the SC of rats performing a two-alternative spatial discrimination task using auditory and/or visual stimuli. We found that a large population of SC neurons showed direction-selective activity before the onset of movement in response to the stimuli irrespective of stimulation modality. Trial-by-trial correlation analysis showed that the premovement activity of many SC neurons increased with faster reaction speed for the contraversive movement, whereas the premovement activity of another population of neurons decreased with faster reaction speed for the ipsiversive movement. When visual and auditory stimuli were presented simultaneously, the premovement activity of a population of neurons for the contraversive movement was enhanced, whereas the premovement activity of another population of neurons for the ipsiversive movement was depressed. Unilateral inactivation of SC using muscimol prolonged reaction times of contraversive movements, but it shortened those of ipsiversive movements. These findings suggest that the difference in activity between the SC hemispheres regulates the reaction speed of motor responses, and multisensory information enlarges the activity difference resulting in faster responses., Japan. Ministry of Education, Culture, Sports, Science and Technology (Grant-in-Aid for Scientific Research on Priority Areas (Molecular Brain Science)), Japan. Ministry of Education, Culture, Sports, Science and Technology (Grant-in-Aid for Young Scientists), Japan. Science and Technology Agency (CREST Program)

The mechanism that controls the selective vulnerability of striatal neurons in Huntington's disease is unclear. Brain-derived neurotrophic factor (BDNF) protects striatal neurons and is regulated by Huntingtin through the interaction with the neuron-restrictive silencer factor. Here, we demonstrate that the downregulation of BDNF by mutant Huntingtin depends on the length and levels of expression of the CAG repeats in cell cultures. To analyze the functional effects of these changes in BDNF in Huntington's disease, we disrupted the expression of bdnf in a transgenic mouse model by cross-mating bdnf(+/ -) mice with R6/1 mice. Thus, we compared transgenic mice for mutant Huntingtin with different levels of BDNF. Using this double mutant mouse line, we show that the deficit of endogenous BDNF modulates the pathology of Huntington's disease. The decreased levels of this neurotrophin advance the onset of motor dysfunctions and produce more severe uncoordinated movements. This behavioral pathology correlates with the loss of striatal dopamine and cAMP-regulated phosphoprotein-32-positive projection neurons. In particular, the insufficient levels of BDNF cause specific degeneration of the enkephalinergic striatal projection neurons, which are the most affected cells in Huntington's disease. This neuronal dysfunction can specifically be restored by administration of exogenous BDNF. Therefore, the decrease in BDNF levels plays a key role in the specific pathology observed in Huntington's disease by inducing dysfunction of striatal enkephalinergic neurons that produce severe motor dysfunctions. Hence, administration of exogenous BDNF may delay or stop illness progression.