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Aquest projecte exposa i valora els efectes del turisme de voluntariats. Per tal de contextualitzar el treball d’investigació, en el marc teòric es realitza un estudi de l’àmbit del turisme de voluntariats, així com dels seus participants i les seves motivacions. El treball d’investigació consta d’una anàlisi dels efectes beneficiosos i perjudicials que rep tant la comunitat local com el voluntari en l’àmbit psicosocial, el cultural i l’econòmic. Per veure la procedència dels perjudicis, s’analitzen també les diverses males pràctiques que tenen lloc dins aquesta activitat i, a continuació, s’exploren diferents opcions de millores que es podrien aplicar per fer més lleus els efectes negatius. El treball d’investigació acaba amb el balanç dels efectes anomenats anteriorment i amb una reflexió sobre la procedència i motivació del turisme de voluntariats en si. Finalment, es conclou que el turisme de voluntariats aporta nombrosos efectes perjudicials, sovint irreversibles, mentre que els efectes positius poden obtenir-se d’altres pràctiques. A més a més, aquesta tipologia de turisme mai podria arribar a solucionar el problema principal: el repartiment desigual de la riquesa This project shows and evaluates the effects of volunteer tourism. In order to contextualize the research work, in the theoretical part you can find some research on the volunteer tourism field, as well as an investigation of its participants and their motivations. The research work consists of an analysis of the beneficial and harmful effects that the local community and the volunteer receive regarding the psychosocial, cultural and economic fields. To discover where these harmful effects come from, there is also an analysis of the bad practices performed in this activity. Following that, there are some possible improvements to make these effects less damaging. The research work ends with a reflection of the effects evaluated previously and the precedence and motivations of volunteer tourism. Finally, the project is concluded by stating that volunteer tourism produces many harmful effects that are sometimes irreversible. Moreover, the beneficial consequences can be achieved from other activities. Additionally, volunteer tourism could never solve the main problem: the unequal distribution of wealth

The main pathways for the repair of DNA double strand breaks (DSBs) are non-homologous end-joining (NHEJ) and homologous recombination directed repair (HDR). These operate mutually exclusive and are activated by 53BP1 and BRCA1, respectively. As HDR can only succeed in the presence of an intact copy of replicated DNA, cells employ several mechanisms to inactivate HDR in the G1 phase of cell cycle. As cells enter S-phase, these inhibitory mechanisms are released and HDR becomes active. However, during DNA replication, NHEJ and HDR pathways are both functional and non-replicated and replicated DNA regions co-exist, with the risk of aberrant HDR activity at DSBs in non-replicated DNA. It has become clear that DNA repair pathway choice depends on inhibition of DNA end-resection by 53BP1 and its downstream factors RIF1 and MAD2L2. However, it is unknown how MAD2L2 accumulates at DSBs to participate in DNA repair pathway control and how the NHEJ and HDR repair pathways are appropriately activated at DSBs with respect to the replication status of the DNA, such that NHEJ acts at DSBs in pre-replicative DNA and HDR acts on DSBs in post-replicative DNA. Here we show that MAD2L2 is recruited to DSBs in H4K20 dimethylated chromatin by forming a protein complex with 53BP1 and RIF1 and that MAD2L2, similar to 53BP1 and RIF1, suppresses DSB accumulation of BRCA1. Furthermore, we show that the replication status of the DNA locally ensures the engagement of the correct DNA repair pathway, through epigenetics. In non-replicated DNA, saturating levels of the 53BP1 binding site, di-methylated lysine 20 of histone 4 (H4K20me2), lead to robust 53BP1-RIF1-MAD2L2 recruitment at DSBs, with consequent exclusion of BRCA1. Conversely, replication-associated 2-fold dilution of H4K20me2 promotes the release of the 53BP1-RIF1-MAD2L2 complex and favours the access of BRCA1. Thus, the differential H4K20 methylation status between pre-replicative and post-replicative DNA represents an intrinsic mechanism that locally ensures appropriate recruitment of the 53BP1-RIF1-MAD2L2 complex at DNA DSBs, to engage the correct DNA repair pathway.

