{"header":{"numFound":27724809,"maxScore":1.0,"queryTime":450,"page":1,"pageSize":10},"results":[{"authors":[{"id":null,"fullName":"Vizcaíno, N. (Nieves)","name":"N.","surname":"Vizcaíno","rank":1,"pid":null},{"id":null,"fullName":"Pérez-Etayo, L. (Lara)","name":"L.","surname":"Pérez-Etayo","rank":2,"pid":null},{"id":null,"fullName":"Conde-Alvarez, R. (Raquel)","name":"R.","surname":"Conde-Alvarez","rank":3,"pid":null},{"id":null,"fullName":"Iriarte, M. (Maite)","name":"M.","surname":"Iriarte","rank":4,"pid":null},{"id":null,"fullName":"Moriyon, I. (Ignacio)","name":"I.","surname":"Moriyon","rank":5,"pid":null},{"id":null,"fullName":"Zuñiga-Ripa, A. (Amaia)","name":"A.","surname":"Zuñiga-Ripa","rank":6,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"keyword","value":"Pyruvate phosphate dikinase"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Metabolism"},"provenance":null},{"subject":{"scheme":"keyword","value":"Virulence"},"provenance":null},{"subject":{"scheme":"keyword","value":"Brucella ovis"},"provenance":null},{"subject":{"scheme":"keyword","value":"Gluconeogenesis"},"provenance":null},{"subject":{"scheme":"keyword","value":"Attenuation"},"provenance":null},{"subject":{"scheme":"keyword","value":"Laboratory models"},"provenance":null},{"subject":{"scheme":"keyword","value":"Vaccine"},"provenance":null}],"mainTitle":"Disruption of pyruvate phosphate dikinase in Brucella ovis PA CO2-dependent and independent strains generates attenuation in the mouse model","subTitle":null,"descriptions":["Brucella ovis is a non-zoonotic rough Brucella that causes genital lesions, abortions and increased perinatal mortal‑ ity in sheep and is responsible for important economic losses worldwide. Research on virulence factors of B. ovis is necessary for deciphering the mechanisms that enable this facultative intracellular pathogen to establish persistent infections and for developing a species-specifc vaccine, a need in areas where the cross-protecting ovine smooth B. melitensis Rev1 vaccine is banned. Although several B. ovis virulence factors have been identifed, there is little information on its metabolic abilities and their role in virulence. Here, we report that deletion of pyruvate phosphate dikinase (PpdK, catalyzing the bidirectional conversion pyruvate ⇌ phosphoenolpyruvate) in B. ovis PA (virulent and CO2-dependent) impaired growth in vitro. In cell infection experiments, although showing an initial survival higher than that of the parental strain, this ppdK mutant was unable to multiply. Moreover, when inoculated at high doses in mice, it displayed an initial spleen colonization higher than that of the parental strain followed by a marked comparative decrease, an unusual pattern of attenuation in mice. A homologous mutant was also obtained in a B. ovis PA CO2-independent construct previously proposed for developing B. ovis vaccines to solve the problem that CO2-dependence represents for large scale production. This CO2-independent ppdK mutant reproduced the growth defect in vitro and the multiplication/clearance pattern in mouse spleens, and is thus an interesting vaccine candidate for the immunoprophylaxis of B. ovis ovine brucellosis."],"publicationDate":"2020-01-01","publisher":null,"embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::00a4bdaf642672c3ae992556cdc24834","originalIds":["50|00064aabbda9::00a4bdaf642672c3ae992556cdc24834","oai:navarra.escire.net:10171/66344"],"pids":[{"scheme":"handle","value":"10171/66344"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":1.1111055E-9,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/66344"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/66344"],"publicationDate":"2020-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"García-García, J. (Jorge)","name":"J.","surname":"García-García","rank":1,"pid":null},{"id":null,"fullName":"Ansorena-Artieda, E. (Eduardo)","name":"E.","surname":"Ansorena-Artieda","rank":2,"pid":null},{"id":null,"fullName":"Milagro-Yoldi, F.I. (Fermín Ignacio)","name":"F. I.","surname":"Milagro-Yoldi","rank":3,"pid":null},{"id":null,"fullName":"Zalba, G. (Guillermo)","name":"G.","surname":"Zalba","rank":4,"pid":null},{"id":null,"fullName":"Miguel-Vázquez, C. (Carlos) de","name":"C.","surname":"Miguel-Vázquez","rank":5,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"NADPH