Los 'fueguinos', Robert Lehmann-Nitsche y el estudio de los onas en la Exposición Nacional de Buenos Aires (1898)

Entre los primeros trabajos del antropólogo alemán Robert Lehmann-Nitsche como jefe del Departamento de Antropología del Museo de La Plata, Argentina, se cuentan las investigaciones sobre los habitantes de Tierra del Fuego, considerados como un 'relicto' evolutivo de la humanidad. Se repasa la importancia de las ferias y exposiciones como espacios de popularización científica y de 'trabajo de campo' para los estudiosos de fines del siglo XIX y principios del XX. Se examina la presentación de los 'fueguinos' en los espacios de las ferias y exposiciones europeas, los debates, los estudios realizados en Europa y el trabajo de Robert Lehmann-Nitsche en la Exposición Nacional de la Industria Argentina (Buenos Aires, 1898).Among the first projects of German anthropologist Robert Lehmann-Nitsche as head of the Museum de La Plata's Department of Anthropology in Argentina was his research on the inhabitants of Tierra del Fuego, deemed evolutionary 'relics' of humanity. The article explores the role of shows and exhibits as spaces where science was popularized and where late nineteenth- and early twentieth-century scholars could do field work. The focus is on the presentation of 'fueguinos' at European shows and exhibits, debates, and studies, especially the work of Robert Lehmann-Nitsche at the National Exhibit of Argentinean Industry, held in Buenos Aires, 1898

Wild-type microglia do not reverse pathology in mouse models of Rett syndrome

Rett syndrome (RTT) is a severe neurodevelopmental disorder caused by mutations in the X chromosomal gene Methyl-CpG-binding Protein 2 (MECP2) (1). RTT treatment so far is symptomatic. Mecp2 disruption in mice phenocopies major features of the syndrome (2) that can be reversed upon re-expression of Mecp2 (3. It has recently been reported that transplantation of wild type (WT) bone marrow (BMT) into lethally irradiated Mecp2tm1.1Jae/y mice prevented neurologic decline and early death by restoring microglial phagocytic activity against apoptotic targets (4). Based on this report, clinical trials of BMT for patients with RTT have been initiated (5). We aimed to replicate and extend the BMT experiments in three different RTT mouse models but found that despite robust microglial engraftment, BMT from WT donors did not rescue early death or ameliorate neurologic deficits. Furthermore, early and specific genetic expression of Mecp2 in microglia did not rescue Mecp2-deficient mice. In conclusion our experiments do not support BMT as therapy for RTT