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1. Evaluating the impact of alternative phenotype definitions on incidence rates across a global data network.

Author

Makadia, Rupa, Shoaibi, Azza, Rao, Gowtham, Ostropolets, Anna, Rijnbeek, Peter, Voss, Erica, Duarte-Salles, Talita, Ramírez-Anguita, Juan, Mayer, Miguel, Maljković, Filip, Denaxas, Spiros, Nyberg, Fredrik, Papez, Vaclav, Sena, Anthony, Alshammari, Thamir, Lai, Lana, Haynes, Kevin, Hripcsak, George, Ryan, Patrick, and Suchard, Marc

Subjects
algorithms, electronic health record, incidence study, phenotype
Abstract

OBJECTIVE: Developing accurate phenotype definitions is critical in obtaining reliable and reproducible background rates in safety research. This study aims to illustrate the differences in background incidence rates by comparing definitions for a given outcome. MATERIALS AND METHODS: We used 16 data sources to systematically generate and evaluate outcomes for 13 adverse events and their overall background rates. We examined the effect of different modifications (inpatient setting, standardization of code set, and code set changes) to the computable phenotype on background incidence rates. RESULTS: Rate ratios (RRs) of the incidence rates from each computable phenotype definition varied across outcomes, with inpatient restriction showing the highest variation from 1 to 11.93. Standardization of code set RRs ranges from 1 to 1.64, and code set changes range from 1 to 2.52. DISCUSSION: The modification that has the highest impact is requiring inpatient place of service, leading to at least a 2-fold higher incidence rate in the base definition. Standardization showed almost no change when using source code variations. The strength of the effect in the inpatient restriction is highly dependent on the outcome. Changing definitions from broad to narrow showed the most variability by age/gender/database across phenotypes and less than a 2-fold increase in rate compared to the base definition. CONCLUSION: Characterization of outcomes across a network of databases yields insights into sensitivity and specificity trade-offs when definitions are altered. Outcomes should be thoroughly evaluated prior to use for background rates for their plausibility for use across a global network.

Published
2023

2. Developing a clinical decision support system software prototype that assists in the management of patients with self-harm in the emergency department: protocol of the PERMANENS project

Author

Mortier, Philippe, Amigo, Franco, Bhargav, Madhav, Conde, Susana, Ferrer, Montse, Flygare, Oskar, Kizilaslan, Busenur, Latorre Moreno, Laura, Leis, Angela, Mayer, Miguel Angel, Pérez-Sola, Víctor, Portillo-Van Diest, Ana, Ramírez-Anguita, Juan Manuel, Sanz, Ferran, Vilagut, Gemma, Alonso, Jordi, Mehlum, Lars, Arensman, Ella, Bjureberg, Johan, Pastor, Manuel, and Qin, Ping

Published
2024
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3. Akkermansia muciniphila-induced trained immune phenotype increases bacterial intracellular survival and attenuates inflammation

Author

Peña-Cearra, Ainize, Palacios, Ainhoa, Pellon, Aize, Castelo, Janire, Pasco, Samuel Tanner, Seoane, Iratxe, Barriales, Diego, Martin, Jose Ezequiel, Pascual-Itoiz, Miguel Ángel, Gonzalez-Lopez, Monika, Martín-Ruiz, Itziar, Macías-Cámara, Nuria, Gutiez, Naiara, Araujo-Aris, Sarai, Aransay, Ana Mª, Rodríguez, Héctor, Anguita, Juan, and Abecia, Leticia

Published
2024
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5. Contextualising adverse events of special interest to characterise the baseline incidence rates in 24 million patients with COVID-19 across 26 databases: a multinational retrospective cohort study

Author

Voss, Erica A, Shoaibi, Azza, Lai, Lana Yin Hui, Blacketer, Clair, Alshammari, Thamir, Makadia, Rupa, Haynes, Kevin, Sena, Anthony G, Rao, Gowtham, van Sandijk, Sebastiaan, Fraboulet, Clement, Boyer, Laurent, Le Carrour, Tanguy, Horban, Scott, Morales, Daniel R, Roldán, Jordi Martínez, Ramírez-Anguita, Juan Manuel, Mayer, Miguel A, de Wilde, Marcel, John, Luis H, Duarte-Salles, Talita, Roel, Elena, Pistillo, Andrea, Kolde, Raivo, Maljković, Filip, Denaxas, Spiros, Papez, Vaclav, Kahn, Michael G, Natarajan, Karthik, Reich, Christian, Secora, Alex, Minty, Evan P, Shah, Nigam H, Posada, Jose D, Morales, Maria Teresa Garcia, Bosca, Diego, Juanino, Honorio Cadenas, Holgado, Antonio Diaz, Jiménez, Miguel Pedrera, Balazote, Pablo Serrano, Barrio, Noelia García, Şen, Selçuk, Üresin, Ali Yağız, Erdogan, Baris, Belmans, Luc, Byttebier, Geert, Malbrain, Manu LNG, Dedman, Daniel J, Cuccu, Zara, Vashisht, Rohit, Butte, Atul J, Patel, Ayan, Dahm, Lisa, Han, Cora, Bu, Fan, Arshad, Faaizah, Ostropolets, Anna, Nyberg, Fredrik, Hripcsak, George, Suchard, Marc A, Prieto-Alhambra, Dani, Rijnbeek, Peter R, Schuemie, Martijn J, and Ryan, Patrick B

Subjects
Lung, Brain Disorders, Patient Safety, Hematology, Infectious Diseases, 2.4 Surveillance and distribution, Aetiology, Good Health and Well Being, COVID-19, Observational research, OMOP CDM, Adverse events of special interest
Abstract

