Dipòsit Digital de la Universitat de Barcelona
El Dipòsit Digital de la Universitat de Barcelona és el repositori institucional que conté en format digital els materials derivats de l'activitat docent, investigadora i institucional de la comunitat universitària.
Enviaments recents
TesiUna aproximació a la Vida secreta de Salvador Dalí per Salvador Dalí: Una obra literària entre el somni, el pensament, la fabulació i la realitat. Introducció a l’estudi d’un dels clàssics contemporanis del segle XX
(Universitat de Barcelona, 2025-11-07) Vidal i Sapé, Artur; Cabré, Rosa, 1945-; Marrugat, Jordi, 1978-; Universitat de Barcelona. Departament de Filologia Catalana i Lingüística General
[cat] En aquesta tesi es parlarà de Dalí escriptor, sobre la seva obra Vida secreta de Salvador Dalí per Salvador Dalí, publicada el 1942 a Nova York. Aquesta obra va suposar un abans i un després pel que fa a la figura del pintor de Figueres. A través d’una anàlisi en profunditat, veurem com Salvador Dalí reformula el concepte d’autobiografia, atorgant-li una dimensió literària innovadora, fins aleshores mai vista. Al llarg de l’anàlisi, també es mostra com aquesta obra va tenir diversos detractors, que van contribuir a allargar l’ombra del mite de Dalí.
TesiRol de los marcadores fecales en la fisiopatología y diagnóstico de la colitis microscópica
(Universitat de Barcelona, 2025-07-11) Batista Pérez, Lissette Altagracia; Zabana Abdo, Yamile; Universitat de Barcelona. Facultat de Medicina i Ciències de la Salut
[spa] La colitis microscópica es una enfermedad inflamatoria crónica caracterizada por la presencia de diarrea acuosa crónica sin lesiones macroscópicas visibles en la mucosa del colon durante una colonoscopia. Esta patología incluye dos formas principales: la colitis colágena y la colitis linfocítica. Actualmente, no se dispone de biomarcadores específicos para esta enfermedad, y a menudo permanece infradiagnosticada. Existe poca evidencia científica sobre el uso o la aplicabilidad de la calprotectina fecal en la colitis microscópica, así como de otros biomarcadores no invasivos. Su fisiopatología no está claramente establecida; tiene un origen multifactorial basado en la interacción entre factores luminales y la inmunidad innata y adaptativa de la mucosa colónica. Esta tesis doctoral está dividida en dos partes principales. En primer lugar, hemos investigado el papel de la calprotectina fecal como marcador diagnóstico de la colitis microscópica. Nuestros resultados han demostrado que los pacientes con colitis microscópica activa presentan niveles significativamente más altos de calprotectina fecal en comparación con aquellos con diarrea crónica funcional, una condición que a menudo se confunde con la colitis microscópica. Esto sugiere que la calprotectina fecal puede ser un biomarcador valioso, ya que los niveles elevados de calprotectina fecal son frecuentes en pacientes con colitis microscópica. Aunque no tiene una alta precisión diagnóstica , puede resultar útil en el diagnóstico, especialmente en mujeres mayores de 60 años con diarrea acuosa crónica. En la segunda parte de la tesis, nos hemos centrado en el papel de la microbiota intestinal en la fisiopatología de la colitis microscópica. Hemos observado un estado de disbiosis intestinal en pacientes con colitis microscópica, caracterizado por alteraciones en la composición y diversidad de la microbiota. Sin embargo, la pérdida de diversidad microbiana fue similar en los diferentes grupos con diarrea (colitis microscópica, diarrea funcional, malabsorción de sales biliares) en comparación con los controles sanos. Este desequilibrio podría desempeñar un papel fundamental en la patogénesis de la enfermedad. Nuestros estudios han sido pioneros en la evaluación de la microbiota antes de la realización de un lavado colónico, lo que ha permitido analizar el impacto de este procedimiento en la composición microbiana. Un número considerable de pacientes con colitis microscópica lograron la remisión clínica sin necesidad de tratamiento tras la colonoscopia, lo que sugiere que los cambios inducidos por el polietilenglicol en la microbiota intestinal podrían desempeñar un papel relevante. En conclusión, esta tesis doctoral aporta nuevas evidencias sobre la importancia de la calprotectina fecal como herramienta diagnóstica en la colitis microscópica y destaca el papel clave de la microbiota intestinal en su fisiopatología. Estos hallazgos contribuyen a una mejor comprensión de esta enfermedad y refuerzan la necesidad de un abordaje multidisciplinar para su diagnóstico y tratamiento.
