Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload

Autores
Maniscalchi, Athina; Benzi Juncos, Oriana Nicole; Conde, Melisa Ailén; Funk, Melania Iara; Alza, Natalia Paola; Salvador, Gabriela Alejandra
Año de publicación
2023
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Iron (Fe) accumulation in specific brain areas and ferroptosis are associated with various neurodegenerative disorders. We have previously established an in vivo model of Fe overload (C57BL/6 mice treated with Fe 333 mg/kg) with midbrain neurodegeneration and lipid cacostasis. Our aim was to study the link between lipid metabolism alterations and ferroptosis taking into account neuroglial metabolism. In midbrain of Fe-overloaded animals, we detected a decrease in the expression of SLC7A11 and an increase in ACSL4 (p<0.001), both markers of ferroptosis. We found that cholesterol (chol) was elevated in midbrain of Fe-treated mice, coincidentally with SREBP2 and ABCA1 upregulation (p<0.001). In addition, increased levels of CPT1c (p<0.001) were observed after Fe overload, indicating an enhanced β-oxidation for the removal of fatty acid released by lipolysis. In the open field test, Fe-overloaded mice displayed motor impairment, with a lower rearing activity, a shorter time spent in the central square, and a longer time in the periphery (p<0.001). Next, we investigated chol metabolism in dopaminergic neurons and astrocytes exposed to Fe overload with ferric citrate ammonium (FAC). Chol content in neurons (N27), astrocytes (C6), and mouse primary glial culture was increased both in intracellular compartments as well as in secretomes after Fe treatment (p<0.001). This rise correlated with an increase in chol de novo synthesis and transport, respectively, by means of HMGCR and ABCA1 upregulation (p<0.001). To study the link between chol accumulation and ferroptosis, cells were exposed to the inhibitor ferrostatin (FER). We found that FER reduced chol levels when cells were exposed to FAC (p<0.001). Our findings indicate that altered chol metabolism could be a biomarker of midbrain neurodegeneration triggered by ferroptosis, with motor impairment as a final outcome
Fil: Maniscalchi, Athina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Benzi Juncos, Oriana Nicole. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Conde, Melisa Ailén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Funk, Melania Iara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Alza, Natalia Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Química; Argentina
Fil: Salvador, Gabriela Alejandra. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Reunión Conjunta SAIC SAB AAFE AACYTAL 2023; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); XXV Jornadas Anuales de la Sociedad Argentina de Biología (SAB); LV Reunión Anual de la Asociación Argentina de Farmacología Experimental (AAFE); VIII Reunión Científica Regional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio (AACYTAL)
Mar del Plata
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Biología
Asociación Argentina de Farmacología Experimental
Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio
Materia
CHOLESTEROL
MIDBRAIN
NEURODEGENERATION
IRON
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/228687
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overloadManiscalchi, AthinaBenzi Juncos, Oriana NicoleConde, Melisa AilénFunk, Melania IaraAlza, Natalia PaolaSalvador, Gabriela AlejandraCHOLESTEROLMIDBRAINNEURODEGENERATIONIRONhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Iron (Fe) accumulation in specific brain areas and ferroptosis are associated with various neurodegenerative disorders. We have previously established an in vivo model of Fe overload (C57BL/6 mice treated with Fe 333 mg/kg) with midbrain neurodegeneration and lipid cacostasis. Our aim was to study the link between lipid metabolism alterations and ferroptosis taking into account neuroglial metabolism. In midbrain of Fe-overloaded animals, we detected a decrease in the expression of SLC7A11 and an increase in ACSL4 (p<0.001), both markers of ferroptosis. We found that cholesterol (chol) was elevated in midbrain of Fe-treated mice, coincidentally with SREBP2 and ABCA1 upregulation (p<0.001). In addition, increased levels of CPT1c (p<0.001) were observed after Fe overload, indicating an enhanced β-oxidation for the removal of fatty acid released by lipolysis. In the open field test, Fe-overloaded mice displayed motor impairment, with a lower rearing activity, a shorter time spent in the central square, and a longer time in the periphery (p<0.001). Next, we investigated chol metabolism in dopaminergic neurons and astrocytes exposed to Fe overload with ferric citrate ammonium (FAC). Chol content in neurons (N27), astrocytes (C6), and mouse primary glial culture was increased both in intracellular compartments as well as in secretomes after Fe treatment (p<0.001). This rise correlated with an increase in chol de novo synthesis and transport, respectively, by means of HMGCR and ABCA1 upregulation (p<0.001). To study the link between chol accumulation and ferroptosis, cells were exposed to the inhibitor ferrostatin (FER). We found that FER reduced chol levels when cells were exposed to FAC (p<0.001). Our findings indicate that altered chol metabolism could be a biomarker of midbrain neurodegeneration triggered by ferroptosis, with motor impairment as a final outcomeFil: Maniscalchi, Athina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Benzi Juncos, Oriana Nicole. