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3. Cuidados en los últimos días de vida en los pacientes hospitalizados en medicina interna

Author

Díez-Manglano, Jesús, Isasi de Isasmendi Pérez, Soledad, Rubio Gómez, Marta, Martín Pérez, Magdalena, Díez García, Luis Felipe, Vallejo Maroto, Ignacio, Ocaña Losada, Cristina, Giner Escobar, Pilar, Díaz Pérez, Catalina, Caballero Granado, Javier, García Font, Resfa María, Jódar Lorente, Francisco J., Pérez Vázquez, Gloria, Ferro Expósito, Ana Belén, Amaya González, María Luisa, Gamboa Antiñolo, Fernando, González Molina, Álvaro, Gómez Hernández, Mercedes, Guzmán García, Marcos, Benítez León, Lola, Montero Rivas, Lorena, Ruiz Mariscal, María, Gómez Aguirre, Noelia, González García, María Pilar, Martín Algora, Isabel, Bueno Castel, María Carmen, Ruiz Laiglesia, Fernando, Bejarano Tello, Esperanza, Cabrerizo García, José Luis, Guiral Fernández, Nuria, Camera, Luis, Gauna, Carla, Abad Requejo, Pedro, Martínez Gutiérrez, Rocío, Fernández Regueiro, Rebeca, Sánchez Vidal, María Teresa, Alfonso Mejido, Joaquín, García Carús, Enrique, Calvo Rodríguez, Carmen Elena, Martínez García, Paula, Ruiz Olivares, Sixto, Fullana Barcelo, María Isabel, González Arencibia, Carmen, Ros Vilamajó, Rosa, Monedero Prieto, María José, González Becerra, Concepción, Pérez, Sofía, Martín Plata, Andrea, Portilla Chocarro, Raquel, Dueñas Gutiérrez, Carlos, Estrada Álvarez, Francisco, Peña Balbuena, Sonia, Rodríguez Galindo, Raúl, Cobos Siles, Marta María, Sánchez Muñoz, Luis Ángel, Castañón López, Ana, Sanz Lobo, Celia, Chimeno Viñas, María Montserrat, Contreras Uriel, María Ángeles, Gil Domínguez, Judit, Medrano González, Francisco, Machín Lázaro, José Manuel, Magallanes Gamboa, Jeffrey, Rodríguez Galdeano, Mónica, Castro Giménez, Joaquín, Barberá Farré, José Ramón, Núñez Aragón, Raquel, Masanés Torán, Ferrán, Barbé, José, Güell Farré, Elena, Torres Bonafonte, Olga, Lozano Miñana, Ana, Moras Sarabia, Desirée, Pérez, Rosa, Arnau i Fernández, Dolors, Formiga, Francesc, Fernández Fernández, Javier, Castro Salomó, Antoni, Qanneta, Rami, Pardo Ortega, María Victoria, Estrada Díaz, Cristina, Monterroso Pintado, Yasmina, García Cors, Montserrat, Almendros Rivas, María Cruz, Domingo Albin, Dolors, Roig Morera, Jaume, Galofré Álvaro, Nuria, Toro Parodi, Aythami, Loureiro Sánchez, Mario, de la Guerra Acebal, Carla, Zubizarreta García, Javier, Benavente Claveras, Iasone, Martí Cabanes, Juan, Sanz Lázaro, Ignacio, Barquero Romero, José, Nevado López-Alegría, Leticia, Arévalo Lorido, José Carlos, Casariego Vales, Emilio, Lorenzo Vizcaya, Ana María, Macía Rodríguez, Cristina, Pérez Fernández, Silvia, Sesma Sánchez, Pascual, Jiménez-Beatty, María Dolores, González Vázquez, Laura, Brea Hernando, Ángel, Castiella Herrero, Jesús, González Anglada, María Isabel, Gracia Lorenzo, Virginia M., Pérez Martín, Alejandro, García Melcón, Gerardo, Gómez Antúnez, María, Quesada Simón, María Angustias, Gil Gil, Fuensanta, Asenjo Martínez, María, Mancebo Aragoneses, Lourdes, Calderón Parra, Jorge, Romero Pérez, María del Carmen, Curbelo García, José, Laguna Cuesta, Fernando, Segovia Abad, María Eugenia, Fontecha Ortega, María, Lara Martínez, Guillermina, Pinos Blanco, Ana, Rodil Fraile, Raquel, Martínez Litago, Elisabel, Echeverría Echeverría, Aitziber, Priego Valladares, Manuel, Trescoli Serrano, Carlos, Vicente Mas, Josep, Torregrosa Suau, Óscar, Gil Tomás, Eva, Castillo Rubio, Rafael, Murcia Zaragoza, José Manuel, Román Sánchez, Pilar, García Herola, Ana, Tenllado Doblas, Pedro Pablo, Blázquez Encinar, Julio César, Castellano Vela, Enrique, Carrizo, Néstor, Giner Galvañ, Vicente, Roca Villanueva, Bernardino Manuel, Pasquau Liaño, Francisco, Pascual Izuel, José María, Díez-Manglano, J., Isasi de Isasmendi Pérez, S., Rubio Gómez, M., Formiga, F., Sánchez Muñoz, L.Á., Castiella Herrero, J., Casariego Vales, E., and Torres Bonafonte, O.H.