BackgroundAdverse events of special interest (AESIs) were pre-specified to be monitored for the COVID-19 vaccines. Some AESIs are not only associated with the vaccines, but with COVID-19. Our aim was to characterise the incidence rates of AESIs following SARS-CoV-2 infection in patients and compare these to historical rates in the general population.MethodsA multi-national cohort study with data from primary care, electronic health records, and insurance claims mapped to a common data model. This study's evidence was collected between Jan 1, 2017 and the conclusion of each database (which ranged from Jul 2020 to May 2022). The 16 pre-specified prevalent AESIs were: acute myocardial infarction, anaphylaxis, appendicitis, Bell's palsy, deep vein thrombosis, disseminated intravascular coagulation, encephalomyelitis, Guillain- Barré syndrome, haemorrhagic stroke, non-haemorrhagic stroke, immune thrombocytopenia, myocarditis/pericarditis, narcolepsy, pulmonary embolism, transverse myelitis, and thrombosis with thrombocytopenia. Age-sex standardised incidence rate ratios (SIR) were estimated to compare post-COVID-19 to pre-pandemic rates in each of the databases.FindingsSubstantial heterogeneity by age was seen for AESI rates, with some clearly increasing with age but others following the opposite trend. Similarly, differences were also observed across databases for same health outcome and age-sex strata. All studied AESIs appeared consistently more common in the post-COVID-19 compared to the historical cohorts, with related meta-analytic SIRs ranging from 1.32 (1.05 to 1.66) for narcolepsy to 11.70 (10.10 to 13.70) for pulmonary embolism.InterpretationOur findings suggest all AESIs are more common after COVID-19 than in the general population. Thromboembolic events were particularly common, and over 10-fold more so. More research is needed to contextualise post-COVID-19 complications in the longer term.FundingNone.

Published
2023

6. Supporting Pharmacovigilance Signal Validation and Prioritization with Analyses of Routinely Collected Health Data: Lessons Learned from an EHDEN Network Study

Author

Gauffin, Oskar, Brand, Judith S., Vidlin, Sara Hedfors, Sartori, Daniele, Asikainen, Suvi, Català, Martí, Chalabi, Etir, Dedman, Daniel, Danilovic, Ana, Duarte-Salles, Talita, García Morales, Maria Teresa, Hiltunen, Saara, Jödicke, Annika M., Lazarevic, Milan, Mayer, Miguel A., Miladinovic, Jelena, Mitchell, Joseph, Pistillo, Andrea, Ramírez-Anguita, Juan Manuel, Reyes, Carlen, Rudolph, Annette, Sandberg, Lovisa, Savage, Ruth, Schuemie, Martijn, Spasic, Dimitrije, Trinh, Nhung T. H., Veljkovic, Nevena, Vujovic, Ankica, de Wilde, Marcel, Zekarias, Alem, Rijnbeek, Peter, Ryan, Patrick, Prieto-Alhambra, Daniel, and Norén, G. Niklas

Published
2023
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9. Mitochondrial dysfunction promotes microbial composition that negatively impacts on ulcerative colitis development and progression

Author

Peña-Cearra, Ainize, Song, Deguang, Castelo, Janire, Palacios, Ainhoa, Lavín, Jose Luis, Azkargorta, Mikel, Elortza, Felix, Fuertes, Miguel, Pascual-Itoiz, Miguel Angel, Barriales, Diego, Martín-Ruiz, Itziar, Fullaondo, Asier, Aransay, Ana M., Rodríguez, Hector, Palm, Noah W., Anguita, Juan, and Abecia, Leticia

Published
2023
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11. Anti-miR-518d-5p overcomes liver tumor cell death resistance through mitochondrial activity.

Author

Fernández-Tussy, Pablo, Rodríguez-Agudo, Rubén, Fernández-Ramos, David, Barbier-Torres, Lucía, Zubiete-Franco, Imanol, Davalillo, Sergio López de, Herraez, Elisa, Goikoetxea-Usandizaga, Naroa, Lachiondo-Ortega, Sofia, Simón, Jorge, Lopitz-Otsoa, Fernando, Juan, Virginia Gutiérrez-de, McCain, Misti V, Perugorria, Maria J, Mabe, Jon, Navasa, Nicolás, Rodrigues, Cecilia MP, Fabregat, Isabel, Boix, Loreto, Sapena, Victor, Anguita, Juan, Lu, Shelly C, Mato, José M, Banales, Jesus M, Villa, Erica, Reeves, Helen L, Bruix, Jordi, Reig, Maria, Marin, Jose JG, Delgado, Teresa C, and Martínez-Chantar, María L

Subjects
Biochemistry and Cell Biology, Oncology and Carcinogenesis
Abstract

Dysregulation of miRNAs is a hallmark of cancer, modulating oncogenes, tumor suppressors, and drug responsiveness. The multi-kinase inhibitor sorafenib is one of the first-line drugs for advanced hepatocellular carcinoma (HCC), although the outcome for treated patients is heterogeneous. The identification of predictive biomarkers and targets of sorafenib efficacy are sorely needed. Thus, selected top upregulated miRNAs from the C19MC cluster were analyzed in different hepatoma cell lines compared to immortalized liver human cells, THLE-2 as control. MiR-518d-5p showed the most consistent upregulation among them. Thus, miR-518d-5p was measured in liver tumor/non-tumor samples of two distinct cohorts of HCC patients (n = 16 and n = 20, respectively). Circulating miR-518d-5p was measured in an independent cohort of HCC patients receiving sorafenib treatment (n = 100), where miR-518d-5p was analyzed in relation to treatment duration and patient's overall survival. In vitro and in vivo studies were performed in human hepatoma BCLC3 and Huh7 cells to analyze the effect of miR-518d-5p inhibition/overexpression during the response to sorafenib. Compared with healthy individuals, miR-518d-5p levels were higher in hepatic and serum samples from HCC patients (n = 16) and in an additional cohort of tumor/non-tumor paired samples (n = 20). MiR-518d-5p, through the inhibition of c-Jun and its mitochondrial target PUMA, desensitized human hepatoma cells and mouse xenograft to sorafenib-induced apoptosis. Finally, serum miR-518d-5p was assessed in 100 patients with HCC of different etiologies and BCLC-stage treated with sorafenib. In BCLC-C patients, higher serum miR-518d-5p at diagnosis was associated with shorter sorafenib treatment duration and survival. Hence, hepatic miR-518d-5p modulates sorafenib resistance in HCC through inhibition of c-Jun/PUMA-induced apoptosis. Circulating miR-518d-5p emerges as a potential lack of response biomarker to sorafenib in BCLC-C HCC patients.