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Conde, Melisa Ailén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Funk, Melania Iara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Alza, Natalia Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Química; ArgentinaFil: Salvador, Gabriela Alejandra. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaReunión Conjunta SAIC SAB AAFE AACYTAL 2023; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); XXV Jornadas Anuales de la Sociedad Argentina de Biología (SAB); LV Reunión Anual de la Asociación Argentina de Farmacología Experimental (AAFE); VIII Reunión Científica Regional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio (AACYTAL)Mar del PlataArgentinaSociedad Argentina de Investigación ClínicaSociedad Argentina de BiologíaAsociación Argentina de Farmacología ExperimentalAsociación Argentina de Ciencia y Tecnología de Animales de LaboratorioFundación Revista MedicinaLuthy, Isabel AliciaPerez Martinez, Silvina LauraSimonovich, VenturaPinto, Gabriel2023info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/228687Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload; Reunión Conjunta SAIC SAB AAFE AACYTAL 2023; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); XXV Jornadas Anuales de la Sociedad Argentina de Biología (SAB); LV Reunión Anual de la Asociación Argentina de Farmacología Experimental (AAFE); VIII Reunión Científica Regional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio (AACYTAL); Mar del Plata; Argentina; 2023; 147-1470025-76801669-9106CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.saic.org.ar/reuniones-anuales-previasNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T12:59:48Zoai:ri.conicet.gov.ar:11336/228687instacron: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:34982025-09-10 12:59:48.727CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
title Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
spellingShingle Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
Maniscalchi, Athina
CHOLESTEROL
MIDBRAIN
NEURODEGENERATION
IRON
title_short Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
title_full Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
title_fullStr Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
title_full_unstemmed Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
title_sort Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload
dc.creator.none.fl_str_mv Maniscalchi, Athina
Benzi Juncos, Oriana Nicole
Conde, Melisa Ailén
Funk, Melania Iara
Alza, Natalia Paola
Salvador, Gabriela Alejandra
author Maniscalchi, Athina
author_facet Maniscalchi, Athina
Benzi Juncos, Oriana Nicole
Conde, Melisa Ailén
Funk, Melania Iara
Alza, Natalia Paola
Salvador, Gabriela Alejandra
author_role author
author2 Benzi Juncos, Oriana Nicole
Conde, Melisa Ailén
Funk, Melania Iara
Alza, Natalia Paola
Salvador, Gabriela Alejandra
author2_role author
author
author
author
author
dc.contributor.none.fl_str_mv Luthy, Isabel Alicia
Perez Martinez, Silvina Laura
Simonovich, Ventura
Pinto, Gabriel
dc.subject.none.fl_str_mv CHOLESTEROL
MIDBRAIN
NEURODEGENERATION
IRON
topic CHOLESTEROL
MIDBRAIN
NEURODEGENERATION
IRON
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Iron (Fe) accumulation in specific brain areas and ferroptosis are associated with various neurodegenerative disorders. We have previously established an in vivo model of Fe overload (C57BL/6 mice treated with Fe 333 mg/kg) with midbrain neurodegeneration and lipid cacostasis. Our aim was to study the link between lipid metabolism alterations and ferroptosis taking into account neuroglial metabolism. In midbrain of Fe-overloaded animals, we detected a decrease in the expression of SLC7A11 and an increase in ACSL4 (p<0.001), both markers of ferroptosis. We found that cholesterol (chol) was elevated in midbrain of Fe-treated mice, coincidentally with SREBP2 and ABCA1 upregulation (p<0.001). In addition, increased levels of CPT1c (p<0.001) were observed after Fe overload, indicating an enhanced β-oxidation for the removal of fatty acid released by lipolysis. In the open field test, Fe-overloaded mice displayed motor impairment, with a lower rearing activity, a shorter time spent in the central square, and a longer time in the periphery (p<0.001). Next, we investigated chol metabolism in dopaminergic neurons and astrocytes exposed to Fe overload with ferric citrate ammonium (FAC). Chol content in neurons (N27), astrocytes (C6), and mouse primary glial culture was increased both in intracellular compartments as well as in secretomes after Fe treatment (p<0.001). This rise correlated with an increase in chol de novo synthesis and transport, respectively, by means of HMGCR and ABCA1 upregulation (p<0.001). To study the link between chol accumulation and ferroptosis, cells were exposed to the inhibitor ferrostatin (FER). We found that FER reduced chol levels when cells were exposed to FAC (p<0.001). Our findings indicate that altered chol metabolism could be a biomarker of midbrain neurodegeneration triggered by ferroptosis, with motor impairment as a final outcome
