Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts
- Autores
- Sequeyra, Aldana Soledad; Pieralisi, Azul Victoria; Cevey, Ágata Carolina; Mirkin, Gerardo Ariel Isidoro; Goren, Nora Beatriz; Penas, Federico Nicolás
- Año de publicación
- 2021
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Chronic chagasic cardiomyopathy is characterized by parasite persistence, chronic inflammation and cardiac cell (Mc) death that may end lead to fbrosis and cardiac insuffciency. Activated fbroblasts (Fb) are involved in this process. Previous results from our group show that fenonofbrate (Fen), a PPARalpha ligand, modulates the expression of inflammatory mediators, prevents fbrosis and restores cardiac function in Trypanosoma cruzi (Tc) -infected mice. To deepen into the knowledge of the role of Mc and Fb in these events, in the present work we used an in vitro model of neonatal murine cardiac cells. We studied the modulator role of Fen on the inflammatory response of Mc and Fb infected with Tc. Mc and Fb were characterized by the expression of troponin C and s alpha-SMA, respectively, using Western blot (Wb). Wb and RT-qPCR analysis showed that Tc stimulated the expression of pro-inflammatory and pro-fbrotic enzymes like NOS2 and MMP-9 in Mc and Fb, whereas treatment with Fen (100µM) inhibited such expression in both cell lineages. In addition, after 48 h of infection we observed increased expression of CTGF, MMP-2 and TGF-beta by RT-qPCR in Mc and Fb, whereas Fen inhibited such increment (p<0.05). Besides, the rise of TNF-alpha and IL-6 after 2 to 6h of infection was precluded by Fen. Furthermore, while NFkB was activated at 30 min post-infection in Mc and Fb since cytoplasmic IkBalpha was signifcantly reduced as determined by Wb, treatment with Fen precluded such activation. Finally, the ability of Mc- and Fb -conditioned media to promote the expression of NOS2 in Fb and Mc was analyzed. Both media induced the expression of NOS2 in Fb and Mc while Fen inhibited its expression as assessed by Wb. These results emphasize the role of Mc and Fb in the inflammatory and pro-fbrotic response to Tc and the interaction between these cell lineages that Fen is able to modulate.
Fil: Sequeyra, Aldana Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Pieralisi, Azul Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Cevey, Ágata Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Mirkin, Gerardo Ariel Isidoro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones en Microbiología y Parasitología Médica. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones en Microbiología y Parasitología Médica; Argentina
Fil: Goren, Nora Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
Fil: Penas, Federico Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina
XVI Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXIX Reunión Anual de la Sociedad Argentina de Inmunología; LIII Reunión Anual de La Asociación Argentina de Farmacología Experimental y XI Reunión Anual de la Asociación Argentina de Nanomedicinas
Ciudad Autónoma de Buenos Aires
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Inmunología
Asociación Argentina de Farmacología Experimental
Asociación Argentina de Nanomedicinas - Materia
-
FENOFIBRATE
CARDIOMYOCYES
FIBROBLASTS
CHAGAS - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/280743
Ver los metadatos del registro completo
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Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblastsSequeyra, Aldana SoledadPieralisi, Azul VictoriaCevey, Ágata CarolinaMirkin, Gerardo Ariel IsidoroGoren, Nora BeatrizPenas, Federico NicolásFENOFIBRATECARDIOMYOCYESFIBROBLASTSCHAGAShttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Chronic chagasic cardiomyopathy is characterized by parasite persistence, chronic inflammation and cardiac cell (Mc) death that may end lead to fbrosis and cardiac insuffciency. Activated fbroblasts (Fb) are involved in this process. Previous results from our group show that fenonofbrate (Fen), a PPARalpha ligand, modulates the expression of inflammatory mediators, prevents fbrosis and restores cardiac function in Trypanosoma cruzi (Tc) -infected mice. To deepen into the knowledge of the role of Mc and Fb in these events, in the present work we used an in vitro model of neonatal murine cardiac cells. We studied the modulator role of Fen on the inflammatory response of Mc and Fb infected with Tc. Mc and Fb were characterized by the expression of troponin C and s alpha-SMA, respectively, using Western blot (Wb). Wb and RT-qPCR analysis showed that Tc stimulated the expression of pro-inflammatory and pro-fbrotic enzymes like NOS2 and MMP-9 in Mc and Fb, whereas treatment with Fen (100µM) inhibited such expression in both cell lineages. In addition, after 48 h of infection we observed increased expression of CTGF, MMP-2 and TGF-beta by RT-qPCR in Mc and Fb, whereas Fen inhibited such increment (p<0.05). Besides, the rise of TNF-alpha and IL-6 after 2 to 6h of infection was precluded by Fen. Furthermore, while