Published
2019
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10. Palliative Sedation in Patients Hospitalized in Internal Medicine Departments

Author

Díez-Manglano, Jesús, de Isasmendi Pérez, Soledad Isasi, Gómez, Marta Rubio, Pérez, Magdalena Martín, Díez García, Luis Felipe, Maroto, Ignacio Vallejo, Losada, Cristina Ocaña, Roldán, Susana Moya, Pérez, Catalina Díaz, Granado, Javier Caballero, García Font, Resfa María, Jódar Lorente, Francisco J., Vázquez, Gloria Pérez, Expósito, Ana belén Ferro, Amaya González, María Luisa, Antiñolo, Fernando Gamboa, Molina, Álvaro González, Hernández, Mercedes Gómez, García, Marcos Guzmán, León, Lola Benítez, Rivas, Lorena Montero, Mariscal, María Ruiz, Aguirre, Noelia Gómez, González García, María Pilar, Algora, Isabel Martín, Bueno Castel, María Carmen, Laiglesia, Fernando Ruiz, Tello, Esperanza Bejarano, Cabrerizo García, José Luis, Fernández, Nuria Guiral, Camera, Luis, Gauna, Carla, Requejo, Pedro Abad, Gutiérrez, Rocío Martínez, Regueiro, Rebeca Fernández, Sánchez Vidal, María Teresa, Mejido, Joaquín Alfonso, Carús, Enrique García, Calvo Rodríguez, Carmen Elena, García, Paula Martínez, Olivares, Sixto Ruiz, Fullana Barcelo, María Isabel, Arencibia, Carmen González, Vilamajó, Rosa Ros, José Monedero Prieto, María, Becerra, Concepción González, Pérez, Sofía, Plata, Andrea Martín, Chocarro, Raquel Portilla, Gutiérrez, Carlos Dueñas, Álvarez, Francisco Estrada, Balbuena, Sonia Peña, Galindo, Raúl Rodríguez, Cobos Siles, Marta María, Sánchez Muñoz, Luis Ángel, López, Ana Castañón, Lobo, Celia Sanz, Chimeno Viñas, María Montserrat, Contreras Uriel, María Ángeles, Domínguez, Judit Gil, González, Francisco Medrano, Machín Lázaro, José Manuel, Gamboa, Jeffrey Magallanes, Galdeano, Mónica Rodríguez, Giménez, Joaquín Castro, Barberá Farré, José Ramón, Aragón, Raquel Núñez, Torán, Ferrán Masanés, Barbé, José, Farré, Elena Güell, Bonafonte, Olga Torres, Miñana, Ana lozano, Sarabia, Desirée Moras, Pérez, Rosa, Arnau i Fernández, Dolors, Formiga, Francesc, Fernández, Javier Fernández, Salomó, Antoni Castro, Qanneta, Rami, Pardo Ortega, María Victoria, Díaz, Cristina Estrada, Pintado, Yasmina Monterroso, Cors, Montserrat García, Almendros Rivas, María Cruz, Albin, Dolors Domingo, Morera, Jaume Roig, Álvaro, Nuria Galofré, Parodi, Aythami Toro, Sánchez, Mario Loureiro, Acebal, Carla de la Guerra, García, Javier Zubizarreta, Claveras, Iasone Benavente, Cabanes, Juan Martí, Lázaro, Ignacio Sanz, Romero, José Barquero, López-Alegría, Leticia Nevado, Arévalo Lorido, José Carlos, Vales, Emilio Casariego, Lorenzo Vizcaya, Ana María, Rodríguez, Cristina Macía, Fernández, Silvia Pérez, Sánchez, Pascual Sesma, Jiménez-Beatty, María Dolores, Vázquez, Laura González, Hernando, Ángel Brea, Herrero, Jesús Castiella, González Anglada, María Isabel, Gracia Lorenzo, Virginia M., Martín, Alejandro Pérez, Melcón, Gerardo García, Antúnez, María Gómez, Quesada Simón, María Angustias, Gil, Fuensanta Gil, Martínez, María Asenjo, Aragoneses, Lourdes Mancebo, Parra, Jorge Calderón, Pérez, María del Carmen Romero, García, José Curbelo, Cuesta, Fernando Laguna, Segovia Abad, María Eugenia, Ortega, María Fontecha, Martínez, Guillermina Lara, Blanco, Ana Pinos, Fraile, Raquel Rodil, Litago, Elisabel Martínez, Echeverría, Aitziber Echeverría, Valladares, Manuel Priego, Serrano, Carlos Trescoli, Mas, Josep Vicente, Suau, Óscar Torregrosa, Tomás, Eva Gil, Rubio, Rafael Castillo, Murcia Zaragoza, José Manuel, Sánchez, Pilar Román, Herola, Ana García, Tenllado Doblas, Pedro Pablo, Blázquez Encinar, Julio César, Vela, Enrique Castellano, Carrizo, Néstor, Galvañ, Vicente Giner, Roca Villanueva, Bernardino Manuel, Liaño, Francisco Pasquau, Pascual Izuel, José María, Isasi de Isasmendi Pérez, Soledad, García Fenoll, Rosa, Sánchez, Luis Ángel, Formiga, Françesc, Giner Galvañ, Vicente, Dueñas, Carlos, Roca, Bernardino, Estrada Díaz, Cristina, and Casariego Vales, Emilio

