Long non-coding RNAs mediate the association between short-term PM exposure and circulating biomarkers of systemic inflammation.

Although short-term fine particulate matter (PM) exposure is associated with systemic inflammation, the effect of lncRNA on these association remains unknown. This study aims to investigate whether the plasma lncRNA mediate the effect of short-term PM exposure on systemic inflammation. In this cross-sectional study, plasma Clara cell protein 16 (CC16), interleukin 6 (IL-6), IL-8, tumor necrosis factor-α (TNF-α) and lncRNA expression levels were measured in 161 adults between March and April in 2018 in Shijiazhuang, China.

Upregulation of Circ_0035266 Contributes to the Malignant Progression of Inflammation-Associated Malignant Transformed Cells Induced by Tobacco-Specific Carcinogen NNK.

Cigarette smoking-induced chronic inflammation has been considered a vital driver of lung tumorigenesis. The compounds 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific carcinogen, and lipopolysaccharide (LPS), an inflammatory inducer, are important components of tobacco smoke which have been implicated in inflammation-driven carcinogenesis. However, the biological effects and underlying mechanisms of LPS-mediated inflammation on NNK-induced tumorigenesis are still unclear.

The involvement of copper, circular RNAs, and inflammatory cytokines in chronic respiratory disease.

Exposure to high concentrations of copper is associated with pulmonary inflammation and chronic respiratory disease (CRD). Epigenetic modulation of noncoding RNAs contributes to the development of several CRDs. It is unknown whether epigenetic modulation is involved in copper mediated pulmonary inflammation and CRD.

Circular RNA circNIPBL promotes NNK-induced DNA damage in bronchial epithelial cells via the base excision repair pathway.

Environmental chemical exposure often causes DNA damage, which leads to cellular dysfunction and the development of diseases. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific carcinogen that is known to cause DNA damage, while remains unknown about the underlying mechanism. In this study, simulated doses of NNK exposure in smokers, ranging from 50 to 300 μM, were used to detect the DNA damage effects of NNK in two human bronchial epithelial cells, 16HBE and BEAS-2B.

Circular RNA circ_Cabin1 promotes DNA damage in multiple mouse organs via inhibition of non-homologous end-joining repair upon PM exposure.

Fine particulate matter (PM) has been shown to induce DNA damage. Circular RNAs (circRNAs) have been implicated in various disease processes related to environmental chemical exposure. However, the role of circRNAs in the regulation of DNA damage response (DDR) after PM exposure remains unclear.

Tobacco-Related Exposure Upregulates Circ_0035266 to Exacerbate Inflammatory Responses in Human Bronchial Epithelial Cells.

One of the most carcinogenic chemicals found in cigarette tobacco smoke is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which has been confirmed to be associated with the etiology of diverse cancers. Lipopolysaccharide (LPS), another biologically active component of cigarette smoke, is a risk factor which enhances NNK-induced lung tumorigenesis due to chronic lung inflammation. Although inflammatory responses play critical roles in the initiation of many tumors, our knowledge about the mechanisms of NNK+LPS on inflammation is currently limited.

Circular RNA circBbs9 promotes PM-induced lung inflammation in mice via NLRP3 inflammasome activation.

Fine particulate matter (PM) is one of the most important components of environmental pollutants, and is associated with pulmonary injury. However, the biological mechanisms of pulmonary damage caused by PM are poorly defined, especially the molecular pathways related to inflammation. Following system exposure to PM for 3 months in normal mice and in chronic obstructive pulmonary disease (COPD) model mice, it was found that PM exposure increased the expression of IL-1β and IL-18 in lung tissues via NLRP3 activation, and these effects were more intense in COPD model mice.

Circular RNA 0039411 Is Involved in Neodymium Oxide-induced Inflammation and Antiproliferation in a Human Bronchial Epithelial Cell Line via Sponging miR-93-5p.

Adverse health effects induced by neodymium oxide (Nd2O3) particles have raised concern as a result of their increasing applications in various arenas. However, information on their potential cytotoxicity is currently limited. In the present study, we investigated the underlying cytotoxicity of Nd2O3 in human bronchial epithelial cells (16HBE) and the potential mechanisms mediated by circular RNAs (circRNAs).

The Frequency of Unhealthy Food Advertising on Mainland Chinese Television (TV) and Children and Adolescents' Risk of Exposure to Them.

Objective: To conduct an analysis of the frequency of unhealthy food advertising on mainland Chinese television (TV) and children and adolescents' risk of exposure to them.

Methods: The frequencies of all types of advertisements (ads) on forty TV channels in mainland China, the exact ad broadcast times, and the name and brand of all snacks and western fast foods advertised were recorded from 0800 hours to 2400 hours on both a weekday and a weekend day in a week. The difference in the frequencies of the diverse types of ads over eight time intervals (each time interval was 2 hours) were compared, and the trends in ad frequencies during the time intervals were described.