oxidase 5"},"provenance":null},{"subject":{"scheme":"keyword","value":"Lipid homeostasis"},"provenance":null},{"subject":{"scheme":"keyword","value":"Glucose uptake"},"provenance":null},{"subject":{"scheme":"keyword","value":"Caveolin 1"},"provenance":null},{"subject":{"scheme":"keyword","value":"Obesity"},"provenance":null},{"subject":{"scheme":"keyword","value":"Glut4"},"provenance":null}],"mainTitle":"Endothelial Nox5 expression modulates glucose uptake and lipid accumulation in mice fed a high-fat diet and 3T3-L1 adipocytes treated with glucose and palmitic acid","subTitle":null,"descriptions":["Obesity is a global health issue associated with insulin resistance and altered lipid homeostasis. It has been described that reactive oxygen species (ROS) derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) activity are involved in the development of these pathologies. The present study describes the role of endothelial NOX5 expression over adipose tissue by using two experimental systems: NOX5 conditional knock-in mice fed with a high-fat diet and 3T3-L1 adipocytes cultured with conditioned media of NOX5-expressing endothelial cells previously treated with glucose and palmitic acid. Animals expressing NOX5 presented lower body weight gain and less mesenteric and epididymal adipose mass compared to control mice fed with the same diet. NOX5-expressing mice also showed significantly lower glycaemia and improved insulin-induced glucose uptake. In addition, Glut4 and Caveolin 1 (Cav1) expression were significantly increased in the adipose tissue of these animals. Likewise, 3T3-L1 adipocytes treated with conditioned media from NOX5-expressing endothelial cells, incubated with high glucose and palmitic acid, presented a reduction in lipid accumulation and an increase in glucose uptake. Moreover, a significant increase in the expression of Glut4 and Cav1 was also detected in these cells. Taken together, all these data support that, in response to a highly caloric diet, NOX5 endothelial activity may regulate glucose sensitivity and lipid homeostasis in the adipose tissue."],"publicationDate":"2021-01-01","publisher":null,"embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::00c85adf8aca6a405708ce0e0d2f8b91","originalIds":["50|00064aabbda9::00c85adf8aca6a405708ce0e0d2f8b91","oai:navarra.escire.net:10171/60372"],"pids":[{"scheme":"handle","value":"10171/60372"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":1.272318E-9,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/60372"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/60372"],"publicationDate":"2021-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Camacho, A.I. (A.I.)","name":"A. I.","surname":"Camacho","rank":1,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"keyword","value":"Vacunas"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Materias Investigacion::Farmacia"},"provenance":null},{"subject":{"scheme":"keyword","value":"Microbiología"},"provenance":null}],"mainTitle":"Towards a non-living vaccine for shigellosis","subTitle":null,"descriptions":["Shigellosis is an acute invasive enteric infection caused by Shigella spp. with an incidence of 165 millions episodes leading to 1.1 millions deaths. Considering bacteria easily spread from person to person and the emergence of multidrug- resistant Shigella strains, WHO gave high priority for the development of a shigellosis vaccine in 1991. Unfortunately, none of the proposals have an acceptable success. On this context, our proposal is based of the employment of an acellular vaccine for mucosal administration, containing relevant antigens from Shigella. Moreover, in order to increase its efficacy, it was propose the use of nanoparticles as adjuvants. Considering pathogenesis of Shigella, we select outer membrane vesicles (OMVs) as the subcellular extract. Since they are part of the outer membrane of bacteria, OMV extraction seems to be a effective strategy for isolation of the most relevant antigens of bacteria. Nevertheless, safety of this kind of subcellular vaccines is usually hampered with a lower inherent immunogenicity. Consequently, in order to obtain an adequate immune response and obtain a delivery system that allow mucosal administration, the antigenic extract from Shigella would be