Published
2020
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12. QJE-STD-20-136.R2-Supplementary_Material – Supplemental material for Developmental trajectories of metacognitive processing and executive function from childhood to older age

Author

Filippi, Roberto, Ceccolini, Andrea, Periche-Tomas, Eva, and Bright, Peter

Subjects
FOS: Psychology, 170199 Psychology not elsewhere classified
Abstract

Supplemental material, QJE-STD-20-136.R2-Supplementary_Material for Developmental trajectories of metacognitive processing and executive function from childhood to older age by Roberto Filippi, Andrea Ceccolini, Eva Periche-Tomas and Peter Bright in Quarterly Journal of Experimental Psychology

Published
2020
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13. Thiazolidinediones can rapidly activate AMP-activated protein kinase in mammalian tissues

Author

LeBrasseur, Nathan K., Kelly, Meghan, Tsao, Tsu-Shuen, Farmer, Stephen R., Saha, Asish K., Ruderman, Neil B., and Tomas, Eva

Subjects
Enzymes -- Research, Insulin -- Research, Diabetes -- Research, Metabolism -- Research, Biological sciences
Abstract

Thiazolidinediones (TZDs) are insulin-sensitizing agents used in the treatment of type 2 diabetes. A widely held view is that their action is secondary to transcriptional events that occur when TZDs bind to the nuclear receptor PPAR[gamma] in the adipocyte and stimulate adipogenesis. It has been proposed that this increases insulin sensitivity, at least in part, by increasing the expression and release of adiponectin, an adipokine that activates the fuel-sensing enzyme AMP-activated protein kinase (AMPK). In this study, we report that TZDs also acutely activate AMPK in skeletal muscle and other tissues by a mechanism that is likely independent of PPAR[gamma]-regulated gene transcription. Thus incubation of isolated rat EDL muscles in medium containing 5 [micro]M troglitazone for 15 min (too brief to be attributable to transcription) significantly increased pAMPK and pACC. At a concentration of 100 [micro]M, troglitazone maximally increased these parameters and caused twofold increases in 2-deoxy-D-glucose uptake and the oxidation of exogenous [[sup.14]C]palmitate. Time course studies revealed that troglitazone-induced increases in pAMPK and pACC abundance at 15 min were paralleled by an increase in the AMP-to-ATP ratio and that by 60 min all of these parameters had returned to baseline values. Increases in pAMPK and pACC were also observed in skeletal muscle, liver, and adipose tissue in intact rats 15 min after the administration of a single dose of troglitazone (10 mg/kg, ip). Likewise, troglitazone and another TZD, pioglitazone, caused rapid increases in pAMPK and pACC of equal magnitude in Swiss 3T3 fibroblasts with and without sufficient PPAR[gamma] to mediate the expression of target genes. The results indicate that TZDs can act within minutes to activate AMPK in mammalian tissues. They suggest that this effect is associated with a change in cellular energy state and that it is not dependent on PPAR[gamma]-mediated gene transcription. acetyl-coenzyme A carboxylase; adiponectin; diabetes; insulin sensitivity; metabolism

