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X-WR-CALDESC:Events for Institute for Bioengineering of Catalonia
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BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20201204T110000
DTEND;TZID=Europe/Madrid:20201204T130000
DTSTAMP:20260517T233751
CREATED:20201201T133153Z
LAST-MODIFIED:20201202T090027Z
UID:80134-1607079600-1607086800@ibecbarcelona.eu
SUMMARY:PhD Thesis Defense: Arnau Biosca
DESCRIPTION:Discovery of protein aggregation in Plasmodium parasites and development of a combinational antimalarial therapy at the nanoscale\nArnau Biosca\, Nanomalaria Group \nThis thesis defense will take place ONLINE on the 4th December at 11.00 using the “BB Collaborate” streaming platform.
URL:https://ibecbarcelona.eu/event/phd-thesis-defense-arnau-biosca/
CATEGORIES:PhD Thesis Defence
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20201204T110000
DTEND;TZID=Europe/Madrid:20201204T130000
DTSTAMP:20260517T233751
CREATED:20201202T085923Z
LAST-MODIFIED:20201202T092538Z
UID:80148-1607079600-1607086800@ibecbarcelona.eu
SUMMARY:PhD Thesis Defense: Javier Rodriguez Benítez
DESCRIPTION:Characterization and interpretation of cardiovascular and cardiorespiratory dynamics in cardiomyopathy patients\nJavier Rodriguez Benítez\, member of Biomedical Signal Processing and Interpretation (BIOSPIN) Group  \nFriday 4th December 2020\, at 11.00 am \nThis defense will be transmitted online at Google meet\, using this link \n 
URL:https://ibecbarcelona.eu/event/phd-thesis-defense-javier-rodriguez-benitez/
CATEGORIES:PhD Thesis Defence
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BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20201210T153000
DTEND;TZID=Europe/Madrid:20201210T170000
DTSTAMP:20260517T233751
CREATED:20201209T122744Z
LAST-MODIFIED:20201210T124825Z
UID:80273-1607614200-1607619600@ibecbarcelona.eu
SUMMARY:PhD Thesis Defense: Anna Vila Giraut
DESCRIPTION:Hydrogel co-networks of gelatin methacryloyl and poly(ethylene glycol)diacrylate sustain 3D functional in vitro models of intestinal mucosa\nAnna Vila Giraut\, Biomimetic systems for cell engineering Group\nConventional in vitro cell culture models do not possess the complexity that the native tissues offer. Because of this\, the functional properties of the tissues are not properly mimicked\, which causes poorly predictive capabilities. Engineered tissues\, which combine biofabrication and tissue engineering techniques\, try to overcome this gap by providing the cells with an environment similar to the native tissue\, recapitulating (I) the physicochemical and mechanical properties of the cellular matrix\, (II) the multicellular complexity of the different tissue compartments\, and (III) the 3D structures of the tissues. These new engineered models are key factors to improve the platforms for basic research studies\, testing new drugs or modelling diseases. Among all the engineered tissues\, the intestinal mucosa is not well represented. The intestinal mucosa is formed by the epithelium\, which is a multicellular monolayer laying on top of the lamina propria\, a connective tissue containing several cell types (mesenchymal cells\, immune cells). The gold standard intestinal models are based on epithelial cell lines derived from colon cancer cells grown on the hard porous membranes of the Transwell® inserts. The lack of the intestinal stromal compartment and the growth on a hard surface give high transepithelial electrical resistance and low apparent permeability. Therefore\, the development of better in vitro platforms\, which integrates both compartments and provides epithelium-lamina propria cell interactions\, is highly desirable. \nIn this work\, we describe an easy and cost-effective method to engineer a 3D intestinal mucosa model that combines both the epithelium and the lamina propria compartments. To build the 3D scaffolds we chose hydrogels as materials to mimic the physicochemical and mechanical properties of intestinal tissue. Thus\, hydrogel conetworks of gelatin methacryolyl (GelMA)\, a natural polymer\, and poly(ethylene glycol) diacrylate (PEGDA)\, a synthetic polymer\, are photopolymerized. On one hand\, GelMA provides