11 research outputs found
The global and national burden of chronic kidney disease attributable to ambient fine particulate matter air pollution: A modelling study
Introduction: We aimed to integrate all available epidemiological evidence to characterise an exposure-response model of ambient fine particulate matter (PM
Methods: We collected data from prior studies on the association of PM
Results: The exposure-response function exhibited evidence of an increase in risk with increasing PM
Conclusion: The global burden of CKD attributable to P
Persistence of Sulfadoxine-Pyrimethamine Resistance Despite Reduction of Drug Pressure in Malawi
A comprehensive survey of polymorphisms conferring anti-malarial resistance in Plasmodium falciparum
Author Correction: Convergent Pathways in Idiopathic Autism Revealed by Time Course Transcriptomic Analysis of Patient-Derived Neurons
MOESM1 of The effect of local variation in malaria transmission on the prevalence of sulfadoxine–pyrimethamine resistant haplotypes and selective sweep characteristics in Malawi
Additional file 1: DHFR and DHPS microsatellite haplotypes. Description: Table of DHFR and DHPS microsatellite haplotypes. Reference strains V1S, 3D7 and HB3. “C”=Chikwawa, rural-high, “T”=Thyolo, rural-moderate, and “N”=Ndirande, urban-low. Mita 2011 (22) and Alam 2011 (21) refer to other publications which provide microsatellite haplotypes identified and shared between Southeast Asian and Malawian parasites at the pfdhps locus
Convergent Pathways in Idiopathic Autism Revealed by Time Course Transcriptomic Analysis of Patient-Derived Neurons
Potentially pathogenic alterations have been identified in individuals with autism spectrum disorders (ASDs) within a variety of key neurodevelopment genes. While this hints at a common ASD molecular etiology, gaps persist in our understanding of the neurodevelopmental mechanisms impacted by genetic variants enriched in ASD patients. Induced pluripotent stem cells (iPSCs) can model neurodevelopment in vitro, permitting the characterization of pathogenic mechanisms that manifest during corticogenesis. Taking this approach, we examined the transcriptional differences between iPSC-derived cortical neurons from patients with idiopathic ASD and unaffected controls over a 135-day course of neuronal differentiation. Our data show ASD-specific misregulation of genes involved in neuronal differentiation, axon guidance, cell migration, DNA and RNA metabolism, and neural region patterning. Furthermore, functional analysis revealed defects in neuronal migration and electrophysiological activity, providing compelling support for the transcriptome analysis data. This study reveals important and functionally validated insights into common processes altered in early neuronal development and corticogenesis and may contribute to ASD pathogenesis