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Particulate matter (PM) emissions from anthropogenic sources contribute substantially to air pollution. The unequal adverse health effects caused by source-emitted PM emphasize the need to consider the discrepancy of PM-bound chemicals rather than solely focusing on the mass concentration of PM when making air pollution control strategies. Here, we present a dataset about chemical compositions of real-world PM emissions from typical anthropogenic sources in China, including industrial (power, industrial boiler, iron & steel, cement, and other industrial process), residential (coal/biomass burning, and cooking), and transportation sectors (on-road vehicle, ship, and non-exhaust emission). The data was obtained under the same strict quality control condition on field measurements and chemical analysis, minimizing the uncertainty caused by different study approaches. The concentrations of PM-bound chemical components, including toxic elements and PAHs, exhibit substantial discrepancies among different emission sectors. This dataset provides experimental data with informative inputs to emission inventories, air quality simulation models, and health risk estimation. The obtained results can gain insight into understanding on source-specific PMs and tailoring effective control strategies., (© 2024. The Author(s).)

Cooking emission is known to be a significant anthropogenic source of air pollution in urban areas, but its toxicities are still unclear. This study addressed the toxicities of fine particulate matter (PM 2.5 ) and gaseous organics by combining chemical fingerprinting analysis with cellular assessments. The cytotoxicity and reactive oxygen species activity of gaseous organics were ∼1.9 and ∼8.3 times higher than those of PM 2.5 , respectively. Moreover, these values of per unit mass PM 2.5 were ∼7.1 and ∼15.7 times higher than those collected from ambient air in Shanghai. The total oleic acid equivalent quantities for carcinogenic and toxic respiratory effects of gaseous organics, as estimated using predictive models based on quantitative structure-property relationships, were 1686 ± 803 and 430 ± 176 μg/mg PM 2.5 , respectively. Both predicted toxicities were higher than those of particulate organics, consistent with cellular assessment. These health risks are primarily attributed to the high relative content and toxic equivalency factor of the organic compounds present in the gas phase, including 7,9-di- tert -butyl-1-oxaspiro(4,5)deca-6,9-diene-2,8-dione, 2-ethylhexanoic acid, and 2-phenoxyethoxybenzene. Furthermore, these compounds and fatty acids were identified as prominent chemical markers of cooking-related emissions. The obtained results highlight the importance of control measures for cooking-emitted gaseous organics to reduce the personal exposure risks.

Osteosarcoma (OS), occurring in mesenchymal tissues and with a high degree of malignancy, is most common in children and adolescents. At present, we intend to figure out the expression and functions of miR-29a-3p in OS development. Reverse transcription-polymerase chain reaction (RT-PCR) was adopted to monitor the expression of miR-29a-3p and IGF1 in OS tissues and adjacent non-tumor tissues. Then, the 3- (4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT) assay, colony formation experiment, western blot and Transwell assay were conducted to validate OS cell proliferation, colony formation ability, apoptosis, migration and invasion. Next, the association between miR-29a-3p and IGF1 was corroborated by the dual-luciferase reporter assay and the Pearson correlation analysis. Finally, WB was implemented to test the levels of autophagy-related proteins LC3-I/LC3-II, Beclin-1, p62, and the IGF-1 R/PI3k/Akt/FOXO3 axis in OS cells. As a result, miR-29a-3p was down-regulated in OS tissues (versus adjacent non-tumor tissues) and OS cell lines. Overexpressing miR-29a-3p aggravated apoptosis, dampened cell proliferation, colony formation, migration and invasion, and promoted autophagy of OS cells. IGF1 was identified as a target of miR-29a-3p. IGF1 induced oncogenic effects in OS by activating IGF-1 R/ PI3k/Akt pathway, and it dampened the tumor-suppressive effect of miR-29a-3p on OS. Taken together, miR-29a-3p repressed the OS evolvement through inducing autophagy and inhibiting IGF1 mediated PI3k/Akt/FOXO3 pathway.

