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 performed RNA-seq and proteomics on naturally infested green ash (F. pennsylvanica) trees at low, medium and high levels of increasing emerald ash borer (A. planipennis) infestation. Our integrative analysis of the RNA-Seq and proteomics data identified 14 proteins and 4 transcripts that contribute most to the difference between highly infested and low infested trees.
Project description:The goal of our study was to determine the effect the TRPV1 I585V SNP has on lung cells. NHBE cells, obtained from 4 different donor (Lonza), were genotyped to identify the presence of the TRPV1 SNP I585V. Of the 4 patient samples, 2 were heterozygous for the I585V SNP and 2 expressed WT TRPV1. These cells were plated in 12 well plates and treated with Coal Fly Ash (CFA) at multiple concentrations and capsasian. Differences between the patient samples were assessed.
Project description:ASH-1 orthologs are H3K36-specific methyltransferases that are conserved from fungi to humans but are poorly understood, in part because they are typically essential for viability. Here we examine the H3K36 methylation pathway of Neurospora crassa, which we find has just two H3K36 methyltransferases, ASH-1 and RNA polymerase II-associated SET-2. Our investigation of the interplay between SET-2 and ASH-1 uncovered a regulatory mechanism connecting ASH-1-catalyzed H3K36 methylation to repression of poorly transcribed genes. Our findings provide new insight into ASH-1 function, H3K27me2/3 establishment, and repression at facultative heterochromatin.
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.
