104 research outputs found

    Plan de marketing dirigido al centro residencial para personas mayores San Martín Egoitza

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    Este trabajo de fin de grado consiste en la realización de un plan de marketing dirigido a un centro residencial para personas mayores, San Martín Egoitza, ubicado en Azpeitia. El trabajo tiene la estructura habitual de un plan de marketing (análisis de la situación, objetivos, estrategias, acciones y control)

    Euskara ikastaro erdi-presentziala HEOn, B1 maila

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    Hizkuntzen irakaskuntzan informazio eta komunikazio teknologiek (IKTek) egin dezaketen ekarpenaren inguruko hausnarketa eta esparru horretarako lagin baten azalpena aurkituko dituzu HezIkt18 graduondoan ikasitakoak bateratzen dituen txosten honetan. Arlo eta eremu zabalak izaki, testuingurua orokorretik Eibarko HEOn egin ohi dugun lanera arteko eta hemen proposatzen den tresnarako bidea deskribatu dela ikusiko du irakurleak. Hezkuntzako araudia, komunikazio gaitasunak eta digitalak, ohiko jarduna eta beste hainbat esparru xehatu dira. Ohiko aurrez aurreko jarduna online egindakoarekin uztartzeko ahalegina da hemen aurkeztutakoa. Ikastetxearen helburuak eta ikasleenak bat egingo lukeen gune bat eratzea, alegia, ikasleek euskaraz jarduteko gaitasuna eskuratzea erraztuko duen testuinguru aproposa. Beraien kasa, autonomiaz baina irakaslearen babes, gidaritza eta laguntzarekin (haietariko bakoitzari egokituta) osatu beharreko ibilbidea da taxutu duguna. Lanarentzako oinarri teorikoa ezartzeko e-learningaz, eskola erdi-presentzialaz eta eskura izandako metodoez jardun ostean, B1 mailako euskara ikastaro hau diseinatzeko baliatu dudan metodologiaren berri eman dut. Jarraian, UEUri esker eskura izan dudan Moodle plataforman egituratutako ikastaroaren nondik norakoen kontaketa zehatzagoa ere eskaintzen da. Azkenik, ondorioen atalean halako lanen ekarpenaz, berrerabilgarritasunaz eta aurrerago egin daitezkeen hobekuntzez hitz-aspertuan aritu naiz

    Evaluación de la infiltración micocárdica en amiloidosis mediante cardiorresonancia magnética

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    La amiloidosis cardiaca (AC) es una enfermedad infiltrativa causada por el depósito de fibrillas anormales insolubles en el espacio intersticial del miocardio. A pesar de que la forma de cadenas ligeras (AL) es el tipo más común de amiloidosis sistémica con afectación cardiaca, las formas familiar de transtiretina (TTR) y senil pueden también involucrar al corazón. La AC debe ser considerada en el diagnóstico diferencial de la insuficiencia cardiaca con función sistólica de ventrículo izquierdo (VI) preservada, especialmente cuando se detecta un patrón de llenado restrictivo, e incluso en ausencia de afectación conocida de otros órganos. En este sentido, los signos clásicos electrocardiográficos (ECG) y ecocardiográficos han sido extensamente utilizados para su diagnóstico. Sin embargo, aunque presentan una excelente especificidad adolecen de suficiente sensibilidad para detectar la enfermedad en fases iniciales. Por otro lado, el diagnóstico definitivo con biopsia endomiocárdica (BEM) no está extensamente disponible y tampoco está exento de potenciales complicaciones..

    Data on interleukin (IL)-2- and IL-15-dependent changes in IL-2Rβ and IL-2Rγ complexes

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    We provide detailed datasets from our analysis of the proteins that associate with IL-2Rbeta and IL-2Rgamma in T-cells stimulated with IL-2 or IL-15 compared with resting T-cells, as identified by SILAC-based quantitative proteomics. We also include quantitative data regarding site-specific phosphorylation events observed both in IL-2Rbeta and IL-2Rgamma. Moreover, we provide results demonstrating the specific protein recruitment capacity of four of those site-specific phosphorylations. The proteomics and phosphoproteomics data described in this article is associated with a research article entitled "Characterization of receptor-associated protein complex assembly in Interleukin (IL)-2- and IL-15-activated T-lymphocytes" (Osinalde et al., 2016 [1]). The mass spectrometry data have been deposited to the ProteomeEXchange Constorium with the identifier PXD002386

    Aly: a possible E2F interacting protein

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    Comunicaciones a congreso

    How to Inactivate Human Ubiquitin E3 Ligases by Mutation

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    E3 ubiquitin ligases are the ultimate enzymes involved in the transfer of ubiquitin to substrate proteins, a process that determines the fate of the modified protein. Numerous diseases are caused by defects in the ubiquitin-proteasome machinery, including when the activity of a given E3 ligase is hampered. Thus, inactivation of E3 ligases and the resulting effects at molecular or cellular level have been the focus of many studies during the last few years. For this purpose, site-specific mutation of key residues involved in either protein interaction, substrate recognition or ubiquitin transfer have been reported to successfully inactivate E3 ligases. Nevertheless, it is not always trivial to predict which mutation(s) will block the catalytic activity of a ligase. Here we review over 250 site-specific inactivating mutations that have been carried out in 120 human E3 ubiquitin ligases. We foresee that the information gathered here will be helpful for the design of future experimental strategies.This work was supported by Spanish MINECO (grant SAF2016-76898-P) cofinanced with FEDER funds. JR was funded with a postdoctoral fellowship from the University of the Basque Country (UPV/EHU)

    Neuronal Proteomic Analysis Of The Ubiquitinated Substrates Of The Disease-Linked E3 Ligases Parkin And Ube3a

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    Both Parkin and UBE3A are E3 ubiquitin ligases whose mutations result in severe brain dysfunction. Several of their substrates have been identified using cell culture models in combination with proteasome inhibitors, but not in more physiological settings. We recently developed the (bio)Ub strategy to isolate ubiquitinated proteins in flies and have now identified by mass spectrometry analysis the neuronal proteins differentially ubiquitinated by those ligases. This is an example of how flies can be used to provide biological material in order to reveal steady state substrates of disease causing genes. Collectively our results provide new leads to the possible physiological functions of the activity of those two disease causing E3 ligases. Particularly, in the case of Parkin the novelty of our data originates from the experimental setup, which is not overtly biased by acute mitochondrial depolarisation. In the case of UBE3A, it is the first time that a nonbiased screen for its neuronal substrates has been reported.The authors thank Michael Clague for insightful comments on an early version of the manuscript. Ugo Mayor, Nerea Osinalde, and Jesus M. Arizmendi are supported by the Spanish MINECO (Grant no. SAF2016-76898-P)
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