encapsulated in Gantrez® AN, a copolymer of ether and maleic anhydride (PMV/MA) with bioadhesive properties."],"publicationDate":"2015-01-01","publisher":"Servicio de Publicaciones de la Universidad de Navarra","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Irache, J.M. (Juan Manuel)","Gamazo, C. (Carlos)","Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::017afd50582efced6a10bc18d318b743","originalIds":["50|00064aabbda9::017afd50582efced6a10bc18d318b743","oai:navarra.escire.net:10171/38071"],"pids":[{"scheme":"handle","value":"10171/38071"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":5.99466E-10,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/38071"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/38071"],"publicationDate":"2015-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Moody, T.W. (T.W.)","name":"T. W.","surname":"Moody","rank":1,"pid":null},{"id":null,"fullName":"Coy, D. (D.)","name":"D.","surname":"Coy","rank":2,"pid":null},{"id":null,"fullName":"Montuenga-Badia, L.M. (Luis M.)","name":"L. M.","surname":"Montuenga-Badia","rank":3,"pid":null},{"id":null,"fullName":"Cuttitta, F. (Frank)","name":"F.","surname":"Cuttitta","rank":4,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Adrenomedullin"},"provenance":null},{"subject":{"scheme":"keyword","value":"cAMP"},"provenance":null},{"subject":{"scheme":"keyword","value":"PAMP"},"provenance":null},{"subject":{"scheme":"keyword","value":"Growth"},"provenance":null}],"mainTitle":"Proadrenomedullin NH(2)-terminal 20 peptide (PAMP) and adrenomedullin bind to teratocarcinoma cells.","subTitle":null,"descriptions":["Proadrenomedullin NH(2-)terminal 20 peptide (PAMP) and adrenomedullin (ADM) bind to teratocarcinoma cells. The effects of PAMP and ADM on teratocarcinoma cells were investigated. (125)I-PAMP bound to PA1 cells with moderate affinity (K(d) = 110 nM) to a single class of sites (B(max) = 110 000/cell). Specific (125)I-PAMP binding was inhibited by PAMP (IC(50) of 100 nM) but not ADM, calcitonin gene-related peptide (CGRP), or amylin. Specific (125)I-ADM binding was inhibited with high affinity by ADM, CGRP, and CGRP(8-37) (IC(50) values of 10, 10, and 15 nM respectively) but not PAMP or amylin. ADM elevated cAMP (ED(50) value of 100 nM), whereas PAMP had no effect on basal cAMP but inhibited the increase in cAMP caused by 10 nM ADM. Also, the increase in cAMP caused by ADM was inhibited CGRP(8-37), suggesting that ADM is binding to CGRP receptors. ADM (100 nM) stimulated transiently c-fos mRNA, whereas PAMP (1000 nM) had little effect; however, PAMP inhibited the increase in c-fos mRNA caused by ADM. ADM stimulated [(3)H]thymidine uptake into PA1 cells, whereas PAMP inhibited the increase in thymidine uptake caused by ADM. These results indicate that ADM and PAMP are both biologically active in teratocarcinoma cells."],"publicationDate":"2000-01-01","publisher":"Elsevier BV","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::02140b24a201d82dc145caa12ae87ad1","originalIds":["50|00064aabbda9::02140b24a201d82dc145caa12ae87ad1","oai:navarra.escire.net:10171/20171"],"pids":[{"scheme":"handle","value":"10171/20171"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":2.1985837E-10,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/20171"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/20171"],"publicationDate":"2000-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Agueda, B. (Beatriz)","name":"B.","surname":"Agueda","rank":1,"pid":null},{"id":null,"fullName":"Parlade, J. (Javier)","name":"J.","surname":"Parlade","rank":2,"pid":null},{"id":null,"fullName":"Miguel-Velasco, A.M. (Ana Maria) de","name":"A. M.","surname":"Miguel-Velasco","rank":3,"pid":null},{"id":null,"fullName":"Martinez-Peña, F. 