NFkB was activated at 30 min post-infection in Mc and Fb since cytoplasmic IkBalpha was signifcantly reduced as determined by Wb, treatment with Fen precluded such activation. Finally, the ability of Mc- and Fb -conditioned media to promote the expression of NOS2 in Fb and Mc was analyzed. Both media induced the expression of NOS2 in Fb and Mc while Fen inhibited its expression as assessed by Wb. These results emphasize the role of Mc and Fb in the inflammatory and pro-fbrotic response to Tc and the interaction between these cell lineages that Fen is able to modulate.Fil: Sequeyra, Aldana Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Pieralisi, Azul Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Cevey, Ágata Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Mirkin, Gerardo Ariel Isidoro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones en Microbiología y Parasitología Médica. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones en Microbiología y Parasitología Médica; ArgentinaFil: Goren, Nora Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaFil: Penas, Federico Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; ArgentinaXVI Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXIX Reunión Anual de la Sociedad Argentina de Inmunología; LIII Reunión Anual de La Asociación Argentina de Farmacología Experimental y XI Reunión Anual de la Asociación Argentina de NanomedicinasCiudad Autónoma de Buenos AiresArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de InmunologíaAsociación Argentina de Farmacología ExperimentalAsociación Argentina de NanomedicinasFundación Revista Medicina2021info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/280743Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts; XVI Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXIX Reunión Anual de la Sociedad Argentina de Inmunología; LIII Reunión Anual de La Asociación Argentina de Farmacología Experimental y XI Reunión Anual de la Asociación Argentina de Nanomedicinas; Ciudad Autónoma de Buenos Aires; Argentina; 2021; 114-1141669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.reunionbiociencias.com.ar/wp-content/uploads/2021/11/Revista-Medicina-2021.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2026-02-06T12:25:32Zoai:ri.conicet.gov.ar:11336/280743instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982026-02-06 12:25:32.51CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| title |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| spellingShingle |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts Sequeyra, Aldana Soledad FENOFIBRATE CARDIOMYOCYES FIBROBLASTS CHAGAS |
| title_short |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| title_full |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| title_fullStr |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| title_full_unstemmed |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| title_sort |
Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts |
| dc.creator.none.fl_str_mv |
Sequeyra, Aldana Soledad Pieralisi, Azul Victoria Cevey, Ágata Carolina Mirkin, Gerardo Ariel Isidoro Goren, Nora Beatriz Penas, Federico Nicolás |
| author |
Sequeyra, Aldana Soledad |
| author_facet |
Sequeyra, Aldana Soledad Pieralisi, Azul Victoria Cevey, Ágata Carolina Mirkin, Gerardo Ariel Isidoro Goren, Nora Beatriz Penas, Federico Nicolás |
| author_role |
author |
| author2 |
Pieralisi, Azul Victoria Cevey, Ágata Carolina Mirkin, Gerardo Ariel Isidoro Goren, Nora Beatriz Penas, Federico Nicolás |
| author2_role |
author author author author author |
| dc.subject.none.fl_str_mv |
FENOFIBRATE CARDIOMYOCYES FIBROBLASTS CHAGAS |
| topic |
FENOFIBRATE CARDIOMYOCYES FIBROBLASTS CHAGAS |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
Chronic chagasic cardiomyopathy is characterized by parasite persistence, chronic inflammation and cardiac cell (Mc) death that may end lead to fbrosis and cardiac insuffciency. Activated fbroblasts (Fb) are involved in this process. Previous results from our group show that fenonofbrate (Fen), a PPARalpha ligand, modulates the expression of inflammatory mediators, prevents fbrosis and restores cardiac function in Trypanosoma cruzi (Tc) -infected mice. To deepen into the knowledge of the role of Mc and Fb in these events, in the present work we used an in vitro model of neonatal murine cardiac cells. We studied the modulator role of Fen on the inflammatory response of Mc and Fb infected with Tc. Mc and Fb were characterized by the expression of troponin C and s alpha-SMA, respectively, using Western blot (Wb). Wb and RT-qPCR analysis showed that Tc stimulated the expression of pro-inflammatory and pro-fbrotic enzymes like NOS2 and MMP-9 in Mc and Fb, whereas treatment with Fen (100µM) inhibited such expression in both cell lineages. In addition, after 48 h of infection we observed increased expression of CTGF, MMP-2 and TGF-beta by RT-qPCR in Mc and Fb, whereas Fen inhibited such increment (p<0.05). Besides, the rise of TNF-alpha and IL-6 