28 research outputs found

    Congenital Zika syndrome is associated with maternal protein malnutrition

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    Zika virus (ZIKV) infection during pregnancy is associated with a spectrum of developmental impairments known as congenital Zika syndrome (CZS). The prevalence of this syndrome varies across ZIKV endemic regions, suggesting that its occurrence could depend on cofactors. Here, we evaluate the relevance of protein malnutrition for the emergence of CZS. Epidemiological data from the ZIKV outbreak in the Americas suggest a relationship between undernutrition and cases of microcephaly. To experimentally examine this relationship, we use immunocompetent pregnant mice, which were subjected to protein malnutrition and infected with a Brazilian ZIKV strain. We found that the combination of protein restriction and ZIKV infection leads to severe alterations of placental structure and embryonic body growth, with offspring displaying a reduction in neurogenesis and postnatal brain size. RNA-seq analysis reveals gene expression deregulation required for brain development in infected low-protein progeny. These results suggest that maternal protein malnutrition increases susceptibility to CZS.Fil: Barbeito Andrés, Jimena. Universidade Federal do Rio de Janeiro; Brasil. Universidad Nacional Arturo Jauretche. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos. Provincia de Buenos Aires. Ministerio de Salud. Hospital Alta Complejidad en Red El Cruce Dr. Néstor Carlos Kirchner Samic. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos; ArgentinaFil: Pezzuto, Paula. Universidade Federal do Rio de Janeiro; BrasilFil: Higa, Luiza. Universidade Federal do Rio de Janeiro; BrasilFil: Dias, André Alves. Universidade Federal do Rio de Janeiro; BrasilFil: Vasconcelos, Janaina. Universidade Federal do Parå; BrasilFil: Santos, T. M. P.. Universidade Federal do Rio de Janeiro; BrasilFil: Ferreira, Jéssica. Universidade Federal do Rio de Janeiro; BrasilFil: Ferreira, R. O.. Universidade Federal do Rio de Janeiro; BrasilFil: Dutra, F. F.. Universidade Federal do Rio de Janeiro; BrasilFil: Rossi, A. D.. Universidade Federal do Rio de Janeiro; BrasilFil: Barbosa, R. V.. Universidade Federal Do Rio de Janeiro. Centro Nacional de Biologia Estrutural E Bioimagem.; BrasilFil: Amorim, C. K. N.. Evandro Chagas Institute; BrasilFil: de Souza, M. P. C.. Evandro Chagas Institute; BrasilFil: Chimelli, L.. Instituto Estadual do Cérebro Paulo Niemeyer ; BrasilFil: Aguiar, R. S.. Universidade Federal do Rio de Janeiro; BrasilFil: Gonzalez, Paula Natalia. Universidad Nacional Arturo Jauretche. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos. Provincia de Buenos Aires. Ministerio de Salud. Hospital Alta Complejidad en Red El Cruce Dr. Néstor Carlos Kirchner Samic. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Unidad Ejecutora de Estudios en Neurociencias y Sistemas Complejos; ArgentinaFil: Lara, F. A.. Oswaldo Cruz Institute; BrasilFil: Castro, M.C.. Harvard University. Harvard School of Public Health; Estados UnidosFil: Molnår, Z.. University of Oxford; Reino UnidoFil: Lopes, R. T.. Universidade Federal do Rio de Janeiro; BrasilFil: Bozza, M. T.. Universidade Federal do Rio de Janeiro; BrasilFil: Vianez, J. L. S. G.. Evandro Chagas Institute; BrasilFil: Barbeito, Claudio Gustavo. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; ArgentinaFil: Cuervo, P.. Oswaldo Cruz Institute; BrasilFil: Bellio, M.. Universidade Federal do Rio de Janeiro; BrasilFil: Tanuri, A.. Universidade Federal do Rio de Janeiro; BrasilFil: Garcez, P. P.. Universidade Federal do Rio de Janeiro; Brasi

    IDENTIFICACIÓN DEL GEN QUE CODIFICA PARA LA PROTEÍNA KMP-11 DE Crithidia spp.: COMPARACIÓN CON SUS ORTÓLOGOS DE OTROS TRIPANOSOMÁTIDOS

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    Kinetoplastida order comprises a group of organisms characterized by the presence of extra-nuclear DNAknown as kinetoplast. Within this highly divergent family of protozoa, the trypanosomatids include manygenera of economical and medical interest since they are pathogenic for humans, plants and insects.Genus Crithidia is formed by a group of monogenetic parasites found in the digestive tract of arthropods.Recent studies have shown the conservative character of the kinetoplastid membrane protein-11 (KMP-11) and its biological and immunological importance in the context of its association with the trypanosomatidmembrane. In this paper, Crithidia spp. KMP-11 protein genes were sequenced. The Crithidia spp. KMP-11 genes have a 279 bp open reading frame which codes for a protein with a molecular weight of 11 kDa.This protein shows a high identity with its orthologues in other trypanosomatids. Phylogenetic analyses,based on the coding nucleotide sequence, support the polyphyletic character of Crithidia genus given thatit is more closely related to T. rangeli, T. cruzi and T. brucei than to Leishmania

    Manquements au droit Ă  l’information du sujet ĂągĂ© cognitivement dĂ©pendant

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    International audienceRĂ©sumĂ© Les auteurs rappellent qu’un des droits fondamentaux du sujet ĂągĂ© cognitivement dĂ©pendant est celui d’ĂȘtre informĂ© clairement de ce qui le concerne (santĂ©, finances, entourage) mais ce droit peut ĂȘtre aisĂ©ment mĂ©connu. Ceci relĂšve sans doute d’intentions altruistes (Ă©viter des souffrances) mais ne prend guĂšre en compte les effets dĂ©lĂ©tĂšres occasionnĂ©s dĂšs lors que le sujet n’est plus considĂ©rĂ© comme acteur de sa propre vie. Ainsi nous pouvons considĂ©rer trois exemples de situations courantes de mĂ©sinformation du sujet ĂągĂ© cognitivementdĂ©pendant : l’annonce du diagnostic de maladie neurocognitive et notamment de maladie d’Alzheimer (annonce partielle ou au seul profit de l’entourage) ; l’absence d’annonce du dĂ©cĂšs d’un proche (enfant-conjoint) dĂšs lors que le sujet ĂągĂ© prĂ©sente une altĂ©ration cognitive patente ; le manque de clartĂ© dans l’annonce de l’institutionnalisation. Cet exposĂ© n’a pas vocation Ă  juger des comportements soignants, mĂ©dicaux ou d’aidants mais Ă  tĂ©moigner des limites d’un systĂšme de prise en soin, marquĂ© par le manque, sinon l’absence, de contrĂŽlesjuridiques concernant notamment l’institutionnalisation

    On the role of age of onset and input in early child bilingualism in Greek and Dutch

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    Although input quantity has been shown to affect language development in bilingual acquisition (e.g., Cobo-Lewis et al. 2002, De Houwer 2008), the relationship between the amount of input and linguistic proficiency is not necessarily direct (e.g., Thordadottir 2008). Furthermore, input effects may be mediated by and interact with other factors. One such factor is age of onset (AO). In particular, it has recently been claimed that the morphosyntactic development of children with AO after 4 years is quantitatively and qualitatively different from those with AO before this age (Meisel 2009). This paper reports on a crosslinguistic study of the acquisition of grammatical gender in English/Dutch and English/Greek bilinguals to examine the effects of input quantity and AO in early child bilingualism
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