Ontology highlight
ABSTRACT:
PROVIDER: PRJNA992273 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25182132_1.fastq.gz | Fastqsanger.gz | |||
| SRR25182132_2.fastq.gz | Fastqsanger.gz | |||
| SRR25182133_1.fastq.gz | Fastqsanger.gz | |||
| SRR25182133_2.fastq.gz | Fastqsanger.gz | |||
| SRR25182134_1.fastq.gz | Fastqsanger.gz |
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Project description:Climate change is impacting human health through a historic rise in wildfire smoke across the United States and the world. Whereas the deleterious effects of wildfire smoke and associated air pollution on asthma outcomes are well-established epidemiologically, genetic risks and molecular mechanisms of how wildfire smoke affects asthma are unknown. This knowledge gap hinders the identification of high-risk individuals and the creation of targeted therapies or recommendations to protect these individuals. Here, we employ a genetic approach to identify common variant (minor allele frequency > 0.05) exposure-conditional genetic risk variants that localize with genomic responses to wood smoke particles (WSP), a model of wildfire smoke exposure, and associate with asthma in the Genetic Epidemiology Research on Aging (GERA) cohort. Our novel approach used nascent transcriptional signatures derived from WSP-exposed Beas-2B airway epithelial cells to reduce the genome sequence for discovery and allow a permutation-based statistical approach to identify 52 candidate SNPs. We applied biologic and bioinformatic filters to prioritize variants for direct testing of allele-dependent transcriptional regulatory function in plasmid reporters. The rs3861144 variant identified by this approach controls WSP responses of airway epithelial cells to SPRY2, which we showed is involved in mechanical injury repair in cell culture. Our results demonstrate that wildfire particulates contribute to asthma risk at the molecular level, and we have identified mechanistic targets and genetic variant candidates to apply for clinical risk prediction and development of targeted therapies for high-risk individuals.
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Project description:Scleractinian corals acquire autotrophic nutrients via the photosynthetic activity of their symbionts and the subsequent transfer of photosynthates. Zooplankton predation by the animal (heterotrophy) is an additional food source. Under stress events, corals loose their symbionts, a phenomena known as bleaching, which eventually leads to starvation, unless corals increase their heterotrophic capacities. Molecular mechanisms by which heterotrophy sustains metabolism in stressed corals remain elusive. Here for the first time, we identify specific genes expressed in heterotrophically fed and unfed corals maintained under normal and light-stress conditions inducing bleaching. Physiological parameters and gene expression profiling showed ominously that fed corals better resisted the stress than unfed corals, by presenting less oxidative damage and protein/DNA degradation. Light stressed and unfed/starved corals (HLS) up-regulated by 140 and 13 times two genes (CP2U1 and CP1A2), which belong to the Cytochrome P450 superfamily, while these genes remained almost unchanged in fed corals (HLF). Other genes of redox regulation, DNA damage response, molecular chaperones, and protein degradation were also up-regulated in HLS corals, presenting higher bleaching, and strong decrease of the photosynthesis performance compared to HLF corals. Several pivotal genes associated with the calcification apparatus such as carbonic anhydrases, calcium-transporting ATPase, calcium channel subunit, and bone morphogenetic proteins (BMPs), were significantly down-regulated only in HLS corals. A parallel decrease in the calcification rates of these later corals was also observed. All together, these results show clearly that heterotrophy helps preventing oxidative stress in corals, and thus avoid the cascade of metabolic problems downstream this stress.
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Project description:Increase in frequency and size of wildfire raises a significant public health concern due to rapid climate change. Epidemiological studies have shown that wildfire smoke exposure can increase the risk of neurological disorders. Our study aims to understand how wildfire smoke particles affect brain endothelial cells using both primary human brain microvascular endothelial cells (HBMEC) and an immortalized human cerebral microvascular endothelial cell line (hCMEC/D3). HBMEC and hCMEC/D3 were exposed to different levels of smoldering eucalyptus smoke particles (10, 30, 50 ug/mL) for 24 hr. Supernatants were collected for LDH and ELISA array, cell lysates were collected for RNAseq, and cells were fixed and stained for tight junction marker (Zonula Occludens-1, ZO-1) via ICC. Our study found that treatment to smoldering eucalyptus particles can increase inflammatory cytokine production dose-dependently in HBMECs and hCMEC/D3. Moreover, RNAseq analyses resulted in dose-dependent changes in HBMEC and hCMEC/D3 from wood smoke treatment that could be mediated via AhR and Nrf2 pathways.
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Project description:The Pacific Northwest (PNW) region contains approximately 97.5% of U.S. commercial hop acreage. In recent years, wildfire events have been increasing in both number and severity within the region. Currently, there is an extensive body of research from the wine industry on the impact of smoke taint in grapes, however, research investigating smoke taint in hops is limited. This study aims to characterize smoke taint in hops through laboratory simulated wildfire smoke exposure coupled with chemical profiling by nontargeted gas chromatography-mass spectrometry (GC-MS). Results reveal that the chemical profiles of smoked hops varied across fuel types. Specifically, several known smoke taint markers, including guaiacol and 4-methylguaiacol, as well as previously unreported compounds such xylopyranose were observed to be elevated in smoked hops compared to controls. This research provides a foundation for future studies to investigate various fuel types and their varying effects on hop quality.
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