«D’or i d’argent. Diàleg entre els brodats i els teixits del Museu Episcopal de Vic i del Musée des Tissus de Lyon» és una exposició coorganitzada entre aquests dos museus, de Vic i de Lió, amb la voluntat d’aplegar esforços per al millor coneixement, estudi i difusió del brodat i del teixit antics. Amb aquest nou projecte, el Museu Episcopal de Vic continua amb la seva línia de col·laboració amb institucions internacionals. En els darrers anys el MEV ha fet exposicions amb el Musée National du Moyen Âge - Thermes de Cluny i amb el Musée des Monuments Français, ambdós de París; ha col·laborat amb el Musée des Augustins de Tolosa de Llenguadoc, amb el MNAC, i ara ha repetit l’experiència, molt satisfactòriament, amb el Musée des Tissus de Lyon., «D’or i d’argent. Diàleg entre els brodats i els teixits del Museu Episcopal de Vic i del Musée des Tissus de Lyon» is an exhibition co-organized by these two museums at Vic and Lyon that aims to join efforts for a better knowledge, study and diffusion of ancient embroideries and textiles. With this new project, tne Episcopal Museum of Vic continues with a line of cooperation with international institutions. In the last years the MEV has collaborated in exhibitions with the Musée national du Moyen Âge -Thermes de Cluny and the Musée des Monuments Français, both in Paris; has also collaborated with the musée des Augustins at Toulouse, with the MNAC at Barcelona, and now repeats the experience, with great satisfaction, with the Musée des Tissus de Lyon.

El 1961 va néixer la revista infantil i juvenil Cavall Fort, destinada a estimular el coneixement i la lectura entre el públic més jove. L’any 2001 el Patronat de la revista confià al MEV el dipòsit permanent del seu fons gràfic, integrat per 4.700 dibuixos originals obra d’artistes amb reconeixement nacional i internacional, entre els quals Joan Miró o Antoni Tàpies. El Museu Episcopal de Vic ha culminat recentment el procés de documentació, catalogació i conservació preventiva d’aquest fons, que resta des d’ara a disposició dels estudiosos i a punt per a la comunicació pública., In 1961 was born Cavall Fort, a magazine for children and young people, with the aim to foster knowledge and reading amongst the youngest public. In 2001 the Board of the publication entrusted Museu Episcopal de Vic with the deposit of its graphical batches, made up of 4.700 original drawings from artists with national and international acknowledgement, such as Joan Miró or Antoni Tàpies. Museu Episcopal de Vic has recently culminated the process of documentation, catalogation and preventive conservation of this batch, which is now available for scholars and ready for public communication.

24 páginas, 9 figuras, Fasciolosis caused by the trematode Fasciola hepatica is a zoonotic neglected disease affecting animals and humans worldwide. Infection occurs upon ingestion of aquatic plants or water contaminated with metacercariae. These release the newly excysted juveniles (FhNEJ) in the host duodenum, where they establish contact with the epithelium and cross the intestinal barrier to reach the peritoneum within 2-3 h after infection. Juveniles crawl up the peritoneum towards the liver, and migrate through the hepatic tissue before reaching their definitive location inside the major biliary ducts, where they mature into adult worms. Fasciolosis is treated with triclabendazole, although resistant isolates of the parasite are increasingly being reported. This, together with the limited efficacy of the assayed vaccines against this infection, poses fasciolosis as a veterinary and human health problem of growing concern. In this context, the study of early host-parasite interactions is of paramount importance for the definition of new targets for the treatment and prevention of fasciolosis. Here, we develop a new in vitro model that replicates the first interaction between FhNEJ and mouse primary small intestinal epithelial cells (MPSIEC). FhNEJ and MPSIEC were co-incubated for 3 h and protein extracts (tegument and soma of FhNEJ and membrane and cytosol of MPSIEC) were subjected to quantitative SWATH-MS proteomics and compared to respective controls (MPSIEC and FhNEJ left alone for 3h in culture medium) to evaluate protein expression changes in both the parasite and the host. Results show that the interaction between FhNEJ and MPSIEC triggers a rapid protein expression change of FhNEJ in response to the host epithelial barrier, including cathepsins L3 and L4 and several immunoregulatory proteins. Regarding MPSIEC, stimulation with FhNEJ results in alterations in the protein profile related to immunomodulation and cell-cell interactions, together with a drastic reduction in the expression of proteins linked with ribosome function. The molecules identified in this model of early host-parasite interactions could help define new tools against fasciolosis., Financial support of the Spanish Ministry of Science Innovation (Projects AGL2015-67023-C2-2-R and PID2019-108782RB-C22), JIN project (RTI2018-093463-J-100) funded by Ministerio de Ciencia, Innovación y Universidades (MCIU), and the Project“CLU-2019-05 – IRNASA/CSIC Unit of Excellence”, funded by the Junta de Castilla y León and cofinanced by the European Union (ERDF “Europe drives our growth”).