Published
2006

22. Evidence against a cognitive advantage in the older bilingual population.

Author

Papageorgiou, Andriani, Periche Tomas, Eva, Filippi, Roberto, and Bright, Peter

Subjects
*RESPONSE inhibition, *MEMORY, *PROBLEM solving, *SHORT-term memory, *MONOLINGUALISM, *TASK performance, *EVIDENCE, *LANGUAGE ability
Abstract

Recent evidence has challenged long-standing claims that multi-language acquisition confers long-term advantages in executive function and may protect against age-related cognitive deterioration. We assessed evidence for a bilingual advantage in older monolingual and bilingual residents matched on age, gender, and socioeconomic status. A comprehensive battery of tests was administered to measure non-verbal reasoning, working memory capacity, visuo-spatial memory, response inhibition, problem solving, and language proficiency. Analyses, including Bayes factors, revealed comparable performance in both groups, with no significant differences on any task (and the only trend, found for the Tower of London task performance, indicated a monolingual advantage). Overall, therefore, our findings run counter to the bilingual advantage hypothesis. We consider the implications of our study and offer suggestions for future work in this area. [ABSTRACT FROM AUTHOR]

Published
2019
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23. Rab11 Is Associated with GLUT4-Containing Vesicles and Redistributes in Response to Insulin

Author

KESSLER, ALEXANDRA, TOMAS, EVA, MUELLER, HEIDI, ZORZANO, ANTONIO, and ECKEL, JUERGEN

Subjects
Insulin -- Physiological aspects, Diabetes -- Research, Health
Abstract

Trafficking of the glucose transporter GLUT4 involves the insulin-regulated movement from intracellular vesicular structures to the cell surface and the subsequent reentry, endosomal processing, and recycling of the transporter. We [...]

Published
2000

24. FGF21 does not require interscapular brown adipose tissue and improves liver metabolic profile in animal models of obesity and insulin-resistance

Author

Bernardo, Barbara, primary, Lu, Min, additional, Bandyopadhyay, Gautam, additional, Li, Pingping, additional, Zhou, Yingjiang, additional, Huang, Jie, additional, Levin, Nancy, additional, Tomas, Eva M., additional, Calle, Roberto A., additional, Erion, Derek M., additional, Rolph, Timothy P., additional, Brenner, Martin, additional, and Talukdar, Saswata, additional

Published
2015
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31. Mice Lacking Adiponectin Show Decreased Hepatic Insulin Sensitivity and Reduced Responsiveness to Peroxisome Proliferator-activated Receptor γ Agonists

Author

Nawrocki, Andrea R., primary, Rajala, Michael W., additional, Tomas, Eva, additional, Pajvani, Utpal B., additional, Saha, Asish K., additional, Trumbauer, Myrna E., additional, Pang, Zhen, additional, Chen, Airu S., additional, Ruderman, Neil B., additional, Chen, Howard, additional, Rossetti, Luciano, additional, and Scherer, Philipp E., additional

Published
2006
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34. Role of Disulfide Bonds in Acrp30/Adiponectin Structure and Signaling Specificity.

Author

Tsu-Shuen Tsao, Tomas, Eva, Murrey, Heather E., Hug, Christopher, Lee, David H., Ruderman, Neil B., Heuser, John E., and Lodish, Harvey F.

Subjects
*SULFIDES, *CHEMICAL bonds, *BLOOD proteins, *LIPIDS, *GLUCOSE, *METABOLISM
Abstract

Acrp30/adiponectin is an adipocyte-derived serum protein with important roles in regulation of lipid and glucose metabolism, but which of its isoforms are biologically active remains controversial. We addressed this issue by first characterizing the structure of each individual Acrp30 oligomer and the determinants responsible for multimer formation. Freeze etch electron microscopy showed the trimer to exhibit a ball-and-stick-like structure containing a large globular sphere, an extended collagen stalk, and a smaller sphere on the opposite end of the stalk. The hexamer consists of two adjacent trimeric globular domains and a single stalk composed of collagen domains from two trimers. Although not necessary for trimer formation or stability, two of the three monomers in an Acrp30 trimer are covalently linked by a disulfide bond between cysteine residues at position 22. In contrast, assembly of hexameric and higher molecular weight (HMW) forms of Acrp30 depends upon formation of Cys[sup 22]-mediated disulfide bonds because their reduction with dithiothreitol or substitution of Cys[sup 22] with alanine led exclusively to trimers. HMW and hexamer isoforms of Acrp30 activated NF-κB in C2C12 cells, but trimers, either natural, formed by reduction of Acrp30 hexamer, or formed by the C22A mutant, did not. In contrast, incubation of isolated rat extensor digitorum longus with naturally formed Acrp30 trimers or trimeric C22A Acrp30 led to increased phosphorylation of AMP-activated protein kinase-α at Thr[sup 172] and its activation. Hexameric and HMW Acrp30 could not activate AMP-activated protein kinase. Thus, trimeric and HMW/hexameric Acrp30 activate different signal transduction pathways, and Acrp30 represents a novel example of the control of ligand signaling via changes in its oligomerization state. [ABSTRACT FROM AUTHOR]