Published
2021

13. eTRANSAFE: data science to empower translational safety assessment

Author

Sanz, Ferran, Pognan, François, Steger-Hartmann, Thomas, Díaz, Carlos, Asakura, Shoji, Amberg, Alexander, Bécourt-Lhote, Nathalie, Blomberg, Niklas, Bosc, Nicolas, Briggs, Katharine, Bringezu, Frank, Brulle-Wohlhueter, Claire, Brunak, Søren, Bueters, Ruud, Callegaro, Giulia, Capella-Gutierrez, Salvador, Centeno, Emilio, Corvi, Javier, Cronin, Mark T. D., Drew, Philip, Duchateau-Nguyen, Guillemette, Ecker, Gerhard F., Escher, Sylvia, Felix, Eloy, Ferreiro, Miguel, Frericks, Markus, Furlong, Laura I., Geiger, Robert, George, Catherine, Grandits, Melanie, Ivanov-Draganov, Dragomir, Kilgour-Christie, Jean, Kiziloren, Tevfik, Kors, Jan A., Koyama, Naoki, Kreuchwig, Annika, Leach, Andrew R., Mayer, Miguel-Angel, Monecke, Peter, Muster, Wolfgang, Nakazawa, Chihiro Miyamoto, Nicholson, Gavin, Parry, Rowan, Pastor, Manuel, Piñero, Janet, Oberhauser, Nils, Ramírez-Anguita, Juan Manuel, Rodrigo, Adrián, Smajic, Aljosa, Schaefer, Markus, Schieferdecker, Sebastian, Soininen, Inari, Terricabras, Emma, Trairatphisan, Panuwat, Turner, Sean C., Valencia, Alfonso, van de Water, Bob, van der Lei, Johan L., van Mulligen, Erik M., Vock, Esther, and Wilkinson, David

Published
2023
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15. miR-873-5p targets mitochondrial GNMT-Complex II interface contributing to non-alcoholic fatty liver disease

Author

Fernández-Tussy, Pablo, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Simón, Jorge, Barbier-Torres, Lucía, Gomez-Santos, Beatriz, Nuñez-Garcia, Maitane, Azkargorta, Mikel, Juan, Virginia Gutiérrez-de, Serrano-Macia, Marina, Rodríguez-Agudo, Rubén, Iruzubieta, Paula, Anguita, Juan, Castro, Rui E, Champagne, Devin, Rincón, Mercedes, Elortza, Felix, Arslanow, Anita, Krawczyk, Marcin, Lammert, Frank, Kirchmeyer, Mélanie, Behrmann, Iris, Crespo, Javier, Lu, Shelly C, Mato, José M, Varela-Rey, Marta, Aspichueta, Patricia, Delgado, Teresa C, and Martínez-Chantar, María L

Subjects
Liver Disease, Biotechnology, Hepatitis, Digestive Diseases, Complementary and Integrative Health, Chronic Liver Disease and Cirrhosis, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Metabolic and endocrine, Good Health and Well Being, Adult, Animals, Antagomirs, Disease Models, Animal, Electron Transport Complex II, Female, Glycine N-Methyltransferase, Hepatocytes, Humans, Lipid Peroxidation, Liver, Male, Mice, Mice, Inbred C57BL, MicroRNAs, Middle Aged, Mitochondria, Non-alcoholic Fatty Liver Disease, Up-Regulation, NASH, GNMT, beta-oxidation, Metabolism, microRNA, β-oxidation, Biochemistry and Cell Biology, Physiology
Abstract

OBJECTIVE:Non-alcoholic fatty liver disease (NAFLD) is a complex pathology in which several dysfunctions, including alterations in metabolic pathways, mitochondrial functionality and unbalanced lipid import/export, lead to lipid accumulation and progression to inflammation and fibrosis. The enzyme glycine N-methyltransferase (GNMT), the most important enzyme implicated in S-adenosylmethionine catabolism in the liver, is downregulated during NAFLD progression. We have studied the mechanism involved in GNMT downregulation by its repressor microRNA miR-873-5p and the metabolic pathways affected in NAFLD as well as the benefit of recovery GNMT expression. METHODS:miR-873-5p and GNMT expression were evaluated in liver biopsies of NAFLD/NASH patients. Different in vitro and in vivo NAFLD murine models were used to assess miR-873-5p/GNMT involvement in fatty liver progression through targeting of the miR-873-5p as NAFLD therapy. RESULTS:We describe a new function of GNMT as an essential regulator of Complex II activity in the electron transport chain in the mitochondria. In NAFLD, GNMT expression is controlled by miR-873-5p in the hepatocytes, leading to disruptions in mitochondrial functionality in a preclinical murine non-alcoholic steatohepatitis (NASH) model. Upregulation of miR-873-5p is shown in the liver of NAFLD/NASH patients, correlating with hepatic GNMT depletion. Importantly, NASH therapies based on anti-miR-873-5p resolve lipid accumulation, inflammation and fibrosis by enhancing fatty acid β-oxidation in the mitochondria. Therefore, miR-873-5p inhibitor emerges as a potential tool for NASH treatment. CONCLUSION:GNMT participates in the regulation of metabolic pathways and mitochondrial functionality through the regulation of Complex II activity in the electron transport chain. In NAFLD, GNMT is repressed by miR-873-5p and its targeting arises as a valuable therapeutic option for treatment.

Published
2019

16. Contextualising adverse events of special interest to characterise the baseline incidence rates in 24 million patients with COVID-19 across 26 databases: a multinational retrospective cohort study

Author

Voss, Erica A., Shoaibi, Azza, Yin Hui Lai, Lana, Blacketer, Clair, Alshammari, Thamir, Makadia, Rupa, Haynes, Kevin, Sena, Anthony G., Rao, Gowtham, van Sandijk, Sebastiaan, Fraboulet, Clement, Boyer, Laurent, Le Carrour, Tanguy, Horban, Scott, Morales, Daniel R., Martínez Roldán, Jordi, Ramírez-Anguita, Juan Manuel, Mayer, Miguel A., de Wilde, Marcel, John, Luis H., Duarte-Salles, Talita, Roel, Elena, Pistillo, Andrea, Kolde, Raivo, Maljković, Filip, Denaxas, Spiros, Papez, Vaclav, Kahn, Michael G., Natarajan, Karthik, Reich, Christian, Secora, Alex, Minty, Evan P., Shah, Nigam H., Posada, Jose D., Garcia Morales, Maria Teresa, Bosca, Diego, Cadenas Juanino, Honorio, Diaz Holgado, Antonio, Pedrera Jiménez, Miguel, Serrano Balazote, Pablo, García Barrio, Noelia, Şen, Selçuk, Üresin, Ali Yağız, Erdogan, Baris, Belmans, Luc, Byttebier, Geert, Malbrain, Manu L.N.G., Dedman, Daniel J., Cuccu, Zara, Vashisht, Rohit, Butte, Atul J., Patel, Ayan, Dahm, Lisa, Han, Cora, Bu, Fan, Arshad, Faaizah, Ostropolets, Anna, Nyberg, Fredrik, Hripcsak, George, Suchard, Marc A., Prieto-Alhambra, Dani, Rijnbeek, Peter R., Schuemie, Martijn J., and Ryan, Patrick B.