Fil: Maniscalchi, Athina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Benzi Juncos, Oriana Nicole. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Conde, Melisa Ailén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Funk, Melania Iara. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Alza, Natalia Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Química; Argentina
Fil: Salvador, Gabriela Alejandra. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Reunión Conjunta SAIC SAB AAFE AACYTAL 2023; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); XXV Jornadas Anuales de la Sociedad Argentina de Biología (SAB); LV Reunión Anual de la Asociación Argentina de Farmacología Experimental (AAFE); VIII Reunión Científica Regional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio (AACYTAL)
Mar del Plata
Argentina
Sociedad Argentina de Investigación Clínica
Sociedad Argentina de Biología
Asociación Argentina de Farmacología Experimental
Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio
description Iron (Fe) accumulation in specific brain areas and ferroptosis are associated with various neurodegenerative disorders. We have previously established an in vivo model of Fe overload (C57BL/6 mice treated with Fe 333 mg/kg) with midbrain neurodegeneration and lipid cacostasis. Our aim was to study the link between lipid metabolism alterations and ferroptosis taking into account neuroglial metabolism. In midbrain of Fe-overloaded animals, we detected a decrease in the expression of SLC7A11 and an increase in ACSL4 (p<0.001), both markers of ferroptosis. We found that cholesterol (chol) was elevated in midbrain of Fe-treated mice, coincidentally with SREBP2 and ABCA1 upregulation (p<0.001). In addition, increased levels of CPT1c (p<0.001) were observed after Fe overload, indicating an enhanced β-oxidation for the removal of fatty acid released by lipolysis. In the open field test, Fe-overloaded mice displayed motor impairment, with a lower rearing activity, a shorter time spent in the central square, and a longer time in the periphery (p<0.001). Next, we investigated chol metabolism in dopaminergic neurons and astrocytes exposed to Fe overload with ferric citrate ammonium (FAC). Chol content in neurons (N27), astrocytes (C6), and mouse primary glial culture was increased both in intracellular compartments as well as in secretomes after Fe treatment (p<0.001). This rise correlated with an increase in chol de novo synthesis and transport, respectively, by means of HMGCR and ABCA1 upregulation (p<0.001). To study the link between chol accumulation and ferroptosis, cells were exposed to the inhibitor ferrostatin (FER). We found that FER reduced chol levels when cells were exposed to FAC (p<0.001). Our findings indicate that altered chol metabolism could be a biomarker of midbrain neurodegeneration triggered by ferroptosis, with motor impairment as a final outcome
publishDate 2023
dc.date.none.fl_str_mv 2023
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Congreso
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/228687
Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload; Reunión Conjunta SAIC SAB AAFE AACYTAL 2023; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); XXV Jornadas Anuales de la Sociedad Argentina de Biología (SAB); LV Reunión Anual de la Asociación Argentina de Farmacología Experimental (AAFE); VIII Reunión Científica Regional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio (AACYTAL); Mar del Plata; Argentina; 2023; 147-147
0025-7680
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/228687
identifier_str_mv Upregulation of cholesterol metabolism as a hallmark of midbrain neurodegeneration induced by iron overload; Reunión Conjunta SAIC SAB AAFE AACYTAL 2023; LXVIII Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); XXV Jornadas Anuales de la Sociedad Argentina de Biología (SAB); LV Reunión Anual de la Asociación Argentina de Farmacología Experimental (AAFE); VIII Reunión Científica Regional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio (AACYTAL); Mar del Plata; Argentina; 2023; 147-147
0025-7680
1669-9106
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.saic.org.ar/reuniones-anuales-previas
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
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eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.coverage.none.fl_str_mv Nacional
dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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