biodegradation and cell adhesion sequences but it lacks long-term mechanical stability. On the other hand\, PEGDA\, is non-biodegradable and does not present cell adhesion motifs. Nevertheless\, it has good mechanical properties. By this technique\, the lamina propria compartment of the intestinal mucosa can be reproduced in vitro. To do that\, GelMA and PEGDA polymers are laden with mesenchymal cells (fibroblasts or myofibroblasts) and/or immune cells (macrophages). We demonstrated that GelMA – PEGDA hydrogel co-networks support the growth of these cells and epithelial monolayers on top of the scaffolds. Embedding fibroblasts or myofibroblasts on the hydrogel conetworks enhance the formation and the maturity of the Caco-2 epithelial monolayers\, providing barrier properties similar to in vivo. The presence of the stromal cells also enhances the recovery of the epithelial integrity when the epithelium is temporally damaged. Finally\, an immunocompetent model is obtained by the encapsulation of macrophages in the constructs. The presence of macrophages does not influence the formation of the epithelium. However\, when the epithelial monolayer is disrupted\, the presence of mesenchymal and immune cells in the stromal compartment increases cytokine secretion in a synergistic manner. Our model can successfully mimic the interactions between stromal and epithelial compartments found in vivo intestinal tissue\, offering a potential platform to be used to study absorption and toxicity of drugs\, as well as cell behaviour under physiological and pathological conditions. \nLocation: The defense will be online. People are invited to attend upon receiving a link that you have to request to vd.fisica.recerca@ub.edu
URL:https://ibecbarcelona.eu/event/phd-thesis-defense-anna-vila-giraut/
CATEGORIES:PhD Thesis Defence
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20201211T140000
DTEND;TZID=Europe/Madrid:20201211T170000
DTSTAMP:20260517T233751
CREATED:20201209T121743Z
LAST-MODIFIED:20201210T124757Z
UID:80270-1607695200-1607706000@ibecbarcelona.eu
SUMMARY:PhD Thesis Defense: Elena Lantero
DESCRIPTION:Targeting strategies against Plasmodium and practical applications: blocking parasite development with heparin derivatives and identifying new aptamers for diagnosis\nElena Lantero\, Nanomalaria Group\nThis thesis defense will take place ONLINE on the 11th December at 14.00 using the “BB Collaborate” streaming platform.
URL:https://ibecbarcelona.eu/event/phd-thesis-defense-elena-lantero/
CATEGORIES:PhD Thesis Defence
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20201215T120000
DTEND;TZID=Europe/Madrid:20201215T140000
DTSTAMP:20260517T233751
CREATED:20201203T074210Z
LAST-MODIFIED:20201214T113928Z
UID:80200-1608033600-1608040800@ibecbarcelona.eu
SUMMARY:PhD Thesis Defense: Sock Ching Low
DESCRIPTION:Giving Centre Stage to Top-Down Inhibitory Mechanisms for Selective Attention\nSock Ching Low\, SPECS (Synthetic\, Perceptive\, Emotive and Cognitive Systems) \nSelective attention determines the sensory signals that are processed at higher levels at the expense of others and is biased by higher-order brain regions which anticipate task-relevant stimuli and increase neural sensitivity to them in the sensory cortex. Often\, this is thought to occur through excitation of selected neurons\, but some studies have suggested that it is not the full description of the process. Increasingly\, evidence has pointed to an alternative\, top-down inhibitory biasing mechanism. Here\, we investigated such an inhibitory model of attention. We first showed how sensitivity to stimulus features known to be task-irrelevant are reduced through top-down suppression. Secondly\, we demonstrated a biologically grounded spiking model’s ability to modulate information processing and benchmarked it to physiology. Lastly\, we explored the interaction between the excitatory and inhibitory models of top-down attention in a foraging agent. Our results support the inhibitory model of top-down attention as a biological attentional mechanism and show how it fits into the current zeitgeist of top-down attentional mechanisms. \nThis thesis defense will be held online using “Zoom” using this link.