Published
2023
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17. La fauna de mamíferos del Neolítico Andaluz

Author

Cantal, José Antonio Riquelme, primary, Rodríguez, Irene Riquelme, additional, Anguita, Juan Manuel Garrido, additional, Expósito, Adrián Ruiz, additional, Nieto, Eduardo Ruiz, additional, Ruíz, Alejandro Beltrán, additional, and Sánchez, Laura Aparicio, additional

Published
2023
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19. Conexiones Culturales y Patrimonio Prehistórico

Author

Garrido Anguita, Juan Manuel

Subjects
Social Science / Archaeology
Abstract

José C. Martín de la Cruz is a pioneer scholar whose contributions both to Prehistory and the diffusion of cultural heritage have been acknowledged at an international level. The present volume pays homage to his professional career, by inviting more than 40 international scholars who tackle the study of Prehistory and the dissemination of heritage from several thematic and temporal perspectives. It is thus a multidisciplinary volume in which scholars from different fields investigate Prehistory from its origins to the period immediately before Greek and Phoenician colonization; at the same time, they explore the different ways in which Prehistoric heritage is transmitted. The volume is composed of four different but related parts, organized chronologically and starting with the most recent Prehistory. The first part deals with the intercultural connections which took place during the Bronze Age in the Mediterranean area. The second part goes back in time and investigates the first settlements and early food producing societies. The third examines our remote past and its natural environment. Finally, the closing part includes a set of multidisciplinary chapters which study prehistory from several different scientific fields. All in all, this volume becomes a scientific meeting point where senior professors and junior scholars get together to offer their scientific findings, at the same time as they pay homage to Professor Martín de la Cruz.

Published
2023

20. Calculating daily dose in the Observational Medical Outcomes Partnership Common Data Model

Author

Burkard, Theresa, primary, López‐Güell, Kim, additional, Gorbachev, Artem, additional, Bellas, Lucía, additional, Jödicke, Annika M., additional, Burn, Edward, additional, de Ridder, Maria, additional, Mosseveld, Mees, additional, Gratton, Jasmine, additional, Seager, Sarah, additional, Vojinovic, Dina, additional, Mayer, Miguel Angel, additional, Ramírez‐Anguita, Juan Manuel, additional, Machín, Angela Leis, additional, Oja, Marek, additional, Kolde, Raivo, additional, Bonadt, Klaus, additional, Prieto‐Alhambra, Daniel, additional, Reich, Chistian, additional, and Català, Martí, additional

Published
2024
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21. Incident Use of Hydroxychloroquine for the Treatment of Rheumatoid Arthritis and Systemic Lupus Erythematosus During the COVID‐19 Pandemic

Author

Mercadé‐Besora, Núria, primary, Guo, Yuchen, additional, Du, Mike, additional, Li, Xintong, additional, Ramírez‐Anguita, Juan Manuel, additional, Moreno, Alberto, additional, Valente, António, additional, Villalobos, Felipe, additional, Cheng, Iek Leng, additional, Carrasco‐Ribelles, Lucía A., additional, van Swieten, Maaike M. H., additional, Merkelbach, Manon, additional, Magoya, Mary, additional, Lasalvia, Paolo, additional, Pericàs‐Pulido, Pau, additional, Berg, Paul, additional, Bosco‐Lévy, Pauline, additional, Lillini, Roberto, additional, Ribeiro, Rogerio, additional, Bagga, Trinamjot Kaur, additional, Ramella, Vittoria, additional, Khalid, Sara, additional, Mayer, Miguel Angel, additional, Leis, Angela, additional, Jödicke, Annika M., additional, Burn, Edward, additional, Prieto‐Alhambra, Daniel, additional, Català, Martí, additional, and Prats‐Uribe, Albert, additional

Published
2024
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22. Phenotype Algorithms for the Identification and Characterization of Vaccine-Induced Thrombotic Thrombocytopenia in Real World Data: A Multinational Network Cohort Study

Author

Shoaibi, Azza, Rao, Gowtham A., Voss, Erica A., Ostropolets, Anna, Mayer, Miguel Angel, Ramírez-Anguita, Juan Manuel, Maljković, Filip, Carević, Biljana, Horban, Scott, Morales, Daniel R., Duarte-Salles, Talita, Fraboulet, Clement, Le Carrour, Tanguy, Denaxas, Spiros, Papez, Vaclav, John, Luis H., Rijneek, Peter R., Minty, Evan, Alshammari, Thamir M., Makadia, Rupa, Blacketer, Clair, DeFalco, Frank, Sena, Anthony G., Suchard, Marc A., Prieto-Alhambra, Daniel, and Ryan, Patrick B.

Published
2022
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24. Restoring cellular magnesium balance through Cyclin M4 protects against acetaminophen-induced liver damage

Author

González-Recio, Irene, Simón, Jorge, Goikoetxea-Usandizaga, Naroa, Serrano-Maciá, Marina, Mercado-Gómez, Maria, Rodríguez-Agudo, Rubén, Lachiondo-Ortega, Sofía, Gil-Pitarch, Clàudia, Fernández-Rodríguez, Carmen, Castellana, Donatello, Latasa, Maria U., Abecia, Leticia, Anguita, Juan, Delgado, Teresa C., Iruzubieta, Paula, Crespo, Javier, Hardy, Serge, Petrov, Petar D., Jover, Ramiro, Avila, Matías A., Martín, César, Schaeper, Ute, Tremblay, Michel L., Dear, James W., Masson, Steven, McCain, Misti Vanette, Reeves, Helen L., Andrade, Raul J., Lucena, M. Isabel, Buccella, Daniela, Martínez-Cruz, Luis Alfonso, and Martínez-Chantar, Maria L

Published
2022
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25. MiR-873-5p acts as an epigenetic regulator in early stages of liver fibrosis and cirrhosis.

