Análise espaço-temporal da doença de Chagas e seus fatores de risco ambientais e demográficos no município de Barcarena, Pará, Brasil

To the Federal University of Pará (UFPA), to the Laboratory of Epidemiology and Geoprocessing (EpiGeo) of the University of the State of Pará (UEPA), to the Laboratory of Geoprocessing of the Evandro Chagas Institute (LabGeo/IEC), to the Health Department of the Municipality of Barcarena (SESMUB), to the Coordination for the Improvement of Higher Education Personnel (CAPES) and the National Council for Scientific and Technological Development (CNPq).Universidade do Estado do Pará. Belém, PA, Brazil.Universidade do Estado do Pará. Belém, PA, Brazil.Universidade do Estado do Pará. Belém, PA, Brazil.Universidade do Estado do Pará. Belém, PA, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Secretaria Municipal de Saúde de Barcarena. Barcarena, PA, Brazil.Universidade do Estado do Pará. Belém, PA, Brazil.Universidade do Estado do Pará. Belém, PA, Brazil.Introduction: Chagas disease is a parasitosis considered a serious problem of public health. In the municipality of Barcarena, Pará, from 2007 to 2014, occurred the highest prevalence of this disease in Brazil. Objective: To analyze the disease distribution related to epidemiological, environmental and demographic variables, in the area and period of the study. Methods: Epidemiological and demographic data of Barcarena Health Department and satellite images from the National Institute For Space Research (INPE) were used. The deforestation data were obtained through satellite image classification, using artificial neural network. The statistical significance was done with the χ2 test, and the spatial dependence tests among the variables were done using Kernel and Moran techniques. Results: The epidemiological curve indicated a disease seasonal pattern. The major percentage of the cases were in male, brown skin color, adult, illiterate, urban areas and with probable oral contamination. It was confirmed the spatial dependence of the disease cases with the different types of deforestation identified in the municipality, as well as agglomerations of cases in urban and rural areas. Discussion: The disease distribution did not occur homogeneously, possibly due to the municipality demographic dynamics, with intense migratory flows that generates the deforestation. Conclusion: Different relationships among the variables studied and the occurrence of the disease in the municipality were observed. The technologies used were satisfactory to construct the disease epidemiological scenarios

A human neurodevelopmental model for Williams syndrome

Williams syndrome (WS) is a genetic neurodevelopmental disorder characterized by an uncommon hypersociability and a mosaic of retained and compromised linguistic and cognitive abilities. Nearly all clinically diagnosed individuals with WS lack precisely the same set of genes, with breakpoints in chromosome band 7q11.23(1–5). The contribution of specific genes to the neuroanatomical and functional alterations, leading to behavioral pathologies in humans, remains largely unexplored. Here, we investigate neural progenitor cells (NPCs) and cortical neurons derived from WS and typically developing (TD) induced pluripotent stem cells (iPSCs). WS NPCs have an increased doubling time and apoptosis compared to TD NPCs. Using an atypical WS subject(6, 7), we narrowed this cellular phenotype to a single gene candidate, FZD9. At the neuronal stage, WS-derived layers V/VI cortical neurons were characterized by longer total dendrites, increased numbers of spines and synapses, aberrant calcium oscillation and altered network connectivity. Morphometric alterations observed in WS neurons were validated after Golgi staining of postmortem layers V/VI cortical neurons. This human iPSC model(8) fills in the current knowledge gap in WS cellular biology and could lead to further insights into the molecular mechanism underlying the disorder and the human social brain