21 research outputs found
Acciones gubernamentales frente al cambio climático en la ciudad de Medellín durante el período 2000- 2019
Maestría en Desarrollo Sostenible y Medio Ambiente, Facultad de Ciencias Contables Económicas y Administrativas.El presente estudio tiene como objetivo, analizar las acciones gubernamentales dirigidas a las estrategias de mitigación y adaptación del cambio climático en la ciudad de Medellín durante el período 2000- 2019. El método utilizado fue a partir del análisis documental y entrevistas con representantes públicos de las diferentes secretarías locales y regionales, responsables del tema. Se concluyó que si bien logra evidenciarse, una acentuación sobre aspectos de salud pública y de gestión ambiental en los diferentes planes de desarrollo local durante los períodos analizados, su articulación como tal, con el cambio climático o variabilidad climática, solo se hace visible en el Plan de Desarrollo Medellín Cuenta con Vos 2016-2019, en el cual aparece claramente definido y articulado el concepto de Salud Ambiental, desde aspectos como calidad del agua, vectores, seguridad alimentaria y contaminación atmosférica
Diagnóstico de la calidad del agua para la cuenca baja del río quindío con macroinvertebrados acuáticos como indicadores ambientales
El agua es la base de la vida. Desde la creación del mundo todos los seres han necesitado de este elemento por formar parte de su composición, para su mantenimiento o bien como medio de vida. (Seoanez, 1999). Pero la actividad humana casi por definición altera el entorno, y en especial las corrientes superficiales (ríos y quebradas), que actúan como colectores naturales de los desechos, siendo estos los ambientes mas afectados.
Existen distintos tipos de alteraciones, que pueden afectar los ambientes acuáticos, pero en general casi todos ellos causan algún daño a la calidad de vida de sus habitantes. Por ello se han ideado distintos medios para su control y evaluación; uno de ellos es la utilización de los organismos que viven permanentemente en el río y que se ven afectados por alteraciones a veces mínimas. (Domínguez, 1997).Introducción1. Objetivos2. Marco Teórico3. Estado del arte4. MetodologíaPregradoLicenciado en Biología y Educación Ambienta
Violencias basadas en género: la otra tragedia de Colombia
This book, a product of academic and discursive activity, develops five chapters of scientific dissemination in which it presents an interdisciplinary analysis of the phenomena that extend in gender violence against women. The first chapter deals with the factual circumstances for the imputation of femicide in Colombia; the second chapter constructs a clinical psychological approach to the aggressor; the third chapter establishes an analysis of femicide from the logics of evolutionary and developmental psychology; the fourth chapter refers to the warp and woof of the brand of violence against women; the fifth chapter analyzes the cultural, social and educational elements of hegemonic machismo as a precipitating, maintaining and creating factor of violence against women.
This publication seeks to contribute to the social, academic and scientific expansion of gender-based violence as another of Colombia's most atrocious tragedies that require a refined view on the part of divergent and critically grounded thinking.PublishedEste libro, producto de la actividad académica y discursiva, desarrolla cinco capítulos de divulgación científica en los cuales presenta un análisis interdisciplinario de los fenómenos que se extienden en las violencias basadas en género en contra de la mujer. El primer capítulo trabaja las circunstancias fácticas para la imputación del feminicidio en Colombia; el segundo construye una aproximación clínica psicológica del feminicida, el tercero establece un análisis del feminicidio desde las lógicas de la psicología evolutiva y del desarrollo, el cuarto refiere las urdimbres a propósito de la marca de violencia en contra de la mujer; el quinto capítulo analiza los elementos culturales, sociales y educativos del machismo hegemónico como factor precipitador, mantenedor y creador de las violencias en contra de la mujer.
Con esta publicación se busca contribuir a la expansión social, académica y científica de las violencias basadas en género como otra de las tragedias más atroces de Colombia que requieren de miradas afinadas por parte del pensamiento divergente y crítico fundamentado
The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism.
International audienceAlthough multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions
Convergence of Genes and Cellular Pathways Dysregulated in Autism Spectrum Disorders.
International audienceRare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 × 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 × 10(-15), ∼3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation
A novel approach of homozygous haplotype sharing identifies candidate genes in autism spectrum disorder
Autism spectrum disorder (ASD) is a highly heritable disorder of complex and heterogeneous aetiology. It is primarily characterized by altered cognitive ability including impaired language and communication skills and fundamental deficits in social reciprocity. Despite some notable successes in neuropsychiatric genetics, overall, the high heritability of ASD (~90%) remains poorly explained by common genetic risk variants. However, recent studies suggest that rare genomic variation, in particular copy number variation, may account for a significant proportion of the genetic basis of ASD. We present a large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD. Our strategy, homozygous haplotype (HH) mapping, aims to detect homozygous segments of identical haplotype structure that are shared at a higher frequency amongst ASD patients compared to parental controls. The analysis was performed on 1,402 Autism Genome Project trios genotyped for 1 million single nucleotide polymorphisms (SNPs). We identified 25 known and 1,218 novel ASD candidate genes in the discovery analysis including CADM2, ABHD14A, CHRFAM7A, GRIK2, GRM3, EPHA3, FGF10, KCND2, PDZK1, IMMP2L and FOXP2. Furthermore, 10 of the previously reported ASD genes and 300 of the novel candidates identified in the discovery analysis were replicated in an independent sample of 1,182 trios. Our results demonstrate that regions of HH are significantly enriched for previously reported ASD candidate genes and the observed association is independent of gene size (odds ratio 2.10). Our findings highlight the applicability of HH mapping in complex disorders such as ASD and offer an alternative approach to the analysis of genome-wide association data
Analysis of shared heritability in common disorders of the brain
ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders
Volumen 18 Número 1
Revista seriada del Instituto Humboldt en asocio con el Invemar, el Instituto de Ciencias Naturales (ICN) y el Missouri Botanical Garden, como una estrategia para ampliar la base del conocimiento de uno de los países con mayor diversidad biológica del mundo.
Inicia como una publicación de listados de especies pero en 2005 amplía su espectro temático hacia la sistemática y la biogeografía. En 2010, a propósito del Año Internacional de la Biodiversidad y en pro del conocimiento, la conservación y el uso sostenible de la biodiversidad, se abre a un público más amplio, considerando trabajos inéditos de investigación sobre botánica, zoología, ecología, biología, limnología, pesquerías, conservación, manejo de recursos y uso de la biodiversidad, con buena aceptación por parte de la comunidad científica y académica. En 2013, en asocio con el SiB Colombia y con el apoyo de la GBIF, se institucionaliza la inclusión de Artículos de Datos (Data Papers) en Biota Colombiana
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The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism
Although multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions
Biota Colombiana Volumen 18 No. 1 (2017)
Volumen 18 Número 1 de la revista Biota ColombianaBogotá, Colombi