Articulando saberes con los pueblos originarios en la Argentina

El presente trabajo intenta dar cuenta de reflexiones en torno a la producción de conocimiento surgidas a partir de una determinada práctica antropológica en tanto miembros del Programa Permanente de Extensión, Investigación y Desarrollo en Comunidades Indígenas de la Facultad de Filosofía y Letras de la UBA. El objetivo general del Programa es vincular y articular en forma sistemática y permanente proyectos y actividades de investigación en distintos campos del conocimiento con acciones de fortalecimiento comunitario, capacitación y práctica solidaria. A lo largo de más de 20 años la perspectiva desde la cual abordamos las diversas acciones, se ha ido modificando de manera paralela, por un lado, a los niveles de compromiso que fuimos adquiriendo a medida que el trabajo se desarrollaba, y por otro, a las condiciones sociohistóricas que lo enmarcaban. Por último, nuestro trabajo ha estado condicionado por las particulares situaciones que fue atravesando la universidad, en especial la práctica extensionista. Por ello, se intentará dar cuenta de la discusión entre diferentes perspectivas sobre el significado y objetivos de la extensión universitaria y la práctica de la misma, así como la necesidad de su jerarquización. Uno de los proyectos más importantes de nuestro espacio – el Observatorio Colectivo para Pueblos Originarios (OCOPO)- se encuentra inserto en el ámbito universitario pero con el involucramiento y la participación permanente y orgánica de comunidades y organizaciones de pueblos originarios, y asume las tareas de: diagnosticar las problemáticas que atraviesan a dichos pueblos, relevar y sistematizar las políticas públicas a ellos referidas, promover la vinculación entre las diferentes organizaciones y/o comunidades, acompañar las iniciativas de las mismas, tendiendo a su fortalecimiento organizativo. Asimismo, este proyecto nos ha permitido tanto profundizar la relación con diversas organizaciones y comunidades indígenas del país, como dar cuenta de los diferentes conflictos, haciendo visible la cuestión indígena. Atendiendo a nuestra trayectoria, algunas de las preguntas que nos pueden guiar en el camino de la reflexión acerca de nuestra forma de entender el quehacer antropológico: ¿en calidad de qué somos “demandados” por los pueblos originarios?; ¿por qué construir un espacio de estas características al interior del ámbito académico universitario?; ¿qué rol tenemos en el marco de la coyuntura académico-política particular que nos atraviesa, y en términos históricos más generales?GT50: Antropólogxs y arqueólogxs en proyectos de extensión universitaria y de comunicación científica. Redes, apropiaciones y tensiones.Universidad Nacional de La Plat

Encontrarse, compartir, construir: notas en torno a la práctica de la extensión universitaria con pueblos originarios