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The described ectomycorrhiza has traits typical of Boletales: whitish with three differentiated plectenchymatous layers in the mantle in plan view forming ring-like structures and rhizomorphs with highly differentiated hyphae. The inflated, smooth cystidia-like clavate end cells on the surface of the rhizomorphs and their slightly twisted external hyphae are additional characterizing features. The Hartig net occupies 1 1/2 rows of cortical cells, partly reaching the endodermis. Not all hyphae have clamps. The identification of the fungal symbiont as B. edulis was confirmed by ITS rDNA sequence comparison between mycorrhizas and sporocarps. The singularity of this symbiotic association, as well as its ecological and practical implications, are discussed."],"publicationDate":"2006-01-01","publisher":"Mycological Society of America","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::02de9221a7b72d0c9cee1062f7d2a095","originalIds":["50|00064aabbda9::02de9221a7b72d0c9cee1062f7d2a095","oai:navarra.escire.net:10171/18758"],"pids":[{"scheme":"handle","value":"10171/18758"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":2.8089814E-10,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/18758"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/18758"],"publicationDate":"2006-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Agorreta, J. 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This study evaluates the effects of hypoxia, an important feature of ALI, on NOS2 expression in a rat model of ALI caused by exposure to hypoxia and LPS. Exposure to hypoxia alone had no effect on the expression of NOS2 in rat lungs. LPS treatment resulted in a significant increase in NOS2 in the lungs, which was further enhanced by concomitant exposure to hypoxia. Immunohistochemical analysis and in situ hybridization showed no changes in the expression of NOS2 in lung resident cells under any conditions. The increase in NOS2 levels is mainly due to the influx of NOS2-expressing inflammatory cells. By morphologic analysis, these inflammatory cells were identified as neutrophils, lymphocytes, and monocytes. In vitro experiments of lung epithelial and endothelial cell lines showed no detectable expression of NOS2 with any of the treatments. In a macrophage cell line, LPS-induced NOS2 expression was not affected by the concomitant exposure to hypoxia. In conclusion, LPS increases NOS2 expression in rat lungs through the recruitment of NOS2-producing leukocytes. Simultaneous exposure to LPS and hypoxia results in a greater influx of inflammatory cells that further enhances NOS2 expression."],"publicationDate":"2003-08-01","publisher":"American Thoracic Society","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::039e0bf556b868c05861aaf7071410ea","originalIds":["50|00064aabbda9::039e0bf556b868c05861aaf7071410ea","oai:navarra.escire.net:10171/16770"],"pids":[{"scheme":"handle","value":"10171/16770"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":2.4319094E-10,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/16770"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/16770"],"publicationDate":"2003-08-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Perez-Echarri, N. (Nerea)","name":"N.","surname":"Perez-Echarri","rank":1,"pid":null},{"id":null,"fullName":"Perez-Matute, P. (Patricia)","name":"P.","surname":"Perez-Matute","rank":2,"pid":null},{"id":null,"fullName":"Marcos, B. (Beatriz)","name":"B.","surname":"Marcos","rank":3,"pid":null},{"id":null,"fullName":"Martinez, J.A. (José Alfredo)","name":"J. A.","surname":"Martinez","rank":4,"pid":null},{"id":null,"fullName":"Moreno-Aliaga, M. J. (María Jesús)","name":"M. J.","surname":"Moreno-Aliaga","rank":5,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Materias Investigacion::Ciencias de la Salud::Diabetes e hipertensión"},"provenance":null},{"subject":{"scheme":"keyword","value":"Materias Investigacion::Ciencias de la Salud::Endocrinología"},"provenance":null}],"mainTitle":"Effects of eicosapentaenoic acid ethyl ester on visfatin and apelin in lean and overweight (cafeteria diet-fed) rats","subTitle":null,"descriptions":["Previous studies have demonstrated that the n-3 fatty acid EPA improves insulin resistance induced by high-fat diets. The aim of the present study was to investigate the potential role of visfatin and apelin in the insulin-sensitising effects of EPA ethyl ester. The effects of EPA on muscle and adipose GLUT mRNA, as well as on liver glucokinase (GK) and glucose-6-phosphatase (G6Pase) activity, were investigated. Male Wistar rats fed on a standard diet or a high-fat cafeteria diet were daily treated by oral administration with EPA ethyl ester (1 g/kg) for 5 weeks. A significant decrease (P,0·01) in white adipose tissue (WAT) visfatin mRNA levels was found in the cafeteria-fed