Author

Fernández-Ramos, David, Fernández-Tussy, Pablo, Lopitz-Otsoa, Fernando, Gutiérrez-de-Juan, Virginia, Navasa, Nicolás, Barbier-Torres, Lucía, Zubiete-Franco, Imanol, Simón, Jorge, Fernández, Agustín F, Arbelaiz, Ander, Aransay, Ana M, Lavín, José Luis, Beraza, Naiara, Perugorria, María J, Banales, Jesus M, Villa, Erica, Fraga, Mario F, Anguita, Juan, Avila, Matias A, Berasain, Carmen, Iruzibieta, Paula, Crespo, Javier, Lu, Shelly C, Varela-Rey, Marta, Mato, José M, Delgado, Teresa C, and Martínez-Chantar, María L

Subjects
Liver, Animals, Mice, Inbred C57BL, Humans, Mice, Carcinoma, Hepatocellular, Liver Cirrhosis, Fibrosis, MicroRNAs, Cell Proliferation, Male, Glycine N-Methyltransferase, Hepatic Stellate Cells, Inbred C57BL, Carcinoma, Hepatocellular, Biochemistry and Cell Biology, Oncology and Carcinogenesis
Abstract

Glycine N-methyltransferase (GNMT) is the most abundant methyltransferase in the liver and a master regulator of the transmethylation flux. GNMT downregulation leads to loss of liver function progressing to fibrosis, cirrhosis, and hepatocellular carcinoma. Moreover, GNMT deficiency aggravates cholestasis-induced fibrogenesis. To date, little is known about the mechanisms underlying downregulation of GNMT levels in hepatic fibrosis and cirrhosis. On this basis, microRNAs are epigenetic regulatory elements that play important roles in liver pathology. In this work, we aim to study the regulation of GNMT by microRNAs during liver fibrosis and cirrhosis. Luciferase assay on the 3'UTR-Gnmt was used to confirm in silico analysis showing that GNMT is potentially targeted by the microRNA miR-873-5p. Correlation between GNMT and miR-873-5p in human cholestasis and cirrhosis together with miR-873-5p inhibition in vivo in different mouse models of liver cholestasis and fibrosis [bile duct ligation and Mdr2 (Abcb4)-/- mouse] were then assessed. The analysis of liver tissue from cirrhotic and cholestatic patients, as well as from the animal models, showed that miR-873-5p inversely correlated with the expression of GNMT. Importantly, high circulating miR-873-5p was also detected in cholestastic and cirrhotic patients. Preclinical studies with anti-miR-873-5p treatment in bile duct ligation and Mdr2-/- mice recovered GNMT levels in association with ameliorated inflammation and fibrosis mainly by counteracting hepatocyte apoptosis and cholangiocyte proliferation. In conclusion, miR-873-5p emerges as a novel marker for liver fibrosis, cholestasis, and cirrhosis and therapeutic approaches based on anti-miR-873-5p may be effective treatments for liver fibrosis and cholestatic liver disease.

Published
2018

26. The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury.

Author

Barbier-Torres, Lucía, Iruzubieta, Paula, Fernández-Ramos, David, Delgado, Teresa C, Taibo, Daniel, Guitiérrez-de-Juan, Virginia, Varela-Rey, Marta, Azkargorta, Mikel, Navasa, Nicolas, Fernández-Tussy, Pablo, Zubiete-Franco, Imanol, Simon, Jorge, Lopitz-Otsoa, Fernando, Lachiondo-Ortega, Sofia, Crespo, Javier, Masson, Steven, McCain, Misti Vanette, Villa, Erica, Reeves, Helen, Elortza, Felix, Lucena, Maria Isabel, Hernández-Alvarez, Maria Isabel, Zorzano, Antonio, Andrade, Raúl J, Lu, Shelly C, Mato, José M, Anguita, Juan, Rincón, Mercedes, and Martínez-Chantar, María Luz

Subjects
Liver, Mitochondria, Liver, Hepatocytes, Animals, Mice, Inbred C57BL, Humans, Mice, Disease Models, Animal, Acetaminophen, Rotenone, Electron Transport Complex I, Mitochondrial Proteins, Molecular Chaperones, RNA, Small Interfering, Uncoupling Agents, Adolescent, Adult, Middle Aged, Female, Male, HSP40 Heat-Shock Proteins, Gene Knockout Techniques, Young Adult, Primary Cell Culture, Drug Overdose, Chemical and Drug Induced Liver Injury, Mitochondria, Inbred C57BL, Disease Models, Animal, RNA, Small Interfering
Abstract

Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen.

Published
2017

27. Role of Aramchol in steatohepatitis and fibrosis in mice.

Author

Iruarrizaga-Lejarreta, Marta, Varela-Rey, Marta, Fernández-Ramos, David, Martínez-Arranz, Ibon, Delgado, Teresa C, Simon, Jorge, Juan, Virginia Gutiérrez-de, delaCruz-Villar, Laura, Azkargorta, Mikel, Lavin, José L, Mayo, Rebeca, Van Liempd, Sebastiaan M, Aurrekoetxea, Igor, Buqué, Xabier, Cave, Donatella Delle, Peña, Arantza, Rodríguez-Cuesta, Juan, Aransay, Ana M, Elortza, Felix, Falcón-Pérez, Juan M, Aspichueta, Patricia, Hayardeny, Liat, Noureddin, Mazen, Sanyal, Arun J, Alonso, Cristina, Anguita, Juan, Martínez-Chantar, María Luz, Lu, Shelly C, and Mato, José M

Subjects
1-carbon metabolism, Lipid metabolism, Mouse model, S-adenosylmethionine
Abstract