URL:https://ibecbarcelona.eu/event/phd-thesis-defense-sock-ching-low/
CATEGORIES:PhD Thesis Defence
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20201221T110000
DTEND;TZID=Europe/Madrid:20201221T130000
DTSTAMP:20260517T233751
CREATED:20201214T081415Z
LAST-MODIFIED:20201214T081428Z
UID:80334-1608548400-1608555600@ibecbarcelona.eu
SUMMARY:PhD Thesis Defense: Laia Lidón Gil
DESCRIPTION:Regulación de la expresión de PrPC como elemento clave en las modificaciones de tau en la enfermedad de Alzheimer\nLaia Lidón\, Molecular and Cellular Neurobiotechnology \nLa enfermedad de Alzheimer (EA) es la causa más común de demencia y tiene una elevada prevalencia a nivel mundial. Se caracteriza por un deterioro cognitivo progresivo y muestra como principales rasgos neuropatológicos la presencia de placas seniles enriquecidas en βamiloide y ovillos neurofibrilares intracelulares constituidos por la proteína tau hiperfosforilada. Una precisa regulación de la fosforilación de tau es esencial para que la proteína ejerza sus funciones normales\, ya que su hiperfosforilación interrumpe procesos neuronales básicos como el transporte axonal. \nPor otro lado\, la proteína priónica celular (PrPC) es una glicoproteína de unión a membrana que en humanos se expresa mayoritariamente en el sistema nervioso central a partir de un único gen\, PRNP. Sus funciones fisiológicas abarcan un conjunto de propiedades neuroprotectoras como la regulación de la homeostasis del calcio\, la actividad anti-apoptótica y la capacidad antioxidante. \nEn los últimos años\, el interés por la PrPC y su implicación en diversas enfermedades neurodegenerativas ha ido en aumento a medida que se han ido conociendo los múltiples rasgos comunes a nivel molecular y/o neuropatológico entre PrPC y dichas enfermedades. Por\nejemplo\, se ha descrito que PrPC interacciona directamente con las proteínas tau\, Aβ y αsinucleína participando así en diversos procesos patológicos y vías de señalización. Es por ello que PrPC ha sido asociada con la EA y otras taupatías o la enfermedad de Parkinson. \nEn este sentido\, se ha descrito que el aumento de expresión de PrPC provoca una reducción de los niveles de tau y una menor susceptibilidad a la fosforilación en modelos experimentales de EA. Además\, ha sido demostrado que durante el curso de la EA se producen cambios de expresión en el perfil de PrPC habiendo un incremento notable en estadios iniciales de la enfermedad\, mientras que en estadios avanzados la expresión de PrPC disminuye coincidiendo con el incremento de depósitos de ptau. Este hecho\, sugiere que PrPC podría estar ejerciendo un rol neuroprotector en las fases iniciales de la enfermedad y\, en cambio\, la reducción de su expresión en fases avanzadas contribuiría a la neurodegeneración y a la progresión de la patología. \nA pesar de ello\, se desconoce cuáles son los desencadenantes de los cambios de expresión de PRNP en la enfermedad y\, por este motivo\, uno de los objetivos principales de la presente tesis ha sido analizar dichos factores. Hemos estudiado diversos estímulos asociados a la EA que pueden estar implicados en la regulación transcripcional de PRNP en etapas iniciales de la enfermedad y nuestros resultados indican que el incremento celular de los niveles de tau promueve la activación del promotor de PRNP. Además\, hemos descrito que la vía de señalización JNK-c-jun-AP1 es la principalmente implicada en la activación del promotor de PRNP por tau. \nPor otro lado\, diversos estudios sugieren que PrPC participa en la diferenciación neuronal de progenitores neuronales\, un proceso altamente influenciado por la actividad de la glucógeno sintasa quinasa-3beta (GSK3β)\, siendo esta inhibida por PrPC . Múltiples trabajos han descrito un desequilibrio en la expresión de las diferentes isoformas de tau (tau3R y tau4R) derivadas del splicing diferencial que sufre el gen de tau\, MAPT\, en enfermedades que cursan acúmulo de tau\, como la EA. En dichas enfermedades también se han encontrado niveles alterados de diversas quinasas\, y entre ellas se encuentra la GSK3β\, que además de incidir sobre la hiperfosforilación de tau\, está directamente implicada en el splicing alternativo de MAPT. Por ello\, otro de los propósitos del presente estudio ha sido analizar la intervención de PrPC \, no solo en la fosforilación de tau y en el mantenimiento de sus niveles de expresión\, sino también\nen la generación de las diferentes isoformas tau3R y tau4R. Mediante el uso de animales transgénicos\, muestras humanas de pacientes con EA y modelos experimentales de estudio de la PrPC \, nuestros resultados corroboran la implicación de PrPC en el splicing alternativo del exón 10 de tau a través de su papel inhibidor de la actividad GSK3β. \n\nThis thesis defense will be held online next 21st December at 11\, in order to be able to attend the defense\, you have to write an email to: doctorat.biologia@ub.edu
URL:https://ibecbarcelona.eu/event/phd-thesis-defense-laia-lidon-gil/
CATEGORIES:PhD Thesis Defence
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