Análisis del discurso del cambio climático

79 p.El cambio climático es un fenómeno natural, el cual, debido a las acciones del ser humano, se ha visto acelerado, generando una serie de repercusiones que son nocivas y puede perjudicar la forma de vida de cada uno de los seres vivos que habitan el planeta. Esta investigación se basa en los informes de las Conferencias de las Partes (COP) de la Convención Mundial de las Naciones Unidas para el Cambio Climático (CMNUCC), en las cuales se juntan distintos países que son parte de las Naciones Unidas y buscan dar solución al avance del cambio climático y a las repercusiones previamente mencionadas. Dicha solución se basa en la creación de medidas, las cuales buscan que se detenga la aceleración de dicho fenómeno, y que los países o pueblos que son vulnerables o han sido afectados por estos cambios en el clima puedan adaptarse a estos. Para el estudio, se planteó la hipótesis de que debido a que el cambio climático pasó de ser una amenaza a una realidad que ya está presente, el discurso en lo relacionado a CMNUCC ha variado en las medidas, cambiando de mitigación a la adaptación del cambio climático. Los objetivos fijados a tratar en el estudio consisten en describir la evolución en el discurso sobre el cambio climático a partir de los informes, estudiando la evolución que hubo en estos y entendiendo las modificaciones que hubo, considerando el contexto en el que fueron generados. Para efecto de la investigación y poder comprobar la hipótesis, se hizo un análisis cualitativo de los informes, teniendo como principal material de estudio los informes de las COP, a partir de los cuales se hizo un análisis de discursos y un estudio de casos de lo que en estos se plasmaba, generando estadísticas de frecuencia de repetición de términos y analizando bases de datos creadas a partir de información relevante recopilada a partir de estos, pudiendo obtener tendencias de uso de términos clave y entender los contextos en los que fueron usados. Con los resultados obtenidos en esta investigación, se obtuvo información de que las medidas de adaptación no reemplazan a las de mitigación, sino que se suman y se complementan, haciendo más eficiente las acciones para el clima mundial de las partes de la CMNUCC

3D cell bioprinting of self-assembling peptide-based hydrogels

Bioprinting of 3D cell-laden constructs with well-defined architectures and controlled spatial distribution of cells is gaining importance in the field of Tissue Engineering. New 3D tissue models are being developed to study the complex cellular interactions that take place during both tissue development and in the regeneration of damaged and/or diseased tissues. Despite advances in 3D printing technologies, suitable hydrogels or ‘bioinks’ with enhanced printability and cell viability are lacking. Here we report a study on the 3D bioprinting of a novel group of self-assembling peptide-based hydrogels. Our results demonstrate the ability of the system to print well-defined 3D cell laden constructs with variable stiffness and improved structural integrity, whilst providing a cell-friendly extracellular matrix “like” microenvironment. Biological assays reveal that mammary epithelial cells remain viable after 7 days of in vitro culture, independent of the hydrogel stiffness

Metabolic dysregulation of the lysophospholipid/autotaxin axis in the chromosome 9p21 gene SNP rs10757274

Background - Common chromosome 9p21 SNPs increase coronary heart disease (CHD) risk, independent of 'traditional lipid risk factors'. However, lipids comprise large numbers of structurally related molecules not measured in traditional risk measurements, and many have inflammatory bioactivities. Here we applied lipidomic and genomic approaches to three model systems, to characterize lipid metabolic changes in common Chr9p21 SNPs which confer ~30% elevated CHD risk associated with altered expression of ANRIL, a long ncRNA. Methods - Untargeted and targeted lipidomics was applied to plasma from Northwick Park Heart Study II (NPHSII) homozygotes for AA or GG in rs10757274, followed by correlation and network analysis. To identify candidate genes, transcriptomic data from shRNA downregulation of ANRIL in HEK293 cells was mined. Transcriptional data from vascular smooth muscle cells differentiated from iPSCs of individuals with/without Chr9p21 risk, non-risk alleles, and corresponding knockout isogenic lines were next examined. Last, an in-silico analysis of miRNAs was conducted to identify how ANRIL might control lysoPL/lysoPA genes. Results - Elevated risk GG correlated with reduced lysophosphospholipids (lysoPLs), lysophosphatidic acids (lysoPA) and autotaxin (ATX). Five other risk SNPs did not show this phenotype. LysoPL-lysoPA interconversion was uncoupled from ATX in GG plasma, suggesting metabolic dysregulation. Significantly altered expression of several lysoPL/lysoPA metabolising enzymes was found in HEK cells lacking ANRIL. In the VSMC dataset, the presence of risk alleles associated with altered expression of several lysoPL/lysoPA enzymes. Deletion of the risk locus reversed expression of several lysoPL/lysoPA genes to non-risk haplotype levels. Genes that were altered across both cell datasets were DGKA, MBOAT2, PLPP1 and LPL. The in-silico analysis identified four ANRIL-regulated miRNAs that control lysoPL genes as miR-186-3p, miR-34a-3p, miR-122-5p, miR-34a-5p. Conclusions - A Chr9p21 risk SNP associates with complex alterations in immune-bioactive phospholipids and their metabolism. Lipid metabolites and genomic pathways associated with CHD pathogenesis in Chr9p21 and ANRIL-associated disease are demonstrated

Access and quality of parks and associations with obesity: A cross-sectional study.

