Habitar Montevideo: 21 miradas sobre la ciudad. Coordinadores: Aguiar, Sebastián; Borrás, Víctor; Cruz, Pablo; Fernández Gabard, Lucía; Pérez Sánchez, Marcelo. 2019. 1ª edición, Montevideo. La Diaria. 606 p.

En el prólogo de este libro, titulado «Caleidoscopio montevideano», Ramiro Segura propone algunos conceptos que permiten reflexionar sobre esta publicación. La noción de caleidoscopio de autores y de miradas sobre un espacio concreto que menciona el prologuista, también puede hacerse extensible al caleidoscopio de posibles receptores, como así también para diferentes acciones a nivel social. Por esto, Habitar Montevideo es un libro de producción y de lecturas interdisciplinarias, de allí que esta reseña sea una mirada más sobre el conjunto de los textos; puesto que, al igual que su producción, la recepción será más o menos especializada sobre un área u otra, por tratarse de un libro que presenta lo que se está haciendo en varios ámbitos, principalmente desde de la Universidad de la República (Udelar), como una de las posibilidades de la extensión universitaria, aunque en sí mismos muchos de los proyectos desde los que parten los textos son proyectos de extensión. Es un libro que toca intereses de todas las clases y de todos los actores que conforman el espacio montevideano, que permite ver de distintos lugares dónde se está parado y observar las orientaciones para seguir adelante. Estos textos también, en su mayoría, surgen de proyectos en proceso o dejan abiertas posibilidades para continuar abordando en el futuro cada una de sus temáticas. Con solo mencionar las orientaciones de las que provienen los autores de los diferentes capítulos se advierte inmediatamente aquel caleidoscopio: arquitectura, sociología, trabajo social, política, psicología, economía, derecho, geografía, letras, comunicación, filosofía y antropología. Como ya había concebido el geógrafo brasileño Milton Santos: «el espacio es el más interdisciplinar de los objetos concretos»(Santos, 1996, p. 59).Imagen de portada: Notable con amantes / técnica mixta y collage sobre mdf (cm. 49 × 40

Memory improvement in the AβPP/PS1 mouse model of familial Alzheimer's disease induced by carbamylated-erythropoietin is accompanied by modulation of synaptic genes

Neuroprotection of erythropoietin (EPO) following long-term administration is hampered by the associated undesirable effects on hematopoiesis and body weight. For this reason, we tested carbamylated-EPO (CEPO), which has no effect on erythropoiesis, and compared it with EPO in the AβPP/PS1 mouse model of familial Alzheimer's disease. Groups of 5-month-old wild type (WT) and transgenic mice received chronic treatment consisting of CEPO (2,500 or 5,000 UI/kg) or EPO (2,500 UI/kg) 3 days/week for 4 weeks. Memory at the end of treatment was assessed with the object recognition test. Microarray analysis and quantitative-PCR were used for gene expression studies. No alterations in erythropoiesis were observed in CEPO-treated WT and AβPP/PS1 transgenic mice. EPO and CEPO improved memory in AβPP/PS1 animals. However, only EPO decreased amyloid-β (Aβ) plaque burden and soluble Aβ40. Microarray analysis of gene expression revealed a limited number of common genes modulated by EPO and CEPO. CEPO but not EPO significantly increased gene expression of dopamine receptors 1 and 2, and adenosine receptor 2a, and significantly down-regulated adrenergic receptor α1D and gastrin releasing peptide. CEPO treatment resulted in higher protein levels of dopamine receptors 1 and 2 in WT and AβPP/PS1 animals, whereas the adenosine receptor 2a was reduced in WT animals. The present results suggest that the improved behavior observed in AβPP/PS1 transgenic mice after CEPO treatment may be mediated, at least in part, by the observed modulation of the expression of molecules involved in neurotransmission

Identification of the GlialCAM interactome: the G protein-coupled receptors GPRC5B and GPR37L1 modulate megalencephalic leukoencephalopathy proteins