Tesi
Novel molecular mechanisms contributing to cognitive impairment in schizophrenia
(Universitat de Barcelona, 2025-07-11) Galán Ganga, Marcos; Giralt Torroella, Albert; Universitat de Barcelona. Departament de Biomedicina
[eng] Schizophrenia is a neuropsychiatric syndrome that affects around 1% of the world population (Marder & Cannon, 2019). Its age of onset typically occurs within the second and third decades of life (Velligan & Rao, 2023). It is characterized by the presence of psychosis (e.g. hallucinations, delusions and disorganized speech), negative symptoms (e.g. social withdrawal, anhedonia and apathy), and cognitive deficits (e.g. social cognition deficits, impaired executive functions and working memory) (Marder & Cannon, 2019). Antipsychotic treatments can help to manage positive symptoms during acute episodes. However, their side effects and limited benefits on sociability and cognition often result in poor medication adherence and increased risk of relapse. Consequently, there is a significant unmet medical need, particularly for treatments targeting those cognitive symptoms that emerge in the premorbid phase and affect nearly 98% of patients (Harvey et al., 2022; Mihaljević-Peleš et al., 2019).
The complexity of the disease relies not only on its wide variety of symptoms, but also from the different heritable and environmental risk factors that influence the development of schizophrenia (Marder & Cannon, 2019; McCutcheon et al., 2020; Jauhar et al., 2022). Research made over the last decades has identified several molecular pathways impaired in the disorder, with neurochemical disturbances related to the dopaminergic and glutamatergic systems having a prominent role in its pathophysiology (Jauhar et al., 2022). Recent evidence has revealed that impaired GABAergic and serotoninergic neurotransmission, neurodevelopmental abnormalities and inflammation could also play a role in the onset and progression of schizophrenia (De Jonge et al., 2017; Gaitonde et al., 2024; Marder & Cannon, 2019; Jauhar et al., 2022; E. E. Lee et al., 2017; Hong & Bang, 2020). Although anatomical and functional dysfunctions have been found in different brain areas from diseased patients, the hippocampus has been suggested to play a pivotal role. Different morphological, electrophysiological, synaptic and molecular impairments affecting this brain region have been associated to schizophrenia and in close relation with to some of its positive, negative and cognitive symptoms (Harrison, 2004; Wegrzyn et al., 2022). Notwithstanding the progresses made to enhance our comprehension of this illness, there remains a need for novel approaches and improved translational models that may recapitulate more accurately its underlying pathological mechanisms.
Latest reports have found altered levels of small RNAs (sRNAs) in post-mortem brain samples of patients affected by schizophrenia and other neuropsychiatric disorders (Yoshino & Dwivedi, 2020). sRNAs are non-coding RNAs with less than 200 nucleotides that do not code for proteins but play an essential role regulating messenger RNA (mRNA) expression, stability and translation, with an important function in health and disease (Yoshino & Dwivedi, 2020). Among the different sRNA biotypes, microRNAs (miRNAs) have been linked to the aetiology of schizophrenia through their direct regulation of neurotransmission and immunological pathways that are known to be altered in the disorder (Zhang et al., 2023; Thomas & Zakharenko, 2021). Moreover, dysregulation of some miRNAs has been found not only in the hippocampus, but also in circulating blood vesicles of affected individuals in association with treatment-resistance and the severity of cognitive symptoms (Barnett et al., 2023). However, most of these studies are largely
descriptive and none of them has been able to directly assess the potential contribution of sRNAs to the onset and/or progression of the cognitive deficits associated with schizophrenia.
Also, genome-wide association studies (GWAS) have found different gene variants associated to cognitive impairment in schizophrenia (Zhao et al., 2022). Some of these risk gene polymorphisms have been located at the forkhead-box P2 (FOXP2) gene, which encodes for a transcription factor involved in regulating synaptic plasticity, neurotransmission and the development of neurons related to language and memory function (Vernes et al., 2007; Lang et al., 2019). FOXP2 has been linked to schizophrenia vulnerability, auditory hallucinations and cognitive deficits in chronic patients with the disorder (Sanjuán et al., 2006; Lang et al., 2019; Sanjuán et al., 2021), although the association of some specific polymorphisms to the disease are still controversial. Furthermore, increased FOXP2 levels have been found in some experimental models of schizophrenia. Nevertheless, it remains to be confirmed whether FOXP2 could mediate the development of the different symptoms associated with schizophrenia and its underlying molecular mechanisms.
In this thesis, we hypothesise that sRNAs dysregulated in the hippocampus of patients with schizophrenia are important contributors to its associated cognitive deficits. Furthermore, we aim to decipher whether altered levels of FOXP2 in the brain of these patients could play a role in the onset and progression of some of those clinical features of the disorder.
