Think Olga: reflections on the cyberfeminist role in brazil

El presente artículo tiene como objetivo identificar la presencia del ciberfeminismo en la Website de la Organización No Gubernamental (ONG) brasileña Think Olga, por medio de acciones que contribuyen con el debate, el empoderamiento y el protagonismo de las mujeres en Internet. A partir de la revisión bibliográfica sobre ciberfeminismo, el artículo realiza un análisis de contenido del site de la ONG para identificar contenidos volcados para el empoderamiento de las mujeres. Concluye que la Think Olga es una iniciativa ciberfeminista que utiliza diversos recursos disponibles en la red para problematizar la cuestión de la mujer en pro de la igualdad entre los géneros.This article aims to identify the presence of cyberfeminism on the website of the Brazilian NGO Think Olga, through actions that contribute to the debate, empowering and leading women on the Internet. Based on the bibliographic review on cyberfeminism, the article carries out a content analysis of the NGO website to identify content intended for the empowerment of women. She concludes that Think Olga is a cyberfeminist initiative that uses various resources available in the network to challenge the issue of women for gender equality. Key words: cyberfeminism. Journalism. Equality. Think Olga NGO

RNA-sequencing suggests extracellular matrix and vasculature dysregulation could impair neurogenesis in schizophrenia cases with elevated inflammation

International audienceA subgroup of schizophrenia cases with elevated inflammation have reduced neurogenesis markers and increased macrophage density in the human subependymal zone (SEZ; also termed subventricular zone or SVZ) neurogenic niche. Inflammation can impair neurogenesis; however, it is unclear which other pathways are associated with reduced neurogenesis. This research aimed to discover transcriptomic differences between inflammatory subgroups of schizophrenia in the SEZ. Total RNA sequencing was performed on SEZ tissue from schizophrenia cases, designated into low inflammation ( n = 13) and high inflammation ( n = 14) subgroups, based on cluster analysis of inflammation marker gene expression. 718 genes were differentially expressed in high compared to low inflammation schizophrenia (FDR p < 0.05) and were most significantly over-represented in the pathway ‘Hepatic Fibrosis/Hepatic Stellate-Cell Activation’. Genes in this pathway relate to extracellular matrix stability (including ten collagens) and vascular remodelling suggesting increased angiogenesis. Collagen-IV, a key element of the basement membrane and fractones, had elevated gene expression. Immunohistochemistry revealed novel collagen-IV+ fractone bulbs within the human SEZ hypocellular gap. Considering the extracellular matrix’s regulatory role in SEZ neurogenesis, fibrosis-related alterations in high inflammation schizophrenia may disrupt neurogenesis. Increased angiogenesis could facilitate immune cell transmigration, potentially explaining elevated macrophages in high inflammation schizophrenia. This discovery-driven analysis sheds light on how inflammation may contribute to schizophrenia neuropathology in the neurogenic niche