Nonalcoholic steatohepatitis (NASH) is the advanced form of nonalcoholic fatty liver disease (NAFLD) which sets the stage for further liver damage. The mechanism for the progression of NASH involves multiple parallel hits including oxidative stress, mitochondrial dysfunction, inflammation and others. Manipulation of any of these pathways may be an approach to prevent NASH development and progression. Aramchol (arachidyl-amido cholanoic acid) is presently in a phase IIb NASH study. The aim of this study was to investigate Aramchol's mechanism of action and its effect on fibrosis using the methionine- and choline-deficient (MCD) diet model of NASH. We collected liver and serum from mice fed a MCD diet containing 0.1% methionine (0.1MCD) for four weeks, which developed steatohepatitis and fibrosis, as well as mice receiving a control diet; the metabolomes and proteomes were determined. 0.1MCD fed mice were given Aramchol (5mg/kg/day for the last 2 weeks); liver samples were analyzed histologically. Aramchol administration reduced features of steatohepatitis and fibrosis in 0.1MCD fed mice. Aramchol downregulated stearoyl-CoA desaturase 1 (SCD1), a key enzyme involved in triglyceride biosynthesis whose loss enhances fatty acid β-oxidation. Aramchol increased the flux through the transsulfuration pathway, leading to a rise in glutathione (GSH) and GSH/GSSG ratio, the main cellular antioxidant that maintains intracellular redox status. Comparison of serum metabolomic pattern between 0.1MCD fed mice and NAFLD patients showed a substantial overlap. Conclusions:Aramchol treatment improved steatohepatitis and fibrosis by 1) decreasing SCD1, and 2) increasing the flux through the transsulfuration pathway maintaining cellular redox homeostasis. We also demonstrated that the 0.1MCD model resembles the metabolic phenotype observed in about 50% of NAFLD patients, which supports the potential use of Aramchol in NASH treatment.

Published
2017

28. Clusters of post-acute COVID-19 symptoms: a latent class analysis across 9 databases and 7 countries

Author

Prieto-Alhambra, Daniel, primary, Güell, Kim López, additional, Català, Martí, additional, Dedman, Daniel, additional, Duarte-Salles, Talita, additional, Kolde, Raivo, additional, López-Blasco, Raúl, additional, Martínez, Álvaro, additional, Mercier, Gregoire, additional, Abellan, Alicia, additional, Arinze, Johnmary, additional, Burkard, Theresa, additional, Burn, Edward, additional, Cuccu, Zara, additional, Delmestri, Antonella, additional, Delseny, Dominique, additional, Khalid, Sara, additional, Kim, Chungsoo, additional, Kim, Ji-woo, additional, Kostka, Kristin, additional, Loste, Cora, additional, Mayer, Miguel, additional, Meléndez-Cardiel, Jaime, additional, Mercadé-Besora, Nuria, additional, Mosseveld, Mees, additional, Nishimura, Akihiko, additional, Nordeng, Hedvig ME, additional, Oyinlola, Jessie O, additional, Paredes, Roger, additional, Pérez-Crespo, Laura, additional, Pineda-Moncusí, Marta, additional, Ramírez-Anguita, Juan Manuel, additional, Trinh, Nhung TH, additional, Uusküla, Anneli, additional, Valdivieso, Bernardo, additional, Xie, Junqing, additional, Mateu, Lourdes, additional, and Jödicke, Annika, additional

Published
2024
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29. Boosting mitochondria activity by silencing MCJ overcomes cholestasis-induced liver injury

Author

Iruzubieta, Paula, Goikoetxea-Usandizaga, Naroa, Barbier-Torres, Lucía, Serrano-Maciá, Marina, Fernández-Ramos, David, Fernández-Tussy, Pablo, Gutiérrez-de-Juan, Virginia, Lachiondo-Ortega, Sofia, Simon, Jorge, Bravo, Miren, Lopitz-Otsoa, Fernando, Robles, Mercedes, Ferre-Aracil, Carlos, Varela-Rey, Marta, Elguezabal, Natalia, Calleja, José Luis, Lu, Shelly C., Milkiewicz, Malgorzata, Milkiewicz, Piotr, Anguita, Juan, Monte, María J., Marin, José J.G., López-Hoyos, Marcos, Delgado, Teresa C., Rincón, Mercedes, Crespo, Javier, and Martínez-Chantar, María Luz

Published
2021
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30. Metabolomic Identification of Subtypes of Nonalcoholic Steatohepatitis

Author

Alonso, Cristina, Fernández-Ramos, David, Varela-Rey, Marta, Martínez-Arranz, Ibon, Navasa, Nicolás, Van Liempd, Sebastiaan M, Trueba, José L Lavín, Mayo, Rebeca, Ilisso, Concetta P, de Juan, Virginia G, Iruarrizaga-Lejarreta, Marta, delaCruz-Villar, Laura, Mincholé, Itziar, Robinson, Aaron, Crespo, Javier, Martín-Duce, Antonio, Romero-Gómez, Manuel, Sann, Holger, Platon, Julian, Van Eyk, Jennifer, Aspichueta, Patricia, Noureddin, Mazen, Falcón-Pérez, Juan M, Anguita, Juan, Aransay, Ana M, Martínez-Chantar, María Luz, Lu, Shelly C, and Mato, José M

Subjects
Digestive Diseases, Chronic Liver Disease and Cirrhosis, Hepatitis, Liver Disease, Aetiology, 2.1 Biological and endogenous factors, Adult, Animals, Biomarkers, Ceramides, Diglycerides, Fatty Acids, Female, Humans, Lipid Metabolism, Male, Metabolome, Methionine Adenosyltransferase, Mice, Mice, Inbred C57BL, Mice, Knockout, Middle Aged, Non-alcoholic Fatty Liver Disease, S-Adenosylmethionine, Triglycerides, Mouse Model, 1-Carbon Metabolism, Prognostic, Clinical Sciences, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology
Abstract