Desde Tartagal hasta Maquinchao hay, de acuerdo a los buscadores de Internet, 2.641.4 kilómetros. En un vehículo veloz representaría unos tres días con sus noches (y tres más de vuelta) unir estos puntos del mapa. En avión se tarda menos pero en realidad no tanto menos, porque un viaje suele empezar mucho antes de subir a ese avión o a cualquier otro medio de transporte. Viajar desde Tartagal o las riberas del Pilcomayo en Salta, hasta el pie de la meseta de Somuncurá, en Río Negro, implica un esfuerzo de voluntad, cuerpo y logística que pocos conocemos. Y también encierra una decisión colectiva, política, organizativa que va más allá de cada persona que viaja, porque no viaja quien lo desea sino quien el colectivo al que pertenece designa. En general, ni siquiera conocemos del todo las historias de quienes emprenden ese viaje, sino solo pequeños tramos, fragmentos de un recorrido que empieza, como decíamos, días antes de partir. Porque antes de salir hay que organizar los compromisos y las obligaciones, resolver quién va a cuidar de los parientes, la huerta o el empleo, hacerse el tiempo y el coraje para abandonar la ciudad o el paraje, subir a un colectivo, o más de uno, que vaya a una ciudad donde hay aeropuerto, pasar escáneres y cacheos, tomar el avión. El camino inverso, viajar de Maquinchao a Salta, es igual de complicado. Hay que abandonar el campo y eso, a algunos, les lleva días de preparativos. Participar de un encuentro de dos o tres días de duración representa quizáunos diez días de abandonar el hogar desde que se traspone la puerta con el bolso hasta que se retorna. Y, sobre todo, expresa una decisión que es producto, y a la vez alimento, de un colectivo. En este artículo queremos dar cuenta de algunas de las prácticas de extensión que desarrollamos desde el Programa Universitario Permanente de Investigación, Extensión y Desarrollo en Comunidades Indígenas de Argentina (Facultad de Filosofía y Letras, Universidad de Buenos Aires), en el marco del Observatorio Colectivo para Pueblos Originarios (OCOPO), iniciativa de nuestro espacio. Y ofrecer algunas reflexiones en torno de los esfuerzos, los resultados y los tiempos de esa práctica de la extensión. Para eso, vamos a narrar algunas instancias y referencias de la trayectoria de nuestro Programa, pero también del desarrollo de dos de los numerosos encuentros entre comunidades y organizaciones indígenas de distintos puntos del país, en cuya articulación y realización colaboramos. Uno se desarrolló en Tartagal, Salta, en 2019. El otro, en Maquinchao, Rio Negro, en 2020. Y la participación implicó el viaje de miembros de comunidades y organizaciones de Río Negro a Salta en 2019 y, a la inversa, de miembros de comunidades y organizaciones de Salta a Río Negro en 2020, justo antes del inicio de las restricciones forzadas por la pandemia.Fil: González, Crispina. Universidad de Buenos Aires. Facultad de Filosofía y Letras; ArgentinaFil: Iñigo Carrera, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Patagonia Norte. Instituto de Investigaciones en Diversidad Cultural y Procesos de Cambio. Universidad Nacional de Río Negro. Instituto de Investigaciones en Diversidad Cultural y Procesos de Cambio; Argentina. Universidad de Buenos Aires. Facultad de Filosofía y Letras; ArgentinaFil: Picciotto, Cecilia. Universidad de Buenos Aires. Facultad de Filosofía y Letras; ArgentinaFil: Schiaffini, Hernán. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Filosofía y Letras; ArgentinaFil: Verzoub, Martín Hernán. Universidad de Buenos Aires. Facultad de Filosofía y Letras; ArgentinaFil: Leguizamón, Juan Martín. Universidad de Buenos Aires. Facultad de Filosofía y Letras; Argentin

Deficits in bioenergetics and impaired immune response in granulocytes from children with autism.

Despite the emerging role of mitochondria in immunity, a link between bioenergetics and the immune response in autism has not been explored. Mitochondrial outcomes and phorbol 12-myristate 13-acetate (PMA)-induced oxidative burst were evaluated in granulocytes from age-, race-, and gender-matched children with autism with severity scores of ≥7 (n = 10) and in typically developing (TD) children (n = 10). The oxidative phosphorylation capacity of granulocytes was 3-fold lower in children with autism than in TD children, with multiple deficits encompassing ≥1 Complexes. Higher oxidative stress in cells of children with autism was evidenced by higher rates of mitochondrial reactive oxygen species production (1.6-fold), higher mitochondrial DNA copy number per cell (1.5-fold), and increased deletions. Mitochondrial dysfunction in children with autism was accompanied by a lower (26% of TD children) oxidative burst by PMA-stimulated reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and by a lower gene expression (45% of TD children's mean values) of the nuclear factor erythroid 2-related factor 2 transcription factor involved in the antioxidant response. Given that the majority of granulocytes of children with autism exhibited defects in oxidative phosphorylation, immune response, and antioxidant defense, our results support the concept that immunity and response to oxidative stress may be regulated by basic mitochondrial functions as part of an integrated metabolic network

Deficits in bioenergetics and impaired immune response in granulocytes from children with autism.