Megalencephalic Leukoencephalopathy with subcortical Cysts (MLC) is a type of vacuolating leukodystrophy, which is mainly caused by mutations in MLC1 or GLIALCAM. The two MLC-causing genes encode for membrane proteins of yet unknown function that have been linked to the regulation of different chloride channels such as the ClC-2 and VRAC. To gain insight into the role of MLC proteins, we have determined the brain GlialCAM interacting proteome. The proteome includes different transporters and ion channels known to be involved in the regulation of brain homeostasis, proteins related to adhesion or signaling as several G protein-coupled receptors (GPCRs), including the orphan GPRC5B and the proposed prosaposin receptor GPR37L1. Focusing on these two GPCRs, we could validate that they interact directly with MLC proteins. The inactivation of Gpr37l1 in mice upregulated MLC proteins without altering their localization. Conversely, a reduction of GPRC5B levels in primary astrocytes downregulated MLC proteins, leading to an impaired activation of ClC-2 and VRAC. The interaction between the GPCRs and MLC1 was dynamically regulated upon changes in the osmolarity or potassium concentration. We propose that GlialCAM and MLC1 associate with different integral membrane proteins modulating their functions and acting as a recruitment site for various signaling components as the GPCRs identified here. We hypothesized that the GlialCAM/MLC1 complex is working as an adhesion molecule coupled to a tetraspanin-like molecule performing regulatory effects through direct binding or influencing signal transduction events

Megalencephalic leukoencephalopathy with subcortical cysts: a personal biochemical retrospective

Megalencephalic leukoencephalopathy with subcortical cysts (MLC) is a rare type of leukodystrophy characterized by dysfunction of the role of glial cells in controlling brain fluid and ion homeostasis. Patients affected by MLC present macrocephaly, cysts and white matter vacuolation, which lead to motor and cognitive impairments. To date, there is no treatment for MLC, only supportive care. MLC is caused by mutations in the MLC1 and GLIALCAM genes. MLC1 is a membrane protein with low identity to the Kv1.1 potassium channel and GlialCAM belongs to an adhesion molecule family. Both proteins form a complex with an as-yet-unknown function that is expressed mainly in the astrocytes surrounding the blood-brain barrier and in Bergmann glia. GlialCAM also acts as an auxiliary subunit of the chloride channel ClC-2, thus regulating its localization at cell-cell junctions and modifying its functional properties by affecting the common gate of ClC-2. Recent studies in Mlc1-,GlialCAM-and Clcn2-knockout mice or Mlc1- knockout zebrafish have provided fresh insight into the pathophysiology of MLC and further details about the molecular interactions between these three proteins. Additional studies have shown that GlialCAM/MLC1 also regulates other ion channels (TRPV4, VRAC) or transporters (Na+/K+-ATPase) in a not-understood manner. Furthermore, it has been shown that GlialCAM/ MLC1 may influence signal transduction mechanisms, thereby affecting other proteins not related with transport such as the EGFreceptor. Here, we offer a personal biochemical retrospective of the work that has been performed to gain knowledge of the pathophysiology of MLC, and we discuss future strategies that may be used to identify therapeutic solutions for MLC patients

Versificar para el común en el siglo XIX : los epigramas de Francisco Acuña de Figueroa

Durante casi doscientos años, Francisco Acuña de Figueroa (1791-1862) ha generado diversos problemas en la crítica literaria uruguaya y es objeto de estudio y de polémica de todas las generaciones que lo sucedieron, desde los más jóvenes intelectuales de su época. En este trabajo se estudiarán sus epigramas, a los que el poeta dedicó el mayor empeño en los últimos años de su vida y se mostrará cómo estos más de mil quinientos poemas, destinados para un público mucho más amplio que el restringido al lector “culto”, representan un alejamiento del proyecto modernizador del siglo XIX.Francisco Acuña de Figueroa (1791-1862) has been a sore spot for Uruguayan literary criticism for almost two hundred years. He has been subject of study and a source of controversy for all subsequent generations, starting with the younger intellectuals of his own time. This work studies his epigrams, to which the poet dedicated himself in his twilight years; it will be shown how these more than 1 500 poems —targeted not at the “cultured reader” but at a wider audience— entail a departure from the modernizing project of the 19th century