rats, which was reversed by EPA administration (P,0·05). Moreover, a negative relationship was observed between homeostatic model assessment (HOMA) and the visfatin:total WAT ratio. In contrast, cafeteria-diet feeding caused a significant increase (P,0·01) in apelin mRNA in visceral WAT. EPA increased (P,0·01) apelin gene expression, and a negative relationship between HOMA index with visceral apelin mRNA and serum apelin:total WAT ratio was also observed. EPA treatment did not induce changes in skeletal muscle GLUT1, GLUT4 or insulin receptor mRNA levels. Neither liver GK and G6Pase activity nor the GK:G6Pase ratio was modified by EPA. These data suggest that somehow the insulin-sensitising effects of EPA could be related to its stimulatory action on both visfatin and apelin gene expression in visceral fat, while changes in skeletal muscle GLUT, as well as in hepatic glucose production, are not likely to be the main contributing factors in the improvement in insulin resistance induced by EPA."],"publicationDate":"2009-01-01","publisher":"Cambridge University Press (CUP)","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::03e18a6233c63c242002b3b3ade72693","originalIds":["50|00064aabbda9::03e18a6233c63c242002b3b3ade72693","oai:navarra.escire.net:10171/6934"],"pids":[{"scheme":"handle","value":"10171/6934"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":3.4183575E-10,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/6934"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/6934"],"publicationDate":"2009-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Gonzalez-Aparicio, M. (Manuela)","name":"M.","surname":"Gonzalez-Aparicio","rank":1,"pid":null},{"id":null,"fullName":"Buñuales, M. (María)","name":"M.","surname":"Buñuales","rank":2,"pid":null},{"id":null,"fullName":"Ortiz-de-Landazuri, I. (Iñaki)","name":"I.","surname":"Ortiz-De-Landazuri","rank":3,"pid":null},{"id":null,"fullName":"Prieto, J. (Jesús)","name":"J.","surname":"Prieto","rank":4,"pid":null},{"id":null,"fullName":"Hernandez-Alcoceba, R. (Rubén)","name":"R.","surname":"Hernandez-Alcoceba","rank":5,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Gene therapy"},"provenance":null},{"subject":{"scheme":"keyword","value":"High-capacity adenovirus"},"provenance":null},{"subject":{"scheme":"keyword","value":"Recombinase"},"provenance":null},{"subject":{"scheme":"keyword","value":"Split-Cre"},"provenance":null},{"subject":{"scheme":"keyword","value":"Dimerizable Cre"},"provenance":null}],"mainTitle":"Application of a split-Cre system for high-capacity adenoviral vector amplification","subTitle":null,"descriptions":["Background and aims: High-capacity adenoviral vectors (HC-AdV) show extended DNA payload and stability of gene expression in vivo due to the absence of viral coding sequences. However, production requires methods to trans-complement viral proteins, usually through Helper Viruses (HV). The Cre/loxP system is frequently employed to remove the packaging signal in HV genomes, in order to avoid their encapsidation. However, chronic exposure to the Cre recombinase in packaging cells is detrimental. We have applied the dimerizable Cre system to overcome this limitation. Methods and results: Cre was split in two fragments devoid of recombinase function (N-terminal 244 and C-terminal 99 amino-acids). In one version of the system, interaction with both moieties was favored by rapamycin-dependent heterodimerization domains (DiCre). Other version contained only Cre sequences (oCre). We generated packaging cells and HVs expressing the complementary fragments and studied their performance for HC-AdV production. We found that both conformations avoided interference with the growth of packaging cells, and the oCre system was particularly suitable for HC-AdV amplification. Conclusions: The split-Cre system improves the performance of packaging cells and can reduce the time and cost of HC-AdV amplification up to 30% and 15%, respectively. This may contribute to the standardization of HC-AdV