Public health is increasingly engaging with multi-faceted obesity prevention efforts. Although parks represent key community assets for broader public health, they may not be distributed equitably and associations with obesity are equivocal. We investigated park access and quality relative to deprivation and obesity with individual-level data from the Yorkshire Health Study. Compared to the least deprived areas, the moderately and most deprived areas had a greater park access and park quality in terms of features and amenities. However, parks in the moderately and most deprived areas also had the most safety concerns and incivilities. Although deprivation was associated with obesity, contrary to current policy guidance, both park access and quality appear less important for understanding variations in obesity within this study. Although sub-group analyses by deprivation tertile revealed that low quality park amenities in highly and moderately deprived areas may be important for understanding obesity prevalence, all other associations were non-significant

Isolation and characterization of neurotoxic astrocytes derived from adult triple transgenic Alzheimer's disease mice

Alzheimer's disease has been considered mostly as a neuronal pathology, although increasing evidence suggests that glial cells might play a key role in the disease onset and progression. In this sense, astrocytes, with their central role in neuronal metabolism and function, are of great interest for increasing our understanding of the disease. Thus, exploring the morphological and functional changes suffered by astrocytes along the course of this disorder has great therapeutic and diagnostic potential. In this work we isolated and cultivated astrocytes from symptomatic 9-10-months-old adult 3xTg-AD mice, with the aim of characterizing their phenotype and exploring their pathogenic potential. These “old” astrocytes occurring in the 3xTg-AD mouse model of Alzheimer's Disease presented high proliferation rate and differential expression of astrocytic markers compared with controls. They were neurotoxic to primary neuronal cultures both, in neuronal-astrocyte co-cultures and when their conditioned media (ACM) was added into neuronal cultures. ACM caused neuronal GSK3β activation, changes in cytochrome c pattern, and increased caspase 3 activity, suggesting intrinsic apoptotic pathway activation. Exposure of neurons to ACM caused different subcellular responses. ACM application to the somato-dendritic domain in compartmentalised microfluidic chambers caused degeneration both locally in soma/dendrites and distally in axons. However, exposure of axons to ACM did not affect somato-dendritic nor axonal integrity. We propose that this newly described old 3xTg-AD neurotoxic astrocytic population can contribute towards the mechanistic understanding of the disease and shed light on new therapeutical opportunities

Metabolic Dysregulation of the Lysophospholipid/Autotaxin Axis in the Chromosome 9p21 Gene SNP rs10757274.

BackgroundCommon chromosome 9p21 single nucleotide polymorphisms (SNPs) increase coronary heart disease risk, independent of traditional lipid risk factors. However, lipids comprise large numbers of structurally related molecules not measured in traditional risk measurements, and many have inflammatory bioactivities. Here, we applied lipidomic and genomic approaches to 3 model systems to characterize lipid metabolic changes in common Chr9p21 SNPs, which confer ≈30% elevated coronary heart disease risk associated with altered expression of ANRIL, a long ncRNA.MethodsUntargeted and targeted lipidomics was applied to plasma from NPHSII (Northwick Park Heart Study II) homozygotes for AA or GG in rs10757274, followed by correlation and network analysis. To identify candidate genes, transcriptomic data from shRNA downregulation of ANRIL in HEK-293 cells was mined. Transcriptional data from vascular smooth muscle cells differentiated from induced pluripotent stem cells of individuals with/without Chr9p21 risk, nonrisk alleles, and corresponding knockout isogenic lines were next examined. Last, an in-silico analysis of miRNAs was conducted to identify how ANRIL might control lysoPL (lysophosphospholipid)/lysoPA (lysophosphatidic acid) genes.ResultsElevated risk GG correlated with reduced lysoPLs, lysoPA, and ATX (autotaxin). Five other risk SNPs did not show this phenotype. LysoPL-lysoPA interconversion was uncoupled from ATX in GG plasma, suggesting metabolic dysregulation. Significantly altered expression of several lysoPL/lysoPA metabolizing enzymes was found in HEK cells lacking ANRIL. In the vascular smooth muscle cells data set, the presence of risk alleles associated with altered expression of several lysoPL/lysoPA enzymes. Deletion of the risk locus reversed the expression of several lysoPL/lysoPA genes to nonrisk haplotype levels. Genes that were altered across both cell data sets were DGKA, MBOAT2, PLPP1, and LPL. The in-silico analysis identified 4 ANRIL-regulated miRNAs that control lysoPL genes as miR-186-3p, miR-34a-3p, miR-122-5p, and miR-34a-5p.ConclusionsA Chr9p21 risk SNP associates with complex alterations in immune-bioactive phospholipids and their metabolism. Lipid metabolites and genomic pathways associated with coronary heart disease pathogenesis in Chr9p21 and ANRIL-associated disease are demonstrated