Project description:Coal is a major energy source that generates diverse environmental impacts through its production, primarily by the release of coal dust particles. An aqueous coal dust extract was obtained from a mineral sample taken from one of the largest coal mines in Colombia (La Loma, Cesar), trace elements by ICP/MS were measured, and its toxicity evaluated using the zebrafish (Danio rerio) vertebrate model. In this study, zebrafish embryos were exposed to different concentrations of aqueous coal extract (0, 0.1, 1, 10, 100 and 1000 parts per million (ppm; μg/mL) to establish acute toxicity, as well as morphological and transcriptome alterations. Trace elements within the coal extract yielding the highest concentrations included Sr, Zn, Ba, As, Cu, Se, Li, Ni, Sb, Rb, Co, and Cr. In addition, Cd and Pb were found in lower concentrations. No significant difference in mortality was observed with survival near 90% in all treatments. A significant decrease in rate of hatching was observed in the 0.1 and 1000 ppm treatment groups at 72 hpf. Furthermore, no significant differences in total body length, head length, or head diameter was observed in any of the treatment groups. Transcriptomic results of zebrafish larvae revealed alterations in 77, 61, and 1,376 genes in the 1, 10, and 100 ppm treatments, respectively. Gene ontology analysis revealed gene alterations associated with hematological system development and function, tissue morphology and development, connective tissue development and function, and embryonic development. Overall, these findings are the first to identify gene expression alterations in response to a developmental aqueous coal dust residue from coal mining.
Project description:Coal mining carries inherent risks of catastrophic gas explosions capable of inflicting severe lung injury. Using a rat model, we explored mechanisms underlying alveolar epithelial damage and repair following a gas explosion. By performing scRNA-sequencing, we revealed that alveolar epithelial cells exhibited the most profound transcriptomic changes after gas explosion compared to other pulmonary cell types.
Project description:DNA, RNA and protein were extracted from the culture and subjected to massive parallel sequencing and nano-LC-MS-MS respectively Combination of these methods enabled the reconstruction of the complete genome sequence of M oxyfera from the metagenome and identification of the functionally relevant enzymes and genes
Project description:Exposure to indoor air pollution generated from the combustion of solid fuels is a major risk factor for a spectrum of cardiovascular and respiratory diseases, including lung cancer. In Chinaâs rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the country. While the elevated disease risk in this population has been linked to the widespread usage of bituminous (smoky) coal as compared to anthracite (smokeless) coal, the underlying physiologic mechanism that smoky coal induces in comparison to other fuel types is unclear. As we have previously used airway gene-expression profiling to gain molecular insights into the physiologic effects of cigarette smoke, here we profiled the buccal epithelium of residents exposed to the burning of smoky and smokeless coal in order to understand the physiologic effects of solid fuels. Buccal mucosa scrapings were collected from healthy, non-smoking female residents of Xuanwei and Fuyuan counties who burn coal indoors. RNA was isolated and hybridized onto Affymetrix Human gene 1.0 ST GeneChips, capturing the gene-expression response of (n=26) smoky coal users and (n=9) smokeless coal users. 24-hour indoor personal exposure levels (PM2.5, Polycyclic Aromatic Hydrocarbons) were also captured during this sampling period.
Project description:We investigated an in vitro experimental exposure model of the MutaMouse flat epithelial (FE1) cells exposed to a complex mixture of carcinogenic PAHs known as coal tar (SRM 1597a) using an Agilent 22k, oligo mouse array platform. Keywords: Toxicology, biomarkers discovery, stress response, complex mixture of carcinogens, PAHs The FE1 cells were exposed to two different sub-toxic concentrations of coal tar (SRM 1597a): 1 mg/ml and 4 mg/ml in a serum free media. After 6h exposure, the cells were washed twice with PBS and re-incubated in fresh media without coal tar. After 4h and 8h incubation, the media were collected for proteomic experiment and the cells were collected from the petri dishes for RNA extraction.
Project description:Exposure to indoor air pollution generated from the combustion of solid fuels is a major risk factor for a spectrum of cardiovascular and respiratory diseases, including lung cancer. In China’s rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the country. While the elevated disease risk in this population has been linked to the widespread usage of bituminous (smoky) coal as compared to anthracite (smokeless) coal, the underlying physiologic mechanism that smoky coal induces in comparison to other fuel types is unclear. As we have previously used airway gene-expression profiling to gain molecular insights into the physiologic effects of cigarette smoke, here we profiled the buccal epithelium of residents exposed to the burning of smoky and smokeless coal in order to understand the physiologic effects of solid fuels.