production."],"publicationDate":"2023-01-01","publisher":"Wiley","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::048a2642dba2b229dd42019aa328702c","originalIds":["oai:navarra.escire.net:10171/66151","50|00064aabbda9::048a2642dba2b229dd42019aa328702c"],"pids":[{"scheme":"handle","value":"10171/66151"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":1.6835128E-9,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/66151"}],"accessRight":{"code":"c_abf2","label":"OPEN","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/66151"],"publicationDate":"2023-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Pastor, L. (Laura)","name":"L.","surname":"Pastor","rank":1,"pid":null},{"id":null,"fullName":"Vettorazzi, A. (Ariane)","name":"A.","surname":"Vettorazzi","rank":2,"pid":null},{"id":null,"fullName":"Enciso-Gadea, J. M. (José Manuel)","name":"J. M.","surname":"Enciso-Gadea","rank":3,"pid":null},{"id":null,"fullName":"Gonzalez-Peñas, E. (Elena)","name":"E.","surname":"Gonzalez-Peñas","rank":4,"pid":null},{"id":null,"fullName":"García-Jalón, J.A. (José Antonio)","name":"J. A.","surname":"García-Jalón","rank":5,"pid":null},{"id":null,"fullName":"Monreal, J.I. (José Ignacio)","name":"J. I.","surname":"Monreal","rank":6,"pid":null},{"id":null,"fullName":"Lopez-de-Cerain, A. (Adela)","name":"A.","surname":"Lopez-De-Cerain","rank":7,"pid":null}],"openAccessColor":null,"publiclyFunded":null,"eoscIfGuidelines":null,"type":"other","language":{"code":"eng","label":"English"},"countries":null,"subjects":[{"subject":{"scheme":"FOS","value":"0301 basic medicine"},"provenance":null},{"subject":{"scheme":"keyword","value":"Kidney transporters"},"provenance":null},{"subject":{"scheme":"FOS","value":"03 medical and health sciences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Sex differences"},"provenance":null},{"subject":{"scheme":"keyword","value":"Ochratoxin a (OTA)"},"provenance":null},{"subject":{"scheme":"keyword","value":"Gene expression"},"provenance":null},{"subject":{"scheme":"keyword","value":"Mycotoxins"},"provenance":null},{"subject":{"scheme":"keyword","value":"Hormones"},"provenance":null}],"mainTitle":"Sex differences in ochratoxin a toxicity in F344 rats after 7 and 21 days of daily oral administration","subTitle":null,"descriptions":["Ochratoxin A (OTA) is a potent renal carcinogen in male rats but not in females. The mechanisms underlying these differences are unknown. The sex-dependent response of F344 rats after a repeated OTA oral administration for 7 (0.50 mg/kg bw) or 21 days (0.21 and 0.50 mg/kg bw) was evaluated. General toxicity, sex and thyroid hormones and histopathology were studied. OTA was quantified (HPLC-FLD) in plasma, kidney and liver and the expression of kidney transporters (RT-qPCR) was studied. After 7 days, kidney histopathology showed more pronounced signs of toxicity in males than in females. After 21 days, a higher toxicity was observed but sex differences disappeared. OTA concentration in plasma and tissues was similar in both sexes. Downregulation was the general OTA-induced effect. Oats' downregulation was slow in males and Oat3 did not change in females. Oatp1 was strongly downregulated in males after 21 days. An opposite effect was observed in Bcrp after 21 days: downregulation in males and upregulation in females. Females showed a dose- and time-dependent decrease of progesterone. Despite the sex differences, the final balance in OTA toxicokinetics at renal cell level does not seem to support a higher accumulation of OTA in male kidneys."],"publicationDate":"2018-01-01","publisher":"Elsevier BV","embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Repositorio de la Universidad de Navarra"],"coverages":null,"bestAccessRight":{"code":"c_16ec","label":"RESTRICTED","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":null,"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"00064aabbda9::049a1971b7a14c6ae1c03b469a160fe3","originalIds":["oai:navarra.escire.net:10171/69062","50|00064aabbda9::049a1971b7a14c6ae1c03b469a160fe3"],"pids":[{"scheme":"handle","value":"10171/69062"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":0.0,"influence":2.1746283E-9,"popularity":8.566651E-10,"impulse":0.0,"citationClass":"C5","influenceClass":"C5","impulseClass":"C5","popularityClass":"C5"}},"projects":null,"organizations":null,"communities":null,"collectedFrom":[{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}],"instances":[{"pids":[{"scheme":"handle","value":"10171/69062"}],"accessRight":{"code":"c_16ec","label":"RESTRICTED","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/","openAccessRoute":null},"type":"Other ORP type","urls":["https://hdl.handle.net/10171/69062"],"publicationDate":"2018-01-01","refereed":"nonPeerReviewed","hostedBy":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"},"collectedFrom":{"key":"openaire____::891381590337449b8dfd6259d4031ae1","value":"NAVARA SCIRE"}}],"links":null,"otherTitles":null,"inDiamondJournal":null,"green":null,"isGreen":null,"isInDiamondJournal":null},{"authors":[{"id":null,"fullName":"Palacios-Ortega, S. 