Electronic cigarettes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA485536 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7685900.fastq.gz | Fastqsanger.gz | |||
| SRR7685901.fastq.gz | Fastqsanger.gz | |||
| SRR7685894.fastq.gz | Fastqsanger.gz | |||
| SRR7685895.fastq.gz | Fastqsanger.gz | |||
| SRR7685896.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Electronic cigarettes (e-cigarettes) have gained their popularity as a substitute for cigarettes or cigars. Despite the widespread use of flavoring chemicals in e-cigarettes, the health impacts of the flavoring compounds, in particular their effects on critical cellular function in the lung, remain largely unknown. The goal of this study was to identify transcriptomic changes and impacted biological pathways in primary human bronchial epithelial cells (HBECs) exposed to flavoring chemicals (diacetyl or 2,3-pentanedione) and to flavored e-cigarette smoke. An airway-liquid interface culturing method was used to differentiate primary human bronchial epithelial cells (HBECs) into mature epithelial cells, which were then treated with 25 ppm diacetyl, 100 ppm 2,3 pentanedione, or e-cigarette smoke solution containing 2 ppm diacetyl. Poly(A)-selected RNA-Seq libraries were prepared with the PrepX RNA-Seq for Illumina Library kit. An Illumina HiSeq 2500 instrument was used to generate 50 base pair single-end reads. STAR was used to align sequencing reads to the hg38 reference genome, and HTSeq was used to quantify transcript levels. DESeq2 was used to perform differential expression analysis.
2019-08-21 | GSE118431 | GEO
Project description:Our study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression change. This RNA-seq study examined the expression profiles of brain frontal cortex samples from mice exposed to classic tobacco flavored blu™ e-cigarettes during gestation and lactation.
2016-02-01 | GSE75858 | GEO
Project description:WS-23 is a synthetic coolant added to disposable 4th generation electronic cigarettes at high doses (up to 40 mg/mL). Here, we show the effects of pure WS-23 on the human bronchial epithelium treated at the air-liquid-interface in a cloud chamber exposure system. Both IPA and DAVID analysis show of the affects of WS-23 are related to impairment of actin cytoskeleton signaling, cell adhesion, cell spreading, and cell movement. Follow up assays on bronchial epithetlial cell line BEAS-2B further support the impairment of actin cytoskeleton signaling and actin depolymerization, as well as inhibition of cell movement, spreading, and gap closure. These results suggest that at the concentrations of WS-23 found in popular disposable electronic cigarettes, there is likely to be an adverse effect on actin cytoskeleton signaling in bronchial epithelial cells of users.
2023-07-25 | MSV000092524 | MassIVE
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:Our study demonstrated that e-cigarettes, both with and without nicotine, induced sex-dependent gene expression change. This RNA-seq study examined the expression profiles of brain frontal cortex samples from mice exposed to classic tobacco flavored blu⢠e-cigarettes during gestation and lactation. Brains were extracted and sectioned from ~1-month-old male and female offspring the week following exposure, RNA was isolated and purified from frontal cotrex tissues, and gene expression profiles were analyzed by RNA Sequencing.
2016-02-01 | E-GEOD-75858 | biostudies-arrayexpress
Project description:Electronic cigarettes (e-cigs) are battery-powered new tobacco products attracting wide attention due to their potential in promoting smoking cessation and uncertainty in long-term health effects. According to the scientific statement from the American Heart Association (AHA), e-cig use may be a potential threat to the cardiopulmonary system and populational studies suggested that e-cig aerosol could enhance arterial stiffness Laboratory evidence suggested that e-cigs could accelerate atherosclerosis and atherosclerosis or aortic aneurysm in mice, while the exact mechanisms of e-cig-related vascular effects remained largely unknown. Here, we investigate the sub-chronic effects of e-cig aerosol on vascular structure, function, and changes in single-cell transcriptome in mice.
2025-01-31 | GSE288003 | GEO
Project description:Electronic cigarettes (EC) are increasing in popularity, but there is only little information on their biologic effects on the oral epithelium, the initial site exposed to EC smoke. We assessed the oral epithelium response to EC by comparing the histology and RNA transcriptome (mRNA and miRNA) of healthy EC vapers to nonsmokers (NS). mRNA was assessed based on: (1) genome-wide; (2) genes previously identified as dysregulated in the oral epithelium of EC vapers vs NS; (3) immune and inflammatory-related genes previously identified as dysregulated in the nasal epithelium of EC vapers compared to NS; (4) genes previously identified as dysregulated in the small airway epithelium of NS following an acute exposure to EC; and (5) genes related to the initial steps of COVID-19 infection. In addition, miRNA was assessed genome-wide. Comparisons were performed using ANOVA, and Benajmini-Hochberg corrected p <0.05 was considered significant. The histology of the epithelium, lamina propria and basal layer in EC vapers appeared normal. Assessment of mRNA and miRNA, based on all gene lists, did not identify any genes significantly modified in the oral epithelium of EC vapers. Assessment of the oral epithelium of healthy EC vapers by histology, mRNA and miRNA demonstrated no abnormalities in response to EC smoke.
2025-06-05 | GSE176492 | GEO
Project description:Differential gene expression of cigarettes and electronic cigarettes
| PRJNA484125 | ENA
Project description:Background: While electronic cigarette (ECIG) use is rapidly rising, their safety profile remains uncertain. The effects of tobacco cigarette (TCIG) smoke on bronchial airway epithelial gene-expression have provided insights into tobacco-related disease pathogenesis. Understanding the impact of electronic cigarettes (ECIGs) on airway gene-expression could provide insights into their potential long-term health effects. Objectives: We sought to compare the bronchial airway gene-expression profiles of former TCIG smokers now using ECIGs with the profiles of former and current TCIG smokers. Methods: We performed gene-expression profiling of bronchial epithelial cells collected from TCIG smokers not using ECIGs (n=21), former smokers using ECIGs (n=15), and current TCIG smokers not using ECIGs (n=9). We then compared our findings with previous studies of the effects of TCIG use on bronchial epithelium, as well an in vitro model of ECIG exposure. Results: Amongst 3,165 genes whose expression varied between the three study groups (q < 0.05), we identified 468 genes significantly altered in ECIG users relative to former smokers (p < 0.05). 79 of these genes were up or down-regulated concordantly between ECIG and TCIG. We did not detect ECIG-associated gene expression changes in known pathways associated with TCIG usage. Genes downregulated in ECIG users are enriched among the genes most downregulated by exposure of airway epithelium to ECIG vapor in vitro. Conclusions: TCIG exposure was associated with a larger number of airway gene-expression changes than with ECIG exposures. ECIGs induce both distinct and shared patterns of gene expression relative to TCIGs in the bronchial airway epithelium.
2019-10-09 | GSE112073 | GEO
Project description:Oral Epithelium Response of Electronic Cigarette Users to Electronic Cigarette
| PRJNA736429 | ENA