Despite the emerging role of mitochondria in immunity, a link between bioenergetics and the immune response in autism has not been explored. Mitochondrial outcomes and phorbol 12-myristate 13-acetate (PMA)-induced oxidative burst were evaluated in granulocytes from age-, race-, and gender-matched children with autism with severity scores of ≥7 (n = 10) and in typically developing (TD) children (n = 10). The oxidative phosphorylation capacity of granulocytes was 3-fold lower in children with autism than in TD children, with multiple deficits encompassing ≥1 Complexes. Higher oxidative stress in cells of children with autism was evidenced by higher rates of mitochondrial reactive oxygen species production (1.6-fold), higher mitochondrial DNA copy number per cell (1.5-fold), and increased deletions. Mitochondrial dysfunction in children with autism was accompanied by a lower (26% of TD children) oxidative burst by PMA-stimulated reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and by a lower gene expression (45% of TD children's mean values) of the nuclear factor erythroid 2-related factor 2 transcription factor involved in the antioxidant response. Given that the majority of granulocytes of children with autism exhibited defects in oxidative phosphorylation, immune response, and antioxidant defense, our results support the concept that immunity and response to oxidative stress may be regulated by basic mitochondrial functions as part of an integrated metabolic network

Reproductive and Developmental Effects Associated with Chronic Arsenic Exposure

Chronic exposure to inorganic arsenic (Asi) is known to cause cancer and non-cancer health effects in humans. The evidence from animal studies clearly shows that As is teratogenic, and the findings of limited human studies suggest that Asi may be associated with several reproductive/developmental outcomes including increased rates of spontaneous abortion, low birth weight, congenital malformations, preeclampsia, and infant mortality. The city of Antofagasta, located in northern Chile, has a history of high As exposure in drinking water. Due to changes in the sources of water, there were considerably high As levels in the public drinking water supply from 1958 to 1970 (over 800 μg/L), which decreased gradually to the current concentrations close to 50 μg/L. A number of studies have reported various health effects associated with the high exposure period, including skin alterations typically linked to As exposure and increases in bladder and lung cancer. An ecologic study was conducted of infant mortality rates in Chile from 1950 to 1996, comparing Antofagasta to the low As exposure areas. Temporal and cross-regional comparisons showed a general steady decline over time in late fetal, neonatal, and post-neonatal mortality rates, for all locations, consistent with improvements in standard of living and health care. However, comparatively high rates were observed in Antofagasta for the three outcomes studied during the 12-year period of the highest As exposure, compared to Santiago and Valparaíso, two locations used as reference groups. While not definitive, these findings support a role for As in the observed increases in mortality rates

Role of p53

BACKGROUND: The tumor suppressor p53 responds to a variety of environmental stressors by regulating cell cycle arrest, apoptosis, senescence, DNA repair, bioenergetics and mitochondrial DNA (mtDNA) copy number maintenance. Developmental abnormalities have been reported in p53-deficient mice, and altered p53 and p53-associated pathways in autism (AU). Furthermore, via the Pten-p53 crosstalk, Pten haploinsufficient-mice have autisticlike behavior accompanied by brain mitochondrial dysfunction with accumulation of mtDNA deletions. METHODS: mtDNA copy number and deletions, and p53 gene copy ratios were evaluated in peripheral blood monocytic cells from children aged 2–5 years with AU (n = 66), race-, gender-, and age-matched typically neurodeveloping children (n = 46), and both parents from each diagnostic group, recruited by the Childhood Autism Risk from Genes and Environment study at the University of California, Davis. RESULTS: mtDNA deletions and higher p53 gene copy ratios were more common in children with AU and their fathers. The incidence of mtDNA deletions in fathers of children with AU was increased 1.9-fold over fathers of typically neurodeveloping children, suggesting a role for deficient DNA repair capacity not driven by paternal age. Deletions in mtDNA and altered p53 gene copy ratios seem to result from genetics (children with severity scores ≥8) and/or act in concert with environmental factors (children with 6–7 severity scores). CONCLUSIONS: Given pro- and antioxidant activities of p53, and associations of genomic instability with disorders other than AU, our study suggests a link between DNA repair capacity, genomic instability in the 17p13.1 region influenced by environmental triggers, and AU diagnosis

