US Sewage Project
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB66906 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Global surveillance of infectious diseases and antimicrobial resistance from sewage
| PRJEB13831 | ENA
Project description:Local surveillance of infectious diseases and antimicrobial resistance from sewage
| PRJEB13832 | ENA
Project description:Surveillance of infectious diseases and antimicrobial resistance from sewage in Kibera (Nairobi, Kenya)
| PRJEB13833 | ENA
Project description:"Modeling the Role of Peroxisome Proliferator-Activated Receptor γ and MicroRNA-146 in Mucosal Immune Responses to Clostridium difficile"
Monica Viladomiu1,2, Raquel Hontecillas1,2, Mireia Pedragosa1,2, Adria Carbo1,2, Stefan Hoops1,2, Pawel Michalak4,5, Katarzyna Michalak4, Richard L. Guerrant2,3, James K. Roche2,3, Cirle A. Warren2,3, Josep Bassaganya-Riera1,2*
1) Nutritional Immunology and Molecular Medicine Laboratory, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 2) Center for Modeling Immunity to Enteric Pathogens, Virginia Tech, Blacksburg, Virginia, United States of America, 3) Division of Infectious Disease and International Health, Center for Global Health, University of Virginia, Charlottesville, Virginia, United States of America, 4) Medical Informatics and Systems Division, Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, Virginia, United States of America, 5) Department of Biological Sciences, Virginia Tech, Blacksburg, Virginia, United States of America
E-mail: jbassaga@vt.edu
This model represents the interaction between Cdiff, miRNA146b, NCOA4, PPARg, IL10 and IL17. Simulation studies show an aberrant expression of miRNA146b with increasing concentrations of Cdiff over time, which results in decreased PPARg activation due to NCOA4 inhibition. As a final result, PPARg is unable to modulate effector and regulatory responses, since results show an upregulation of IL17 expression and downregulation of IL10 production.
2005-01-01 | MODEL1210260004 | BioModels
Project description:The gut microbiome is associated with diverse diseases, but the universal signature of an (un)healthy microbiome remains elusive and there is a need to understand how genetics, exposome, lifestyle and diet shape the microbiome in health and disease. To fill this gap, we profiled bacterial composition, function, antibiotic resistance and virulence factors in the gut microbiomes of 8,208 Dutch individuals from a three-generational cohort comprising 2,756 families. We then correlated this to 241 host and environmental factors, including physical and mental health, medication use, diet, socioeconomic factors and childhood and current exposome.
| EGAS00001005027 | EGA
Project description:To validate the oligo array and to investigate the impact of the environmental stressors on dolphin health at transcriptomic level Collection of blood samples from wild animals in 4 different geographic locations of the South East of the United States
2014-03-26 | E-GEOD-50684 | biostudies-arrayexpress
Project description:Metagenomics analysis of sewage for surveillance of antimicrobial resistance in South Africa
| PRJEB70907 | ENA
Project description:Socioeconomic status (SES), living in poverty, and other social determinants of health contribute to health disparities in the United States. African American (AA) men living below poverty in Baltimore City have a higher incidence of mortality when compared to either white males or AA females living below poverty. Previous studies in our laboratory and elsewhere suggest that environmental conditions are associated with differential gene expression (DGE) patterns in white blood cells, and this may contribute to the onset of diseases in the immune or cardiovascular systems. DGE have also been associated with hypertension and cardiovascular disease (CVD) and correlate with race and gender. However, no studies have investigated how poverty status associates with DGE between male and female AAs and whites living in Baltimore City. We examined DGE in 52 AA and white participants of the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) cohort, who were living above or below 125% of the 2004 federal poverty line at time of sample collection. We performed a microarray to assess DGE patterns in peripheral blood mononuclear cells (PBMCs) from these participants. AA males and females living in poverty had the most genes differentially-expressed compared with above poverty controls. Gene ontology (GO) analysis identified unique and overlapping pathways related to the endosome, single-stranded RNA binding, long-chain fatty-acyl-CoA biosynthesis, toll-like receptor signaling, and others within AA males and females living in poverty and compared with their above poverty controls. We performed RT-qPCR to validate top differentially-expressed genes in AA males. We found that KLF6, DUSP2, RBM34, and CD19 are expressed at significantly lower levels in AA males in poverty and KCTD12 is higher compared to above poverty controls. This study serves as initial link to better understand the biological mechanisms of poverty status with health outcomes and disparities.
2020-10-02 | GSE149256 | GEO
Project description:Investigation of antimicrobial resistance in Escherichia species - ENGAGE Project
| PRJEB21131 | ENA
Project description:<p>The gut microbiota is increasingly recognized for playing a critical role in human health and disease, especially in conferring resistance to both virulent pathogens such as Salmonella, which infects 1.2 million people in the United States every year [1], and opportunistic pathogens like Candida, which causes an estimated 46,000 cases of invasive candidiasis each year in the United States [2]. The dynamics of pathogen-microbiome interactions and the metabolites involved in this process remain largely unknown. </p><p>We use gnotobiotic mice infected with the virulent pathogen Salmonella enterica serovar Typhimurium or the opportunistic pathogen Candida albicans in combination with metagenomics and discovery metabolomics to identify changes in the community and metabolome during infection. To isolate the role of the microbiota in response to pathogens, we compared mice monocolonized with the pathogen, uninfected mice 'humanized' with a synthetic human microbiome, or infected humanized mice. We observe that changes in the community and in biosynthetic gene cluster potential occur within 3 days for the virulent Salmonella enterica serovar Typhimurium, but there are minimal changes with a poorly colonizing Candida albicans. In addition, the metabolome shifts depending on infection status, including changes in glutathione metabolites in response to Salmonella infection. The LC-MS metabolomic fingerprint of the cecum differed between mice monocolonized with either pathogen and humanized infected mice. Specifically, we identified an increase in glutathione disulfide, glutathione cysteine disulfide, inosine 5'-monophosphate, and hydroxybutyrylcarnitine in mice infected with Salmonella in contrast to uninfected mice and mice monocolonized with Salmonella. These metabolites potentially play a role in pathogen-induced oxidative stress. These results provide insight into how the microbiota community members interact with each other and with pathogens on a metabolic level.</p><p><br></p><p>Ref:</p><p>[1] Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, and Griffin PM. Foodborne Illness Acquired in the United States—Major Pathogens. Emerg Infect Dis 2011;17:7-15. doi.org/10.3201/eid1701.P11101</p><p>[2] Centers for Disease Control and Prevention, Antibiotic Resistance Threats in the United States, 2013</p>
2019-09-20 | MTBLS753 | MetaboLights