Ontology highlight
ABSTRACT:
PROVIDER: PRJNA451366 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7054520_1.fastq.gz | Fastqsanger.gz | |||
| SRR7054520_2.fastq.gz | Fastqsanger.gz | |||
| SRR7054521_1.fastq.gz | Fastqsanger.gz | |||
| SRR7054521_2.fastq.gz | Fastqsanger.gz | |||
| SRR7054522_1.fastq.gz | Fastqsanger.gz |
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Project description:Smoking cigarettes is harmful to the cardiovascular system. Considerable attention has been paid to the reduced harm potential of alternative nicotine-containing inhalable products such as e-cigarettes. We investigated the effects of E-vapor aerosols or cigarette smoke (CS) on atherosclerosis progression, cardiovascular function, and molecular changes in the heart and aorta of female ApoE−/− mice. The mice were exposed to aerosols from three different E-vapor formulations: (1) carrier (propylene glycol and vegetable glycerol), (2) base (carrier and nicotine) or (3) test (base and flavor) or to CS from 3R4F reference cigarettes for up to 6 months. Concentrations of CS and base or test aerosols were matched at 35 µg nicotine/L. Exposure to CS, compared with sham-exposed fresh air controls, accelerated atherosclerotic plaque formation, while no such effect was seen for any of the three E-vapor aerosols. Molecular changes indicated disease mechanisms related to oxidative stress and inflammation in general, plus changes in calcium regulation, and altered cytoskeletal organization and microtubule dynamics in the left ventricle. While ejection fraction, fractional shortening, cardiac output, and isovolumic contraction time remained unchanged following E-vapor aerosols exposure, the nicotine-containing base and test aerosols caused an increase in isovolumic relaxation time similar to CS. A nicotine-related increase in pulse wave velocity and arterial stiffness was also observed, but it was significantly lower for base and test aerosols than for CS. These results demonstrate that in comparison with CS, E-vapor aerosols induce substantially lower biological responses associated with smoking-related cardiovascular diseases.
2020-05-12 | E-MTAB-8578 | biostudies-arrayexpress
Project description:Peripheral blood samples were collected before (0 hour) and at 24 hours after exposure from healthy subjects who participated in previous controlled exposures to ultrafine carbon particles (UFP, 50 microg/m3) or filtered air (FA)(n = 3 each). The exposure time was 2 hours. RNA from mononuclear cell fraction (>85% lymphocytes) was extracted, amplified and hybridized to Affymetrix HU133 plus 2 microarrays. We used microarray to explore significantly altered genes after ultrafine carbon particle exposure.
2010-06-30 | GSE19317 | GEO
Project description:Peripheral blood samples were collected before (0 hour) and at 24 hours after exposure from healthy subjects who participated in previous controlled exposures to ultrafine carbon particles (UFP, 50 microg/m3) or filtered air (FA)(n = 3 each). The exposure time was 2 hours. RNA from mononuclear cell fraction (>85% lymphocytes) was extracted, amplified and hybridized to Affymetrix HU133 plus 2 microarrays. We used microarray to explore significantly altered genes after ultrafine carbon particle exposure. Each subject was exposed to filtered air or ultrafine carbon particles. Two peripheral blood samples (pre- and post-exposure) were taken. Mononuclear cells were isolated for gene expression analysis.
2010-06-29 | E-GEOD-19317 | biostudies-arrayexpress
Project description:The purpose of this study was to characterize global gene expression in human airway epithelial cells and identify cellular pathways associated with coarse, fine and ultrafine particulate matter (PM) exposures. Ambient PM was collected in 3 different size fractions from Chapel Hill air, particles were extracted from foam or filter matrices and lyophilized. Human primary airway epithelial cells were exposed to particles at 250μg/ml or vehicle control for 6h in culture. Following exposure, RNA was isolated and hybridized to human HG U133A affymetrix chips. Experiment Overall Design: Human primary epithelial cells were exposed to coarse, fine, ultrafine PM or vehicle control in culture for 6h. Three biological replicates for each treatment (coarse, fine, ultrafine, control) were conducted at (250ug/ml). 12 Affymetrix chips (HG U133A) were used.
2008-06-15 | E-GEOD-7010 | biostudies-arrayexpress
Project description:Electronic cigarette use has increased dramatically over the past three years, despite numerous reports of acute lung injury and even death. In this report we provide evidence from a nonhuman primate model for Electronic Vapor-Induced Lung Injury (EVALI), demonstrating significant lung pathology from electronic vaping (EV). Here we characterized the particle size and pathogenic effects induced by EV exposure of nonhuman primates using the commercial nicotine JUUL® pod modular devices. Vaping aerosols appear to preferentially and exclusively target the bronchioles while bypassing larger bronchi. We demonstrate a significantly smaller particle size, generated by the EV device relative to combustion product aerosols produced by conventional cigarettes. Histopathologically, vaping aerosols appear to preferentially and exclusively target the bronchioles while bypassing larger bronchi which is consistent with a significanlty smaller particle size compared to cigarette smoke. Our immunohistochemical and RNAseq studies provide further evidence for severe small airway inflammation and dysregulation of gene expression within immune cells derived from bronchial lavage, respectively. Our findings raise major concerns regarding the safety of e-cigarettes, and provide a mechanism for the preferential induction of lung injury by EV. Our results, in a species whose lung architecture is the closest possible approximation of that of a human adolescent, suggest the danger of the EV device itself and resultant small particulate aerosols produced, preferentially entering and damaging a highly susceptible part of the respiratory system.
2022-07-01 | GSE199072 | GEO
Project description:Exposure to ambient airborne particulate matter (PM) has been associated with almost 9 million premature deaths per year worldwide. Ports are essential infrastructure for trade and transport, with over 80% of the world’s international trade volume travelling by sea, yet there is little understanding of the potential health effects of PM from ships. Here, we studied the elemental and toxicological characteristics of size-fractionated PM collected at different areas of a busy European mixed-use port. We found that unregulated ultrafine PM, a PM size fraction <100 nm in aerodynamic diameter, originating from a cruise-ship source, was highly enriched compared to ultrafine PM from other sites in tracers of heavy fuel oil combustion (V and Ni), with Co identified as a novel tracer. In cell models of airway and alveolar epithelium, this cruise ship-associated ultrafine PM was markedly more pro-inflammatory than PM from other sites, while simultaneously reducing expression of a range of genes associated with the innate antiviral response. Investigation of the effects of the three metals found to be enriched in our cruise-ship ultrafine PM showed that these effects could be reproduced by vanadium exposure, which reduced interferon signalling and increased permissiveness to viral infection, facilitating replication of the respiratory viruses rhinovirus-16 and SARS-CoV-2. Our findings suggest that, despite a series of regulations introduced over the last 20 years, cruise ship-associated emissions of PM from heavy fuel oil combustion may exert disproportionate effects on health compared to PM from other sources. In particular, the effects manifest themselves through induction of a response with characteristics of a poor viral infection prognosis. More broadly, current regulations, which neglect PM source- and composition-related variations, and ultrafine PM in general, may need strengthening to better mitigate health effects resulting from exposure to PM.
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Project description:Gene expression profiling of the human keratinocytes cell line (HaCaT) exposure to ultrafine, fine, and submicron TiO2 particles were employed to gain insights into the molecular events.
2009-06-15 | GSE16425 | GEO
Project description:Metaproteomics approach was used to investigate the microbial community and diversity of the infant gut to identify different key proteins with metabolic functional roles in the microbiomes of healthy and atopic dermatitis infants in a Thai population-based birth cohort.
2020-09-06 | PXD021324 | JPOST Repository