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Despite the widespread adoption of emergency coronary reperfusion therapy, reperfusion‐induced myocardial injury remains a challenging issue in clinical practice. Following myocardial reperfusion, S100A8/A9 molecules are considered pivotal in initiating and regulating tissue inflammatory damage. Effectively reducing the S100A8/A9 level in ischemic myocardial tissue holds significant therapeutic value in salvaging damaged myocardium. In this study, HA (hemagglutinin)‐ and RAGE (receptor for advanced glycation end products)‐ comodified macrophage membrane‐coated siRNA nanoparticles (MMM/RNA NPs) with siRNA targeting S100A9 (S100A9‐siRNA) are successfully prepared. This nanocarrier system is able to target effectively the injured myocardium in an inflammatory environment while evading digestive damage by lysosomes. In vivo, migration of MMM/RNA NPs to myocardial injury lesions is confirmed in a myocardial ischemia‐reperfusion injury (MIRI) mouse model. Intravenous injection of MMM/RNA NPs significantly reduced S100A9 levels in serum and myocardial tissues, further decreasing myocardial infarction area and improving cardiac function. Targeted reduction of S100A8/A9 by genetically modified macrophage membrane‐coated nanoparticles may represent a new therapeutic intervention for MIRI. [ABSTRACT FROM AUTHOR]

Long non-coding RNA (LncRNA) plays an important role in malignant transformation of cells. This study aimed to explore the role of Lnc-ENST00000535078 in the malignant transformation of immortalized human bronchial epithelial cells (BEAS-2B) induced by coal tar pitch extract (CTPE). The malignant transformation model of BEAS-2B cells exposed to CTPE. Cell proliferation was examined by Cell counting kit-8 (CCK-8) assay. Colony formation assay was used to assess the colony of cells. Cell migration and invasion were detected by Transwell analysis. Cell cycle progression and apoptotic status were assessed by flow cytometry. Differentially expressed genes were screened by RNA sequencing. The results showed that Lnc-ENST00000535078 expression was highest in malignantly transformed BEAS-2B cells passaged to the 30th generation. Knockdown of Lnc-ENST00000535078 inhibited the migration, invasion and anti-apoptotic abilities of malignantly transformed BEAS-2B cells. Transcriptome analysis found 608 differential genes. CCND1 and FOS genes were screened out because of their levels were positive correlation with the expression of Lnc-ENST00000535078, which were consistent with the RNA sequencing results. In conclusion, Low expression of Lnc-ENST00000535078 inhibits the migration and invasion of malignant transformed BEAS-2B cells and promotes apoptosis in these cells. Lnc-ENST00000556926 might affect the malignant transformation of cells through the regulation of CCND1 and FOS. This study may provide a potential target for intervention in CTPE-induced lung cancer. [ABSTRACT FROM AUTHOR]

Benzo(a)pyrene‐7,8‐dihydrodiol‐9,10‐epoxide (BPDE), the metabolite of environmental pollutant benzo(a)pyrene (B(a)P) could induce pulmonary toxicity and inflammation. SIRT1, an NAD+ ‐dependent histone deacetylase, is known to regulate inflammation in the occurrence and development of various diseases, but its effects on BPDE‐induced acute lung injury are still unknown. The present study aimed to explore the role of SIRT1 in BPDE‐induced acute lung injury. Here, human bronchial epithelial (HBE) cells (BEAS‐2B) cells were stimulated with BPDE at different concentrations (0.50, 0.75, and 1.00 μmol/L) for 24 h, we found that the levels of cytokines in the supernatant were increased and the expression of SIRT1 in cells was down‐regulated, at the same time, BPDE stimulation up‐regulated the protein expression of HMGB1, TLR4, and p‐NF‐κBp65 in BEAS‐2B cells. Then the activator and inhibitor of SIRT1 were used before BPDE exposure, it was shown that the activation of SIRT1 significantly attenuated the levels of inflammatory cytokines and HMGB1, and reduced the expression of HMGB1, AC‐HMGB1, TLR4, and p‐NF‐κBp65 protein; while these results were reversed by the inhibition of SIRT1. This study revealed that the SIRT1 activation may protect against BPDE‐induced inflammatory damage in BEAS‐2B cells by regulating the HMGB1/TLR4/NF‐κB pathway. [ABSTRACT FROM AUTHOR]