22 páginas, 8 figuras, Fasciola hepatica is a trematode parasite that infects animals and humans causing fasciolosis, a worldwide-distributed disease responsible for important economic losses and health problems. This disease is of growing public health concern since parasite isolates resistant to the current treatment (triclabendazole) have increasingly been described. F. hepatica infects its vertebrate host after ingestion of the encysted parasite (metacercariae), which are found in the water or attached to plants. Upon ingestion, newly excysted juveniles of F. hepatica (FhNEJ) emerge in the intestinal lumen and cross the intestinal barrier, reach the peritoneum and migrate to the biliary ducts, where adult worms fully develop. Despite the efforts made to develop new therapeutic and preventive tools, to date, protection against F. hepatica obtained in different animal models is far from optimal. Early events of host-FhNEJ interactions are of paramount importance for the infection progress in fasciolosis, especially those occurring at the host-parasite interface. Nevertheless, studies of FhNEJ responses to the changing host environment encountered during migration across host tissues are still scarce. Here, we set-up an ex vivo model coupled with quantitative SWATH-MS proteomics to study early host-parasite interaction events in fasciolosis. After comparing tegument and somatic fractions from control parasites and FhNEJ that managed to cross a mouse intestinal section ex vivo, a set of parasite proteins whose expression was statistically different were found. These included upregulation of cathepsins L3 and L4, proteolytic inhibitor Fh serpin 2, and a number of molecules linked with nutrient uptake and metabolism, including histone H4, H2A and H2B, low density lipoprotein receptor, tetraspanin, fatty acid binding protein a and glutathione-S-transferase. Downregulated proteins in FhNEJ after gut passage were more numerous than the upregulated ones, and included the heath shock proteins HSP90 and alpha crystallin, amongst others. This study brings new insights into early host-parasite interactions in fasciolosis and sheds light on the proteomic changes in FhNEJ triggered upon excystment and intestinal wall crossing, which could serve to define new targets for the prevention and treatment of this widespread parasitic disease., The Spanish Ministerio de Ciencia e Innovación (Projects PID2019-108782RB-C22 and PID2019-108782RB-C21), Spanish Ministerio de Economía, Industria y Competitividad (Projects AGL2015-67023-C2-2-R and AGL2015-67023-C2-1-R), and the Project “CLU-2019-05 – IRNASA/CSIC Unit of Excellence”, funded by the Consejería de Educación, Junta de Castilla y León and co-financed by the European Union (ERDF “Europe drives our growth”). the JIN project ‘ULYSSES’ (RTI2018-093463-J-100) funded by the Spanish Ministerio de Ciencia, Innovación y Universidades.