Role of p53, Mitochondrial DNA Deletions, and Paternal Age in Autism: A Case-Control Study.

BackgroundThe tumor suppressor p53 responds to a variety of environmental stressors by regulating cell cycle arrest, apoptosis, senescence, DNA repair, bioenergetics and mitochondrial DNA (mtDNA) copy number maintenance. Developmental abnormalities have been reported in p53-deficient mice, and altered p53 and p53-associated pathways in autism (AU). Furthermore, via the Pten-p53 crosstalk, Pten haploinsufficient-mice have autisticlike behavior accompanied by brain mitochondrial dysfunction with accumulation of mtDNA deletions.MethodsmtDNA copy number and deletions, and p53 gene copy ratios were evaluated in peripheral blood monocytic cells from children aged 2-5 years with AU (n = 66), race-, gender-, and age-matched typically neurodeveloping children (n = 46), and both parents from each diagnostic group, recruited by the Childhood Autism Risk from Genes and Environment study at the University of California, Davis.ResultsmtDNA deletions and higher p53 gene copy ratios were more common in children with AU and their fathers. The incidence of mtDNA deletions in fathers of children with AU was increased 1.9-fold over fathers of typically neurodeveloping children, suggesting a role for deficient DNA repair capacity not driven by paternal age. Deletions in mtDNA and altered p53 gene copy ratios seem to result from genetics (children with severity scores ≥8) and/or act in concert with environmental factors (children with 6-7 severity scores).ConclusionsGiven pro- and antioxidant activities of p53, and associations of genomic instability with disorders other than AU, our study suggests a link between DNA repair capacity, genomic instability in the 17p13.1 region influenced by environmental triggers, and AU diagnosis

Role of p53, Mitochondrial DNA Deletions, and Paternal Age in Autism: A Case-Control Study.

The tumor suppressor p53 responds to a variety of environmental stressors by regulating cell cycle arrest, apoptosis, senescence, DNA repair, bioenergetics and mitochondrial DNA (mtDNA) copy number maintenance. Developmental abnormalities have been reported in p53-deficient mice, and altered p53 and p53-associated pathways in autism (AU). Furthermore, via the Pten-p53 crosstalk, Pten haploinsufficient-mice have autisticlike behavior accompanied by brain mitochondrial dysfunction with accumulation of mtDNA deletions. mtDNA copy number and deletions, and p53 gene copy ratios were evaluated in peripheral blood monocytic cells from children aged 2-5 years with AU (n = 66), race-, gender-, and age-matched typically neurodeveloping children (n = 46), and both parents from each diagnostic group, recruited by the Childhood Autism Risk from Genes and Environment study at the University of California, Davis. mtDNA deletions and higher p53 gene copy ratios were more common in children with AU and their fathers. The incidence of mtDNA deletions in fathers of children with AU was increased 1.9-fold over fathers of typically neurodeveloping children, suggesting a role for deficient DNA repair capacity not driven by paternal age. Deletions in mtDNA and altered p53 gene copy ratios seem to result from genetics (children with severity scores ≥8) and/or act in concert with environmental factors (children with 6-7 severity scores). Given pro- and antioxidant activities of p53, and associations of genomic instability with disorders other than AU, our study suggests a link between DNA repair capacity, genomic instability in the 17p13.1 region influenced by environmental triggers, and AU diagnosis