Characterization of hippocampal sRNA profiles from patients with schizophrenia revealed novel microRNA (miRNA) species dysregulated in the disorder. To define the contribution of sRNAs to the cognitive-like symptoms of schizophrenia, we developed a novel translational model based on the injection of those sRNAs isolated from the hippocampus of schizophrenia patients or non-affected individuals into the brain of wild-type mice. Animals receiving sRNAs from diseased patients exhibited an impairment in hippocampal-dependent spatial short-term memory in the T-maze test, in comparison with mice receiving sRNAs from healthy controls or vehicle. However, no deficits were found in recognition memory when performing the novel object recognition (NOR) test, along with no changes in anxiety-like levels nor locomotor activity in the open field test. Golgi staining revealed that schizophrenia sRNAs induced a decrease in the spine density of the pyramidal neurons from the cornus ammonis 1 (CA1) hippocampal region. Injected mice showed higher levels of synaptotagmin 2, a presynaptic marker for inhibitory interneurons. This increase mirrors observations made in patients. Furthermore, we also detected subtle morphological changes in mouse hippocampal microglia in response to sRNAs from affected individuals.
We found increased FOXP2 protein levels in the hippocampus and putamen of patients with schizophrenia. These aberrant levels of FOXP2 were recapitulated in the hippocampus, but not in the striatum, of a chronic ketamine mouse model of experimental psychosis. Overexpression of Foxp2 in the hippocampus of wild-type mice using adeno-associated viral (AAV) vectors induced some positive-like symptoms of the
disease, such as hyperlocomotion and alterations in navigation in the open field test. No effects in the negative-like symptoms were found in the three-chamber sociability test. Interestingly, Foxp2 overexpression induced cognitive deficits related to an impairment in recognition memory in the NOR test, while we did not find any differences in the spatial short-term memory when performing the T-maze test. Proteomic analysis of the hippocampus of mice overexpressing Foxp2 revealed a reduction in relevant proteins involved in glutamatergic and GABAergic neurotransmission.
Positive correlation between FOXP2 and SYT2 protein levels in the hippocampus of affected individuals suggests these changes could be concomitant processes in the disorder.
In summary, our results suggest that dysregulated hippocampal sRNAs in schizophrenia are important contributors to its associated cognitive symptoms, while aberrantly increased levels of FOXP2 in the hippocampus of these patients participate in the pathophysiology of the disorder.
ArticleAttribution of the unprecedented heat event of August 2023 in Barcelona (Spain) to observed and projected global warming
(Elsevier B.V., 2024-06-24) Lemus-Canovas, Marc; Montesinos Ciuró, Eduard; Cearreta-Innocenti, Tania; Serrano-Notivoli, Roberto; Royé, Dominic
The study analyses observed and numerical simulations of daily maximum and minimum temperature from 1920 onwards and to investigate the unprecedented heat event that occurred in 21–23 August 2023 in Barcelona. The historical changes in the intensity of such events, their expected future changes under scenarios of +1.5 ◦C, +2 ◦C, and + 3 ◦C, and the future exposure of populations to such kind of events are examined using the flow analogues approach. The findings indicate a significant increase in observed temperatures for similar heatwaves to those occurred in August 2023. The study also emphasises the impact of global warming on the intensification of heat events over the impact of urbanization. Additionally, after examining the role of natural variability in temperature changes, we concluded that global warming is the primary factor driving the increase in heatwave intensity. In terms of the frequency of such events, we found that extreme heat events, such as the August 2023 heatwave, will become 2 and 5 times more likely with a global summer warming of 2 ◦C and 3 ◦C, respectively. This will expose a large portion of the population to dangerous heat levels highlighting the importance of limiting global warming to 1.5 ◦C to mitigate the impacts on urban populations.
ArticleMechanisms of the QBO influence on the tropical troposphere: climatological SST conditions
(Wiley, 2025-11-22) Rodrigo Sánchez, Mario; García-Franco, Jorge Luis; García-Serrano, Javier; Bladé, Ileana; Palmeiro, Froila M.
The Quasi-Biennial Oscillation (QBO), the leading mode of tropical stratospheric variability, is thought to influence the tropical troposphere. Disentangling this influence from the dominant effects of El Niño-Southern Oscillation (ENSO) remains challenging. In this study, we use an atmosphere-only experiment with climatological sea surface temperature to isolate the tropospheric impact of the QBO, while a companion article examines how ENSO further affects this impact. The analysis focuses on the QBO modulation of temperature and zonal wind in the upper troposphere-lower stratosphere (UTLS) and the accompanying effects on static stability, wind shear and vorticity. Our results show that the QBO modifies deep tropical convection over the Maritime Continent region, and affects both the zonal Walker circulation and, more notably, the meridional Hadley circulation. These impacts are highly seasonal, with the strongest effects in summer and autumn. A zonal asymmetry in the vertical structure of the QBO signal and its influence on tropical circulation is identified, with anomalies descending into the upper troposphere over the Indo-Pacific region. Our results also suggest that the timing of this teleconnection is primarily associated with QBO-induced changes in static stability, which exhibit a strong correlation with precipitation and arrive first at the UTLS, followed by changes in wind shear and vorticity.