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Efecto de TNF-a y glucosa","subTitle":null,"descriptions":["Knowledge of the regulatory mechanisms involved in adipocyte differentiation and hypertrophy is essential to understand the nexus between obesity and insulin resistance and will help to design new therapeutic approaches for obesity and diabetes. Previous studies published by our group pointed to caveolin-1 (Cav-1) as one of the genes upregulated in rat visceral white adipose tissue in response to a high fat diet. Cav-1 is an essential constituent of adipocyte caveolae which binds the beta subunit of the insulin receptor (IR) and is implicated in the regulation of insulin signaling. The major objectives of the this work were: to determine changes in expression and activation of Cav-1 during adipocyte differentiation and the role of DNA methylation in the expression changes; to analyze the effect of such changes in the transmission of insulin signaling; to study the effects of external conditions typically associated with obesity, such as inflammation (TNF-α) or high glucose (hyperglycemia), on the expression and activation of Cav-1 and their influence on insulin signaling, both during adipocyte differentiation and in mature adipocytes. In this work, we have found that, during adipocyte differentiation of 3T3-L1 cells, the promoter and first intron of the Cav-1 gene undergo a demethylation process that is accompanied by a strong induction of Cav-1 expression, indicating that epigenetic mechanisms have a pivotal role in this differentiation process. Furthermore, IR, PKB-Akt and Glut-4 expression are also increased during the differentiation process suggesting a coordinated regulation with Cav-1. Activation of Cav-1 protein by phosphorylation arises during the differentiation process, an event that would help to facilitate the maintenance of insulin sensitivity by these fully mature adipocytes. TNF-α-mediated chronic low-grade inflammation of adipose tissue is associated with obesity and insulin resistance. In our study, TNF-α slowed down the differentiation program, hindering the expression of some insulin signaling intermediates without fully eliminating insulin-mediated glucose uptake. In mature adipocytes, TNF-α did not compromise lipid-storage capacity but downregulated the expression of the insulin signaling intermediates, totally blocking insulin-mediated glucose uptake. Insulin sensitivity correlated with the level of activated phospho-Cav-1 in both situations, strongly suggesting the direct contribution of Cav-1 to the maintenance of this physiological response. Finally, adipocytes exposed to high glucose concentrations exhibited impaired metabolic functions, including an increase of oxidative and proinflammatory factors that might favour the development of insulin resistance. Our results demonstrated that both, long-term high glucose exposure during adipogenesis, and short-term incubation of mature adipocytes with high glucose, promoted triglyceride accumulation in 3T3-L1 cells. The short-term exposure of mature adipocytes to high glucose significantly reduced the sensitivity to insulin of Cav-1, IR and protein kinase B (AKT-2) phosphorylation, as well as insulin-induced deoxyglucose uptake. Adipocytes differentiated in the presence of high glucose lost Cav-1 and IR response to insulin-stimulated phosphorylation, but maintained the insulin sensitivity of AKT-2 phosphorylation and deoxyglucose uptake. Moreover, these cells showed an increase of Cav-1, IR and AKT-2 protein content, pointing to an adaptive response induced by the long-term high glucose exposure."],"publicationDate":"2015-01-01","publisher":null,"embargoEndDate":null,"sources":null,"formats":["application/pdf"],"contributors":["Miguel-Vázquez, C. 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