Published
2003
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35. AMP-activated protein kinase and its regulation by adiponectin and interleukin-6

Author

Kelly, Meghan, Ruderman, Neil B., and Tomas, Eva

Abstract

AbstractAMP-activated protein kinase (AMPK) is a fuel-sensing enzyme that responds to decreases in cellular energy state by activating processes that generate adenosine triphosphate (ATP) (e.g. fatty acid oxidation), and inhibiting others that consume ATP but are not acutely necessary for survival (e.g. fatty acid, triglyceride and protein synthesis). In contrast, sustained decreases in AMPK or a failure to activate it appropriately have been implicated in the pathogenesis of the metabolic syndrome. Recent studies suggest that various hormones can activate or inhibit AMPK. One of these hormones, adiponectin (Adn), an adipokine released by the fat cell, activates AMPK in liver, muscle, primary rat adipocytes, cultured endothelium and almost certainly other cells. Low plasma levels of Adn are associated with the metabolic syndrome; thus, in both humans and experimental animals, they are often accompanied by obesity, insulin resistance, ectopic lipid deposition, and a predisposition to both type 2 diabetes and atherosclerotic heart disease. Recent studies suggest that thiazoledinediones (TZDs), agents used to treat diabetes because they diminish insulin resistance, exert this effect in great measure by increasing the synthesis and release of adiponectin by the adipocyte and secondarily increasing AMPK activity in the liver and other tissues. Another cytokine that has been shown to activate AMPK is interleukin-6 (IL-6). Studies in IL-6 knockout (KO) mice have revealed that AMPK activity is diminished in their muscle and adipose tissue at 3 months of age and that, like the adiponectin KO mice, they are predisposed to obesity, glucose intolerance and hypertriglyceridemia. Likewise, when bred on an Apo E–/–they develop more severe atherosclerosis than control mice. Whether AMPK activation by other means prevents the development of the metabolic syndrome in the IL-6 or adiponectin KO mice remains to be determined.

Published
2006
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36. Mice lacking adiponectin show decreased hepatic insulin sensitivity and reduced responsiveness to peroxisome proliferator-activated receptor gamma agonists.

Author

Nawrocki AR, Rajala MW, Tomas E, Pajvani UB, Saha AK, Trumbauer ME, Pang Z, Chen AS, Ruderman NB, Chen H, Rossetti L, and Scherer PE

Subjects
Adenylate Kinase metabolism, Adiponectin deficiency, Adiponectin physiology, Animals, Cell Line, Dietary Fats pharmacology, Glucose Clamp Technique, Glucose Tolerance Test, Male, Mice, Muscles metabolism, PPAR gamma metabolism, Thiazolidinediones pharmacology, Insulin Resistance, Liver metabolism, PPAR gamma agonists
Abstract

The adipose tissue-derived hormone adiponectin improves insulin sensitivity and its circulating levels are decreased in obesity-induced insulin resistance. Here, we report the generation of a mouse line with a genomic disruption of the adiponectin locus. We aimed to identify whether these mice develop insulin resistance and which are the primary target tissues affected in this model. Using euglycemic/insulin clamp studies, we demonstrate that these mice display severe hepatic but not peripheral insulin resistance. Furthermore, we wanted to test whether the lack of adiponectin magnifies the impairments of glucose homeostasis in the context of a dietary challenge. When exposed to high fat diet, adiponectin null mice rapidly develop glucose intolerance. Specific PPARgamma agonists such as thiazolidinediones (TZDs) improve insulin sensitivity by mechanisms largely unknown. Circulating adiponectin levels are significantly up-regulated in vivo upon activation of PPARgamma. Both TZDs and adiponectin have been shown to activate AMP-activated protein kinase (AMPK) in the same target tissues. We wanted to address whether the ability of TZDs to improve glucose tolerance is dependent on adiponectin and whether this improvement involved AMPK activation. We demonstrate that the ability of PPARgamma agonists to improve glucose tolerance in ob/ob mice lacking adiponectin is diminished. Adiponectin is required for the activation of AMPK upon TZD administration in both liver and muscle. In summary, adiponectin is an important contributor to PPARgamma-mediated improvements in glucose tolerance through mechanisms that involve the activation of the AMPK pathway.

Published
2006
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