Background & aimsNonalcoholic fatty liver disease (NAFLD) is a consequence of defects in diverse metabolic pathways that involve hepatic accumulation of triglycerides. Features of these aberrations might determine whether NAFLD progresses to nonalcoholic steatohepatitis (NASH). We investigated whether the diverse defects observed in patients with NAFLD are caused by different NAFLD subtypes with specific serum metabolomic profiles, and whether these can distinguish patients with NASH from patients with simple steatosis.MethodsWe collected liver and serum from methionine adenosyltransferase 1a knockout (MAT1A-KO) mice, which have chronically low levels of hepatic S-adenosylmethionine (SAMe) and spontaneously develop steatohepatitis, as well as C57Bl/6 mice (controls); the metabolomes of all samples were determined. We also analyzed serum metabolomes of 535 patients with biopsy-proven NAFLD (353 with simple steatosis and 182 with NASH) and compared them with serum metabolomes of mice. MAT1A-KO mice were also given SAMe (30 mg/kg/day for 8 weeks); liver samples were collected and analyzed histologically for steatohepatitis.ResultsLivers of MAT1A-KO mice were characterized by high levels of triglycerides, diglycerides, fatty acids, ceramides, and oxidized fatty acids, as well as low levels of SAMe and downstream metabolites. There was a correlation between liver and serum metabolomes. We identified a serum metabolomic signature associated with MAT1A-KO mice that also was present in 49% of the patients; based on this signature, we identified 2 NAFLD subtypes. We identified specific panels of markers that could distinguish patients with NASH from patients with simple steatosis for each subtype of NAFLD. Administration of SAMe reduced features of steatohepatitis in MAT1A-KO mice.ConclusionsIn an analysis of serum metabolomes of patients with NAFLD and MAT1A-KO mice with steatohepatitis, we identified 2 major subtypes of NAFLD and markers that differentiate steatosis from NASH in each subtype. These might be used to monitor disease progression and identify therapeutic targets for patients.

Published
2017

31. Last population of cave lion (Panthera (Leo) spelaea) in the extreme south-west of Europe: Carigüela cave (Southern Iberian Peninsula)

Author

Muséum national d'Histoire naturelle (France), Universidad de Córdoba (España), Ministerio de Economía y Competitividad (España), European Commission, Riquelme Cantal, José Antonio, Garrido Anguita, Juan Manuel, Delgado Huertas, Antonio, Castaños Ugarte, Pedro María, Jiménez Barredo, Fernando, Hasozbek, Altug, Simón-Vallejo, María D., Ávila Ramírez, Rocío, Rivas Carmona, M. del Mar, Cortés-Sánchez, Miguel, Muséum national d'Histoire naturelle (France), Universidad de Córdoba (España), Ministerio de Economía y Competitividad (España), European Commission, Riquelme Cantal, José Antonio, Garrido Anguita, Juan Manuel, Delgado Huertas, Antonio, Castaños Ugarte, Pedro María, Jiménez Barredo, Fernando, Hasozbek, Altug, Simón-Vallejo, María D., Ávila Ramírez, Rocío, Rivas Carmona, M. del Mar, and Cortés-Sánchez, Miguel

Abstract

he revision of the fauna of Carigüela (Píñar, Granada) has yielded the remains of a cave lion hitherto unknown at this site. The comparative morphometric study of the distal humerus fragment has led to its attribution to Panthera spelaea Goldfuss. From two samples of the bone and using the U/Th technique, an absolute dating of 145–148 ka (MIS 6) has been established. The geographical location of the site makes the cave lion of Carigüela, together with that of Solana del Zamborino, the two most southerly records of this species in Europe. In the case of the former, it is the most recent reference of this species for southern Iberia.

Published
2024

34. Incidence of Post-Acute COVID-19 Symptoms in 7 Countries: An International Network Cohort Study

Author

Xie, Junqing, primary, López-Güell, Kim, additional, Dedman, Daniel J., additional, Duarte-Salles, Talita, additional, Kolde, Raivo, additional, Martínez, Álvaro, additional, Mercier, Grégoire, additional, Abellan, Alicia, additional, Arinze, Johnmary T., additional, Cuccu, Zara, additional, Delmestri, Antonella, additional, Delseny, Dominique, additional, Khalid, Sara, additional, Kim, Chungsoo, additional, Kim, Ji-woo, additional, Kostka, Kristin, additional, Loste, Cora, additional, Mayer, Miguel-Angel, additional, Meléndez-Cardiel, Jaime, additional, Mercadé-Besora, Núria, additional, Mosseveld, Mees, additional, Nishimura, Akihito, additional, Nordeng, Hedvig, additional, Oyinlola, Jessie O., additional, Pérez-Crespo, Laura, additional, Pineda-Moncusi, Marta, additional, Ramírez-Anguita, Juan Manuel, additional, Trinh, Nhung TH, additional, Uuskula, Anneli, additional, Valdivieso, Bernardo, additional, Burkard, Theresa, additional, Burn, Edward, additional, Català, Martí, additional, Prieto-Alhambra, Daniel, additional, Paredes, Roger, additional, and Jodicke, Annika, additional

Published
2024
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38. GPCRmd uncovers the dynamics of the 3D-GPCRome

Author

Rodríguez-Espigares, Ismael, Torrens-Fontanals, Mariona, Tiemann, Johanna K. S., Aranda-García, David, Ramírez-Anguita, Juan Manuel, Stepniewski, Tomasz Maciej, Worp, Nathalie, Varela-Rial, Alejandro, Morales-Pastor, Adrián, Medel-Lacruz, Brian, Pándy-Szekeres, Gáspár, Mayol, Eduardo, Giorgino, Toni, Carlsson, Jens, Deupi, Xavier, Filipek, Slawomir, Filizola, Marta, Gómez-Tamayo, José Carlos, Gonzalez, Angel, Gutiérrez-de-Terán, Hugo, Jiménez-Rosés, Mireia, Jespers, Willem, Kapla, Jon, Khelashvili, George, Kolb, Peter, Latek, Dorota, Marti-Solano, Maria, Matricon, Pierre, Matsoukas, Minos-Timotheos, Miszta, Przemyslaw, Olivella, Mireia, Perez-Benito, Laura, Provasi, Davide, Ríos, Santiago, R. Torrecillas, Iván, Sallander, Jessica, Sztyler, Agnieszka, Vasile, Silvana, Weinstein, Harel, Zachariae, Ulrich, Hildebrand, Peter W., De Fabritiis, Gianni, Sanz, Ferran, Gloriam, David E., Cordomi, Arnau, Guixà-González, Ramon, and Selent, Jana

Published
2020
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39. Histone deacetylase 4 promotes cholestatic liver injury in the absence of prohibitin‐1

Author

Barbier-Torres, Lucía, Beraza, Naiara, Fernández-Tussy, Pablo, Lopitz-Otsoa, Fernando, Fernández-Ramos, David, Zubiete-Franco, Imanol, Varela-Rey, Marta, Delgado, Teresa C, Gutiérrez, Virginia, Anguita, Juan, Pares, Albert, Banales, Jesús M, Villa, Erica, Caballería, Juan, Alvarez, Luis, Lu, Shelly C, Mato, Jose M, and Martínez-Chantar, María Luz