after 2 to 6h of infection was precluded by Fen. Furthermore, while NFkB was activated at 30 min post-infection in Mc and Fb since cytoplasmic IkBalpha was signifcantly reduced as determined by Wb, treatment with Fen precluded such activation. Finally, the ability of Mc- and Fb -conditioned media to promote the expression of NOS2 in Fb and Mc was analyzed. Both media induced the expression of NOS2 in Fb and Mc while Fen inhibited its expression as assessed by Wb. These results emphasize the role of Mc and Fb in the inflammatory and pro-fbrotic response to Tc and the interaction between these cell lineages that Fen is able to modulate. Fil: Sequeyra, Aldana Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Pieralisi, Azul Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Cevey, Ágata Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Mirkin, Gerardo Ariel Isidoro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones en Microbiología y Parasitología Médica. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones en Microbiología y Parasitología Médica; Argentina Fil: Goren, Nora Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina Fil: Penas, Federico Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas en Retrovirus y Sida. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas en Retrovirus y Sida; Argentina XVI Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXIX Reunión Anual de la Sociedad Argentina de Inmunología; LIII Reunión Anual de La Asociación Argentina de Farmacología Experimental y XI Reunión Anual de la Asociación Argentina de Nanomedicinas Ciudad Autónoma de Buenos Aires Argentina Sociedad Argentina de Investigación Clínica Sociedad Argentina de Inmunología Asociación Argentina de Farmacología Experimental Asociación Argentina de Nanomedicinas |
| description |
Chronic chagasic cardiomyopathy is characterized by parasite persistence, chronic inflammation and cardiac cell (Mc) death that may end lead to fbrosis and cardiac insuffciency. Activated fbroblasts (Fb) are involved in this process. Previous results from our group show that fenonofbrate (Fen), a PPARalpha ligand, modulates the expression of inflammatory mediators, prevents fbrosis and restores cardiac function in Trypanosoma cruzi (Tc) -infected mice. To deepen into the knowledge of the role of Mc and Fb in these events, in the present work we used an in vitro model of neonatal murine cardiac cells. We studied the modulator role of Fen on the inflammatory response of Mc and Fb infected with Tc. Mc and Fb were characterized by the expression of troponin C and s alpha-SMA, respectively, using Western blot (Wb). Wb and RT-qPCR analysis showed that Tc stimulated the expression of pro-inflammatory and pro-fbrotic enzymes like NOS2 and MMP-9 in Mc and Fb, whereas treatment with Fen (100µM) inhibited such expression in both cell lineages. In addition, after 48 h of infection we observed increased expression of CTGF, MMP-2 and TGF-beta by RT-qPCR in Mc and Fb, whereas Fen inhibited such increment (p<0.05). Besides, the rise of TNF-alpha and IL-6 after 2 to 6h of infection was precluded by Fen. Furthermore, while NFkB was activated at 30 min post-infection in Mc and Fb since cytoplasmic IkBalpha was signifcantly reduced as determined by Wb, treatment with Fen precluded such activation. Finally, the ability of Mc- and Fb -conditioned media to promote the expression of NOS2 in Fb and Mc was analyzed. Both media induced the expression of NOS2 in Fb and Mc while Fen inhibited its expression as assessed by Wb. These results emphasize the role of Mc and Fb in the inflammatory and pro-fbrotic response to Tc and the interaction between these cell lineages that Fen is able to modulate. |
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2021 |
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2021 |
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http://hdl.handle.net/11336/280743 Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts; XVI Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXIX Reunión Anual de la Sociedad Argentina de Inmunología; LIII Reunión Anual de La Asociación Argentina de Farmacología Experimental y XI Reunión Anual de la Asociación Argentina de Nanomedicinas; Ciudad Autónoma de Buenos Aires; Argentina; 2021; 114-114 1669-9106 CONICET Digital CONICET |
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Fenofibrate modulates inflammatory mediators as well as cross-talk between Trypanosoma cruzi- infected cardiomyocytes and fibroblasts; XVI Reunión Anual de la Sociedad Argentina de Investigación Clínica; LXIX Reunión Anual de la Sociedad Argentina de Inmunología; LIII Reunión Anual de La Asociación Argentina de Farmacología Experimental y XI Reunión Anual de la Asociación Argentina de Nanomedicinas; Ciudad Autónoma de Buenos Aires; Argentina; 2021; 114-114 1669-9106 CONICET Digital CONICET |
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eng |
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eng |
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