Atmospheric amines contribute to the nucleation and initial growth of new particles as well as secondary organic aerosol formation, influencing the radiative balance of the Earth's atmosphere. In this study, we develop an ion chromatography (IC) method for separating and quantifying the nine most abundant amines (methylaminium (MMAH + ), dimethylaminium (DMAH + ), trimethylaminium (TMAH + ), ethylaminium (MEAH + ), diethylaminium (DEAH + ), propylaminium (MPAH + ), butylaminium (MBAH + ), ethanolaminium (MEOH + ), and triethanolaminium (TEOH + )) from six common inorganic species in atmospheric aerosols. The retention times of the amines were altered by the addition of acetonitrile to the eluent because acetonitrile can reduce the adsorption of hydrophobic amines on the stationary phase. The developed method achieved the successful separation of DEAH + and TMAH + from inorganic cations, which often coelute with each other in established IC methods. The interference of K + on the determination of MEAH + was eliminated by the complexation of K + with 18-crown-6, which prolonged the retention time of K + . Finally, 9 target amines and 6 common inorganic cations were separated, with a resolution Rs ≥ 1.2 for DEAH + and MPAH + and Rs > 1.5 for other species. The detection limits varied in the range of 0.34-1.48 ng for the 9 amines and 0.19-0.56 ng for the inorganic cations. The developed method was successfully applied for the determination of low molecular weight amines and inorganic cations in PM 2.5 collected from an urban site in Shanghai and an isolated coast of Chongming Island. Eight amines were detected in the urban samples, in which MMAH + and DMAH + dominated. The average amine concentration in the urban aerosols was 76.3 ± 38.4 ng m -3 , which is approximately 4-fold higher than those in the marine samples collected from the coast., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

More than 30% of patients with osteosarcoma succumb to pulmonary metastases. Epithelial-mesenchymal transition (EMT) is a biological process by which tumor cells gain an increased capacity for invasiveness and metastasis. A previous study confirmed the phenomenon of EMT in osteosarcoma, a mesenchymal-derived tumor. However, whether chemotherapy affects EMT remains to be elucidated. In the present study, the osteosarcoma cells were exposed to a sublethal dose of cisplatin, and any surviving cells were assumed to be more resistant to cisplatin. In addition, these cells exhibited a more mesenchymal phenotype. Immunofluorescence analysis revealed that the cisplatin treated cells had an increased long/short axis ratio and increased expression of N-cadherin compared with control cells. A panel of EMT-associated genes was subsequently assessed by quantitative PCR and western blot analysis, and they were observed to be significantly upregulated in the cisplatin treated cells. The in vitro wound healing and Transwell assay indicated that the cisplatin treated cells were more prone to migrate and invade. An in vivo assay showed that the cisplatin-treated xenograft had increased expression of EMT-associated genes, and exhibited increased pulmonary lesions compared with the control, which indicated an elevated capacity to metastasize. The expression of Snail was knocked down by specific small interfering RNA, and it was observed that Snail inhibition promoted cisplatin sensitivity, and cisplatin-induced EMT was significantly blocked. Taken together, the results of the present study supported that idea that Snail participates in cisplatin-induced EMT in osteosarcoma cells, and targeting EMT-transcription factors may offer promise for the therapeutics of osteosarcoma.

The aim of this study was to construct the eukaryotic expression vector pEGFP-N1-hPer2 and assess its expression in the human osteosarcoma cell line MG63. Total mRNA was extracted from human osteosarcoma MG63 cells, the human period 2 (hPer2) gene was obtained by reverse transcription-polymerase chain reaction (RT-PCR) and cloned into the pEGFP-N1 vector, then the recombinant pEGFP-N1-hPer2 plasmid was constructed and transfected into MG63 cells using Lipofectamine 2000. The expression of hPer2 in MG63 cells was measured by quantitative RT-PCR and western blot analysis. The accurate construction of pEGFP-N1-hPer2 was verified by double enzyme digestion and DNA sequencing. hPer2 gene expression in the transfected cells was assessed by RT-qPCR and western blot analysis. In conclusion, the recombinant pEGFP-N1-hPer2 plasmid was constructed successfully, and expressed effectively in MG63 cells.