Ontology highlight
ABSTRACT:
PROVIDER: PRJNA900446 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In the first decade of life, high-asthma risk urban children develop stable phenotypes of respiratory health versus disease that link early life environmental exposures to childhood allergic sensitization and asthma. Moreover, unique patterns of nasal gene expression demonstrate how specific molecular pathways underlie distinct respiratory phenotypes, including allergic and non-allergic asthma.
2021-04-01 | GSE145505 | GEO
Project description:Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical com position, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1(PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In partic ular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regu latory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu win ter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5;and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contrib utes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.
2022-10-30 | GSE216512 | GEO
Project description:Environmental cadmium, with a high average dietary intake, is a severe public health risk. However, the long-term health implications of environmental exposure to cadmium in different life stages remain unclear. We used microarrays to explore the effects of early exposure to low-dose cadmium on hepatic gene expression.
2016-12-31 | GSE83326 | GEO
Project description:Hepatitis B Virus constitutes a major threat to global public health by infecting hepatocytes, initiating and driving the progress to end-stage liver disease and liver cancer. Curing treatment for HBV infection is yet unavailable, mainly due to unmet gaps in current understanding of HBV-host interaction. Here, multi-omics interrogations were conducted to generate the first landscape of HBV-induced global changes in host transcriptome, translatome and proteome, which identified multiple translatomic events that HBV orchestrated to remodel host proteostasis networks and afford micro-environments essential for HBV proliferation and persistence.
2021-03-06 | PXD014908 | Pride
Project description:GenomeTrakr Project: State of Hawaii, Department of Health | Public Health & Environmental Laboratories
| PRJNA514065 | ENA
Project description:GenomeTrakr wastewater project: New Jersey Department of Health - Public Health and Environmental Laboratories
| PRJNA769667 | ENA