In this work, a microfluidic lung chip with membrane supporting cell growth that can produce multiple concentration gradients of gas and liquid is introduced. The chip is composed of a gas gradient layer in the upper part, a porous membrane supporting cell growth in the middle and a liquid gradient layer in the lower part. The gas-liquid interface environment of the cells on the membrane can expose the cells to the gas in the upper layer and the liquid in the lower layer at the same time. Then, the chip is applied to the toxicity testing of formaldehyde in A549 cells. The results showed that at 6 × 10−5 mol/L formaldehyde, the survival rate of the cells in four channels were 90, 87, 81, and 71%, which shows a dose-response trend under the influence of different concentrations of formaldehyde. ROS staining results also showed that formaldehyde exposure at 6 × 10−5 mol/L lead to the increase of ROS level in the cells. These results suggest that the chip based on cell growth on membrane could be used for toxicological evaluation of environmental polluting gases. [ABSTRACT FROM AUTHOR]

Background The primary aim of this study is to examine the association between urinary polycyclic aromatic hydrocarbons (PAHs) and diabetes mellitus (DM) among the US population. Methods We used data from the National Health and Nutritional Examination Survey 2003–16, which is a nationally representative population-based survey of the US non-institutionalized population. Logistic regression analysis was performed to evaluate the association between urinary PAHs and the prevalence of DM using odds ratios (ORs) and 95% confidence intervals (CIs). Results The study sample including 13 792 individuals ≥18 y of age. The average ages of the three PAH tertiles were 42.56±19.67, 42.21±19.51 and 43.39±17.99 y. An increased risk of DM was found with increased odds for the second (OR 1.56 [95% CI 1.36 to 1.79]) and third tertile (OR 1.79 [95% CI 1.55 to 2.06)] of urinary PAH as compared with the first tertile. Similarly, higher chances of DM were observed in the second (men: OR 1.42 [95% CI 1.18 to 1.71]; women: OR 1.76 [95% CI 1.44 to 2.14]) and third tertile (men: OR 1.69 [95% CI 1.38 to 2.08]; women: OR 1.79 [95% CI 1.46 to 2.19]) of urinary PAHs as compared with the first tertile in both men and women. Conclusions A population-based cross-sectional study found a positive association between urinary PAHs and DM in the US population. [ABSTRACT FROM AUTHOR]

In order to investigate smoking behaviors and nicotine exposure levels of cigarette smokers after switching to using heated tobacco products, 50 volunteers who regularly smoked cigarettes were recruited and randomly divided into two groups, one switched to a heated tobacco product known as IQOS and the other group to a domestic heated tobacco product M. Their general smoking characteristics were collected via questionnaires and their smoking parameters were recorded by a CReSS pocket analyzer. The contents of nicotine exposure biomarker in the volunteers'urine samples before and after switching were determined by HPLC-MS/MS. The results showed that: 1) The smoking behaviors of the smokers were basically unchanged after switching to the heated tobacco products, the puffing volume and duration did not change significantly. However, the puffing interval of the two groups significantly shortened from (14.3±8.0) s and (15.3±9.0) s to (9.8±8.3) s and (9.7± 5.4) s, respectively. 2) The contents of total nicotine metabolites and nicotine exposure biomarkers (i.e. cotinine) in the volunteers'urine samples did not change significantly after switching to the heated tobacco products. 3) There was no significant difference of the smoking behaviors between the volunteers switched to IQOS and those to M, and the levels of total nicotine metabolites and cotinine in the urine samples of the two groups were also quite similar. [ABSTRACT FROM AUTHOR]

The development of liver, intestine, lung and other organ chips and multi-organ chip models were summarized in this paper. The chip design and specific applications of these chip models in drug toxicity assessment and environmental toxicological evaluations were introduced emphatically, and the existing researches and application potentials of organ chips in the risk assessment of tobacco products were also discussed. This work provides the insights and ideas for the application of microfluidic organ chips in in vitro toxicological studies of tobacco products and other environmental exposures. In vitro toxicology evaluation plays an important role in the health risk assessment of tobacco products, the simulation of the physiological microenvironment and biological function in organ chips is of great significance in the construction of in vitro models. The application of microfluidic organ chips to in vitro toxicology of tobacco products could provide an innovative experimental platform for studying the formation mechanisms of tobacco-related diseases, and realize the multi-dimensional life analysis on the micro and nano scales. [ABSTRACT FROM AUTHOR]