Person:
Tortajada Alonso, Agustín

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First Name
Agustín
Last Name
Tortajada Alonso
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Inmunología, Oftalmología y ORL
Area
Inmunología
Identifiers
UCM identifierORCIDScopus Author IDWeb of Science ResearcherIDDialnet ID

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Now showing 1 - 3 of 3
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    Project number: PIMCD86/23-24
    Simulación virtual de diagnóstico de inmunodeficiencias congénitas para el asentamiento de conocimientos básicos sobre inmunología
    (0024) Marín Marín, Ana Victoria; Martínez Naves, Eduardo; Regueiro González-Barros, José Ramón; Tortajada Alonso, Agustín; Cubero Palero, Francisco Javier; Allende Martínez, Luis Miguel; González Granado, Luis Ignacio; Muñoz Ruiz, Miguel; Chacón Arguedas, Carlos Daniel; Fernández Megino, Rebeca; Herrero Alonso, Marta; Estévez Benito, Iván; Fernández Boraita, Julia Belén; Franco Jarava, Clara
    La inmunología es una materia transversal que trata conocimientos de biología celular, bioquímica molecular, genética y patología clínica. La docencia que reciben los alumnos de primero de Medicina en nuestra Universidad, cuyas aulas se componen de 80 alumnos aproximadamente, consta de unas 36 horas anuales en una asignatura obligatoria e impartida en el segundo periodo del curso. Dada la gran complejidad inherente en el estudio inmunología, es realmente difícil lograr el interés del grupo por la asignatura a través de las técnicas docentes clásicas. En este proyecto de innovación docente, proponemos una actividad interactiva, parcialmente virtual y con una perspectiva basico-clínica interactiva mediante la cual los alumnos participarán activamente en el diagnóstico de un total de 3 pacientes pediátricos con errores congénitos de la inmunidad durante una única sesión al final del curso. Para ello, dispondremos de 3 casos clínicos reales que describirán enfermedades frecuentes dentro de la especialidad siendo presentados concisamente con datos clínicos a través de la pantalla de la misma aula docente, y de manera simultánea lanzaremos preguntas a través de una plataforma web que permitirá que los alumnos respondan utilizando un “apodo” e individualmente empleando sus teléfonos móviles. Con cada pregunta los alumnos aprenderán a identificar conceptos claves para el diagnóstico de inmunodeficiencias que no pueden abordarse en las clases magistrales por escasez de tiempo, y a la vez autoevaluarán los conocimientos adquiridos hasta el momento.
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    Activation of the Unfolded Protein Response (UPR) Is Associated with Cholangiocellular Injury, Fibrosis and Carcinogenesis in an Experimental Model of Fibropolycystic Liver Disease
    (Cancers, 2021) Chaobo, Chen; Hanghang, Wu; Hui, Ye; Tortajada Alonso, Agustín; Peligros Gómez, María Isabel; Kang, Zheng; Vaquero Martín, Francisco Javier; Bañares Cañizares, Rafael; Martínez Naves, Eduardo; Nevzorova, Yulia; Cubero Palero, Francisco Javier
    Fibropolycystic liver disease is characterized by hyperproliferation of the biliary epithelium and the formation of multiple dilated cysts, a process associated with unfolded protein response (UPR). In the present study, we aimed to understand the mechanisms of cyst formation and UPR activation in hepatocytic c-Jun N-terminal kinase 1/2 (Jnk1/2) knockout mice. Floxed JNK1/2 (Jnkf/f) and Jnk∆hepa animals were sacrificed at different time points during progression of liver disease. Histological examination of specimens evidenced the presence of collagen fiber deposition, increased α-smooth muscle actin (αSMA), infiltration of CD45, CD11b and F4/80 cells and proinflammatory cytokines (Tnf, Tgfβ1) and liver injury (e.g., ALT, apoptosis and Ki67-positive cells) in Jnk∆hepa compared with Jnkf/f livers from 32 weeks of age. This was associated with activation of effectors of the UPR, including BiP/GRP78, CHOP and spliced XBP1. Tunicamycin (TM) challenge strongly induced ER stress and fibrosis in Jnk∆hepa animals compared with Jnkf/f littermates. Finally, thioacetamide (TAA) administration to Jnk∆hepa mice induced UPR activation, peribiliary fibrosis, liver injury and markers of biliary proliferation and cholangiocarcinoma (CCA). Orthoallografts of DEN/CCl4-treated Jnk∆hepa liver tissue triggered malignant CCA. Altogether, these results suggest that activation of the UPR in conjunction with fibrogenesis might trigger hepatic cystogenesis and early stages of CCA.
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    Activation of the Unfolded Protein Response (UPR) Is Associated with Cholangiocellular Injury, Fibrosis and Carcinogenesis in an Experimental Model of Fibropolycystic Liver Disease
    (Cancers, 2021) Chen, Chaobo; Wu, Hanghang; Tortajada Alonso, Agustín; Bañares Cañizares, Rafael; Martínez Naves, Eduardo; Nevzorova, Yulia; Cubero Palero, Francisco Javier
    Fibropolycystic liver disease is characterized by hyperproliferation of the biliary epithelium and the formation of multiple dilated cysts, a process associated with unfolded protein response (UPR). In the present study, we aimed to understand the mechanisms of cyst formation and UPR activation in hepatocytic c-Jun N-terminal kinase 1/2 (Jnk1/2) knockout mice. Floxed JNK1/2 (Jnkf/f) and Jnk∆hepa animals were sacrificed at different time points during progression of liver disease. Histological examination of specimens evidenced the presence of collagen fiber deposition, increased α-smooth muscle actin (αSMA), infiltration of CD45, CD11b and F4/80 cells and proinflammatory cytokines (Tnf, Tgfβ1) and liver injury (e.g., ALT, apoptosis and Ki67-positive cells) in Jnk∆hepa compared with Jnkf/f livers from 32 weeks of age. This was associated with activation of effectors of the UPR, including BiP/GRP78, CHOP and spliced XBP1. Tunicamycin (TM) challenge strongly induced ER stress and fibrosis in Jnk∆hepa animals compared with Jnkf/f littermates. Finally, thioacetamide (TAA) administration to Jnk∆hepa mice induced UPR activation, peribiliary fibrosis, liver injury and markers of biliary proliferation and cholangiocarcinoma (CCA). Orthoallografts of DEN/CCl4-treated Jnk∆hepa liver tissue triggered malignant CCA. Altogether, these results suggest that activation of the UPR in conjunction with fibrogenesis might trigger hepatic cystogenesis and early stages of CCA.