Subjects
Pediatric, Genetics, Perinatal Period - Conditions Originating in Perinatal Period, Chronic Liver Disease and Cirrhosis, Liver Disease, Rare Diseases, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Animals, Cholestasis, Intrahepatic, Histone Deacetylases, Humans, Liver Diseases, Male, Mice, Prohibitins, Repressor Proteins, Medical Biochemistry and Metabolomics, Clinical Sciences, Immunology, Gastroenterology & Hepatology
Abstract

UnlabelledProhibitin-1 (PHB1) is an evolutionarily conserved pleiotropic protein that participates in diverse processes depending on its subcellular localization and interactome. Recent data have indicated a diverse role for PHB1 in the pathogenesis of obesity, cancer, and inflammatory bowel disease, among others. Data presented here suggest that PHB1 is also linked to cholestatic liver disease. Expression of PHB1 is markedly reduced in patients with primary biliary cirrhosis and biliary atresia or with Alagille syndrome, two major pediatric cholestatic conditions. In the experimental model of bile duct ligation, silencing of PHB1 induced liver fibrosis, reduced animal survival, and induced bile duct proliferation. Importantly, the modulatory effect of PHB1 is not dependent on its known mitochondrial function. Also, PHB1 interacts with histone deacetylase 4 (HDAC4) in the presence of bile acids. Hence, PHB1 depletion leads to increased nuclear HDAC4 content and its associated epigenetic changes. Remarkably, HDAC4 silencing and the administration of the HDAC inhibitor parthenolide during obstructive cholestasis in vivo promote genomic reprogramming, leading to regression of the fibrotic phenotype in liver-specific Phb1 knockout mice.ConclusionPHB1 is an important mediator of cholestatic liver injury that regulates the activity of HDAC4, which controls specific epigenetic markers; these results identify potential novel strategies to treat liver injury and fibrosis, particularly as a consequence of chronic cholestasis.

Published
2015

41. Gut microbiome and serum metabolome analyses identify molecular biomarkers and altered glutamate metabolism in fibromyalgia

Author

Clos-Garcia, Marc, Andrés-Marin, Naiara, Fernández-Eulate, Gorka, Abecia, Leticia, Lavín, José L., van Liempd, Sebastiaan, Cabrera, Diana, Royo, Félix, Valero, Alejandro, Errazquin, Nerea, Vega, María Cristina Gómez, Govillard, Leila, Tackett, Michael R., Tejada, Genesis, Gónzalez, Esperanza, Anguita, Juan, Bujanda, Luis, Orcasitas, Ana María Callejo, Aransay, Ana M., Maíz, Olga, López de Munain, Adolfo, and Falcón-Pérez, Juan Manuel

Published
2019
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43. Mitochondrial dysfunction-associated microbiota establishes a transmissible refractory response to anti-TNF therapy during ulcerative colitis

Author

Peña-Cearra, Ainize, primary, Castelo, Janire, additional, Lavín, Jose Luis, additional, Gonzalez-Lopez, Monika, additional, Pascual-Itoiz, Miguel Angel, additional, Fuertes, Miguel, additional, Gutiérrez de Juan, Virginia, additional, Bárcena, Laura, additional, Martín-Ruiz, Itziar, additional, Pellón, Aize, additional, Seoane, Iratxe, additional, Barriales, Diego, additional, Palacios, Ainhoa, additional, Fullaondo, Asier, additional, Rodríguez-Lago, Iago, additional, Martinez-Chantar, María L., additional, Aransay, Ana Mª, additional, Rodriguez, Hector, additional, Anguita, Juan, additional, and Abecia, Leticia, additional

Published
2023
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47. Metabolic rewiring by increased mitochondrial respiration drives immunosuppression in liver cancer

Author

Goikoetxea, Naroa, primary, Egia-Mendikute, Leire, additional, Bravo, Miren, additional, Serrano-Macia, Marina, additional, Delgado, Teresa Cardoso, additional, Ladero, Iraia, additional, Molina, Elena, additional, Lachiondo-Ortega, Sofia, additional, Agudo, Rubén Rodríguez, additional, Castelo, Janire, additional, Barriales, Diego, additional, Iruretagoyena, Begoña Rodriguez, additional, Santamaria, Eva, additional, Mercado-Gómez, Maria, additional, González-Recio, Irene, additional, Rincón, Mercedes, additional, Avila, Matías A, additional, Anguita, Juan, additional, Elguezabal, Natalia, additional, Palazón, Asís, additional, and Martínez-Chantar, María Luz, additional

Published
2023
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48. Silencing hepatic MCJ attenuates non-alcoholic fatty liver disease (NAFLD) by increasing mitochondrial fatty acid oxidation

Author

Barbier-Torres, Lucía, Fortner, Karen A., Iruzubieta, Paula, Delgado, Teresa C., Giddings, Emily, Chen, Youdinghuan, Champagne, Devin, Fernández-Ramos, David, Mestre, Daniela, Gomez-Santos, Beatriz, Varela-Rey, Marta, de Juan, Virginia Gutiérrez, Fernández-Tussy, Pablo, Zubiete-Franco, Imanol, García-Monzón, Carmelo, González-Rodríguez, Águeda, Oza, Dhaval, Valença-Pereira, Felipe, Fang, Qian, Crespo, Javier, Aspichueta, Patricia, Tremblay, Frederic, Christensen, Brock C., Anguita, Juan, Martínez-Chantar, María Luz, and Rincón, Mercedes

Published
2020
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49. The mitochondrial negative regulator MCJ modulates the interplay between microbiota and the host during ulcerative colitis

Author

Pascual-Itoiz, Miguel Angel, Peña-Cearra, Ainize, Martín-Ruiz, Itziar, Lavín, José Luis, Simó, Carolina, Rodríguez, Héctor, Atondo, Estibaliz, Flores, Juana María, Carreras-González, Ana, Tomás-Cortázar, Julen, Barriales, Diego, Palacios, Ainhoa, García-Cañas, Virginia, Pellón, Aize, Fullaondo, Asier, Aransay, Ana Mª, Prados-Rosales, Rafael, Martín, Rebeca, Anguita, Juan, and Abecia, Leticia

Published
2020
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