19 páginas, 6 figuras, 1 tabla, Fasciola hepatica is the main causative agent of fasciolosis, a zoonotic parasitic disease of growing public health concern. F. hepatica metacercariae are ingested by the host and excyst in the intestine, thereby releasing the newly excysted juveniles (FhNEJ), which traverse the gut wall and migrate towards the biliary ducts. Since blocking F. hepatica development is challenging after crossing of the intestinal wall, targeting this first step of migration might result in increased therapeutic success. The intestinal extracellular matrix (ECM) is constituted by a network of structural proteins, including laminin (LM) and fibronectin (FN), that provide mechanical support while acting as physical barrier against intestinal pathogens. Here, we employed ELISA and immunofluorescent assays to test for the presence of LM- and FN-binding proteins on a tegument-enriched antigenic fraction of FhNEJ, and further determined their identity by two-dimensional electrophoresis coupled to mass spectrometry. Additionally, we performed enzymatic assays that revealed for the first time the capability of the juvenile-specific cathepsin L3 to degrade LM, and that LM degradation by FhNEJ proteins is further potentiated in the presence of host plasminogen. Finally, a proteomic analysis showed that the interaction with LM triggers protein changes in FhNEJ that may be relevant for parasite growth and adaptation inside the mammalian host. Altogether, our study provides valuable insights into the molecular interplay between FhNEJ and the intestinal ECM, which may lead to the identification of targetable candidates for the development of more effective control strategies against fasciolosis., This work was supported by the JIN project ‘ULYSSES’ (RTI2018-093463-J-100) funded by the Ministerio de Ciencia, Innovación y Universidades (MCIU), Agencia Estatal de Investigación (AEI) and Fondo Europeo de Desarrollo Regional (FEDER, UE). We also acknowledge the financial support of the project “CLU-2019-05–IRNASA-CSIC Unit of Excellence”, funded by the Junta de Castilla y León and co-funded by the European Union (FEDER “Europe drives our growth”), and the Programme for strengthening research structures “Stairway to excellence” internationalisation aid, co-funded by the European Regional Development Fund. M.S.L. acknowledges the financial support of the Spanish Ministry of Science and Innovation (Project PID2019-108782RB-C22). J.S. and D.B.R. acknowledge the support of the Junta de Castilla y León for their Predoctoral contracts. M.L.G. acknowledges the support of the Spanish Ministry of Science and Innovation for her FPU Predoctoral contract. J.G.M. is supported by the ‘Ramón y Cajal’ program (RYC2020-030575-I) of the Ministerio de Ciencia e Innovación. The proteomics laboratory where LC-MS/MS analysis was performed is a member of Proteored, PRB3 and is supported by grant PT17/0019, of the PE I + D+i 2013–2016, funded by the Instituto de Salud Carlos III (ISCIII) and the European Regional Development Fund (ERDF). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

22 páginas, 8 figuras, The trematode Fasciola hepatica is the most widespread causative agent of fasciolosis, a parasitic disease that mainly affects humans and ruminants worldwide. During F. hepatica infection, newly excysted juveniles (FhNEJ) emerge in the duodenum of the mammalian host and migrate towards their definitive location, the intra-hepatic biliary ducts. Understanding how F. hepatica traverses the intestinal wall and migrates towards the liver is pivotal for the development of more successful strategies against fasciolosis. The central enzyme of the mammalian fibrinolytic system is plasmin, a serine protease whose functions are exploited by a number of parasite species owing to its broad spectrum of substrates, including components of tissue extracellular matrices. The aim of the present work is to understand whether FhNEJ co-opt the functions of their host fibrinolytic system as a mechanism to facilitate trans-intestinal migration., This work was supported by the JIN project ‘ULYSSES’ (RTI2018-093463-J-100 to J.G.M.) funded by the Ministerio de Ciencia, Innovación y Universidades (MCIU), Agencia Estatal de Investigación (AEI) and Fondo Europeo de Desarrollo Regional (FEDER, UE). IRNASA-CSIC group acknowledges funding received from Project “CLU-2019-05 - IRNASA-CSIC Unit of Excellence”, funded by the Junta de Castilla y León cofunded by the European Union (FEDER “Europe drives our growth”) and funding from the Programme for strengthening research structures "Stairway to excellence" internationalisation aid, cofunded by the Junta de Castilla y León and the European Regional Development Fund. M.S.L.acknowledges the financial support of the Spanish Ministry of Science and Innovation (Project PID2019-108782RB-C22). J.S. and D.B.R. acknowledge the support of the Junta de Castilla y León for their Predoctoral contracts. J.G.M. is supported by the ‘Ramón y Cajal’ program (RYC2020-030575-I) of the Ministerio de Ciencia e Innovación. Valencia centre collaboration funded by: CIBER-Consorcio Centro de Investigación Biomédica en Red- (CB21/13/00056), Instituto de Salud Carlos III, Ministry of Science and Innovation and European Union – NextGenerationEU; the Red de Investigación de Centros de Enfermedades Tropicales - RICET (RD16/0027/0023) of the PN de I+D+I, ISCIII-Subdirección General de Redes y Centros de Investigación Cooperativa RETICS, Ministry of Health and Consumption, Madrid; the PROMETEO Program, Programa de Ayudas para Grupos de Investigación de Excelencia (2021/004), Generalitat Valenciana, Valencia, Spain. The proteomics laboratory where LC-MS/MS analysis was performed is a member of Proteored, PRB3 and is supported by grant PT17/0019, of the PE I+D+i 2013-2016, funded by the Instituto de Salud Carlos III (ISCIII) and the European Regional Development Fund (ERDF). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript