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Emphysema, myofibroblast accumulation and airway remodeling can occur in the lungs due to exposure to atmospheric pollution, especially fine particulate matter (PM2.5), leading to chronic obstructive pulmonary disease (COPD). Specifically, bronchial epithelium-fibroblast communication participates in airway remodeling, which results in COPD. An increasing number of studies are now being conducted on the role of exosome-mediated cell-cell communication in disease pathogenesis. Here, we investigated whether exosomes generated from bronchial epithelial cells could deliver information to normal stromal fibroblasts and provoke cellular responses, resulting in airway obstruction in COPD. We studied the mechanism of exosome-mediated intercellular communication between human bronchial epithelial (HBE) cells and primary lung fibroblasts (pLFs). We found that PM2.5-induced HBE-derived exosomes promoted myofibroblast differentiation in pLFs. Then, the exosomal lncRNA expression profiles derived from PM2.5-treated HBE cells and nontreated HBE cells were investigated using an Agilent Human LncRNA Array. Combining coculture assays and direct exosome treatment, we found that HBE cell-derived exosomal HOTAIRM1 facilitated the myofibroblast differentiation of pLFs. Surprisingly, we discovered that exosomal HOTAIRM1 enhanced pLF proliferation to secrete excessive collagen secretion, leading to airway obstruction by stimulating the TGF-β/SMAD3 signaling pathway. Significantly, PM2.5 reduced FEV1/FVC and FEV1 and increased the level of serum exosomal HOTAIRM1 in healthy people; moreover, serum exosomal HOTAIRM1 was associated with PM2.5-related reductions in FEV1/FVC and FVC. These findings show that PM2.5 triggers alterations in exosome components and clarify that one of the paracrine mediators of myofibroblast differentiation is bronchial epithelial cell-derived HOTAIRM1, which has the potential to be an effective prevention and therapeutic target for PM2.5-induced COPD. [ABSTRACT FROM AUTHOR]

In this study, we employed classic electrochemical techniques including cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) to perform electrochemical characterization on atomic-level single-crystal TiO2 electrodes and extract capacitive and resistive properties of single-crystal TiO2 electrode/solution interface in KCl and KCl/K3PO4 at various pH levels. The lattice structure and crystal appearance were characterized using X-ray diffractometry (XRD), scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), and Raman spectroscopy to facilitate the in-depth exploration of heterogeneous reaction dynamics and theory. Furthermore, this study aimed to verify and improve the theory and application of capacitance at the single-crystal TiO2 electrode/solution interface. The electrochemical measurements indicate that, in the same pH, the presence of PO43− significantly increases the total capacitance (CT), outer capacitance (CO), electrical double-layer capacitance (Cdl), and diffusion layer capacitance (Cdiff) at single-crystal TiO2 electrode/solution interface. This enhancement is attributed to the direct interaction between PO43− and the single-crystal TiO2 electrode surface, leading to the specific adsorption of PO43− on the electrode surface, revealing higher current and stronger electrochemical activity in the interaction between TiO2 and PO43−. Additionally, our XPS results indicate the adsorption of PO43− on the single-crystal TiO2 electrode surface. The interaction of PO43− with the TiO2 surface demonstrates increased hydrophilicity and enhanced adsorption capacity through mechanisms such as ligand exchange or cation bridging, thereby augmenting the Cdl at the single-crystal TiO2 electrode/solution interface. [ABSTRACT FROM AUTHOR]

Hollow microspheres Bi2WO6 (HBWO) were prepared by the solvothermal method for the adsorption of U(VI) from aqueous solutions. Batch experiments and characterization analysis investigated the adsorption performance and mechanism. The results showed that the adsorption equilibrium could be reached in 30 min at T = 303 K, pH = 6, CU(VI) = 10 mg/L, m/V = 0.1 g/L. The removal efficiency of HBWO for U(VI) in solution was 95.53%, which was about 20% higher than Bi2WO6 nanosheets. The maximum Langmuir adsorption capacity could reach 523.13 mg/g. FTIR and XPS analysis indicated that the interaction mechanism of U(VI) with HBWO is mainly surface complexation of strong ionic bond (M–O) and hydroxyl (–OH) groups. In addition, HBWO has strong ion selectivity for U(VI) and good regeneration and reuse performance. These results demonstrated that HBWO might potentially remediate actual uranium-containing wastewater. [ABSTRACT FROM AUTHOR]

Fine particulate matter organic extract (Po) was reported to promote inflammation in the lung. Sex differences were reported in many inflammatory diseases. In this study, we investigated the effects of Po exposure on pulmonary inflammatory response and evaluated the role of sex in this process. While mice were exposed to 100 µg/m3 Po for 12 weeks by an inhalation exposure system, the lung histopathological analysis shown obvious inflammation, the cell numbers in bronchoalveolar lavage fluid (BALF) were significantly increased, and most inflammatory cytokines in BALF were upregulated. The results of factorial analysis of variance shown that there was an interaction between sex and Po exposure in the inflammatory cell numbers and the levels of tumor necrosis factor-α (TNF-α), interleukin-5 (IL-5), and growth-related oncogene/keratinocyte chemoattractant (GRO/KC). Notably, these changes and interactions were diminished while Po-exposed mice were administered with the estrogen receptor β (ERβ) antagonist. We speculated that sex might affect the levels of inflammatory indicators in BALF of Po-exposed mice and female mice were more prone to inflammation while exposed to Po. Moreover, ERβ was involved in these processes. To our knowledge, this is the first investigation about the role of sex in Po-induced adverse effects. [ABSTRACT FROM AUTHOR]

Background: Currently, SARS-CoV-2 liver invasion, inflammatory cytokines, and antiviral drugs are widely thought to be associated with liver dysfunction in COVID-19 patients. Besides, previous studies indicated that ACEI/ARB drugs can increase the expression of hepatic ACE2, a cell entry receptor for SARS-CoV-2. This study aims to investigate whether ACEI/ARB aggravates liver injury and the association of inflammatory cytokines and antiviral drugs with liver dysfunction in patients with hypertension and COVID-19.Method: This retrospective study included 127 hypertensive patients with long-term use or nonuse of ACEI/ARBs hospitalized for COVID-19 from January 30 to April 7, 2020, in Tongji hospital of Wuhan, China. Demographic, clinical, laboratory, treatment, and outcome data were collected.Results: Of the 127 patients with COVID-19 and hypertension, 43 taking long-term of ACEI/ARBs and 84 without using ACEI/ARBs. Abnormal liver function was observed in part of ACEI/ARB and non-ACEI/ARB users but without significant differences between these two groups. Serum inflammatory cytokines, IL-6, IL-8, and TNFα, as well as inflammation-related markers, ferritin, procalcitonin, and C-reactive protein, were significantly elevated in patients with liver dysfunction. IL-6 level was positively correlated with liver function tests on admission and highly consistent with the changes of abnormal ALT, AST, and GGT during hospitalization, but the correlations of other inflammatory cytokines were low. There was no significant association between the use of antiviral drugs and liver dysfunction in these patients.Conclusion: The elevation of inflammatory cytokine, IL-6, but not ACEI/ARB and antiviral drugs, is closely associated with liver dysfunction in patients with hypertension and COVID-19. [ABSTRACT FROM AUTHOR]

Hollow microspheres Bi2WO6 (HBWO) were prepared by the solvothermal method for the adsorption of U(VI) from aqueous solutions. Batch experiments and characterization analysis investigated the adsorption performance and mechanism. The results showed that the adsorption equilibrium could be reached in 30 min at T = 303 K, pH = 6, CU(VI) = 10 mg/L, m/V = 0.1 g/L. The removal efficiency of HBWO for U(VI) in solution was 95.53%, which was about 20% higher than Bi2WO6 nanosheets. The maximum Langmuir adsorption capacity could reach 523.13 mg/g. FTIR and XPS analysis indicated that the interaction mechanism of U(VI) with HBWO is mainly surface complexation of strong ionic bond (M–O) and hydroxyl (–OH) groups. In addition, HBWO has strong ion selectivity for U(VI) and good regeneration and reuse performance. These results demonstrated that HBWO might potentially remediate actual uranium-containing wastewater. [ABSTRACT FROM AUTHOR]

Objective: To investigate personal exposures to nitrogen oxides (NO X ) and nitrogen di-oxide (NO 2 ) and the influence of baseline personal characteristics, living environment and daily activity patterns of the participants on the exposures among adults over 35 in Tianjin and Shanghai., Methods: In this panel study, 91 healthy nonsmoking adults aged over 35 from Tianjin and Shanghai participated in our study. The study was conducted in summer and winter. The participants were followed for three times with an interval of at least two weeks. Only participants in Shanghai were followed once in winter because of the COVID-19 pandemic. Twenty-seven participants completed follow-up visits in both seasons. We measured their 24 h personal exposures to NO X and NO 2 and collected their baseline and time-activity information through questionnaire/diary. The linear mixed model was used to analyze the associations between potential influencing factors and personal NO X and NO 2 exposure levels., Results: There were 349 follow-up visits with valid 24 h personal NO 2 and NO X exposure measurements in the two cities. The ave-rage 24 h personal exposures to NO 2 and NO X (volume fraction) in Tianjin participants were 18.0×10 -9 and 26.2×10 -9 in summer, and 31.0×10 -9 and 54.9×10 -9 in winter, respectively; and the average 24 h personal exposures to NO 2 and NO X in Shanghai participants were 38.7×10 -9 and 100.0×10 -9 in summer, and 45.5×10 -9 and 139.2×10 -9 in winter, respectively. The results of univariate regression analysis showed that their personal NO X exposure levels were significantly associated with city, season, gender, average daily cooking times, and ambient NO 2 concentrations measured at fixed-site monitoring stations. In addition to the above factors, the personal NO X exposure levels were also significantly associated with educational level and the personal NO 2 exposure levels were also significantly associated with passive smoking, average daily home time, cooking energy type, residential distance from main traffic road, and use of kitchen ventilators. Multivariate regression analysis showed that the personal exposure levels of NO 2 and NO X were significantly lower in Tianjin than that in Shanghai, were significantly lower in summer than that in winter, and were significantly and positively associated with ambient NO 2 concentrations measured at fixed-site monitoring stations. In addition, personal NO X exposure levels were significantly lower in females than in males, and personal NO 2 exposure levels were significantly positively associated with average daily cooking times and significantly inversely associated with average daily home time. For every interquartile range ( IQR ) increase (12.7×10 -9 ) in ambient NO 2 , the personal NO 2 exposure levels increased by 27.5% (95% CI : 17.0%-38.9%), and personal NO X exposure levels increased by 16.1% (95% CI : 7.1%-25.8%)., Conclusion: Season, city and ambient NO 2 concentrations are significant influencing factors of personal exposure levels of NO 2 and NO X. At the same time, the personal exposures levels of NO 2 are also affected by lifestyle factors. Our study provides scientific evidence for making precise air pollution control decisions and reducing the exposure levels of NO X in the population.

Objective: To evaluate the association of pickled food、fried food and smoked food combined with smoking and alcohol drinking with lung cancer., Methods: A hospital-based case-control study was conducted. A total of 1902 cases(24-90 years old) diagnosed in the Union Hospital and First Affiliated Hospital of Fujian Medical University and Fuzhou General Hospital of Nanjing Military Region and 2026(23-87 years old) controls matched healthy populaition for age(±3 ages) and gender from January 2006 to December 2013. Unconditional Logistic regression was used to analyze the combined effects and interactions of pickled food, fried food and smoked food with smoking and drinking, and to explore their relationship with the risk of lung cancer., Results: The result of unconditional Logistic regression analysis demonstrated that fried food and smoked food were risk factors of lung cancer. Compare with the people whose fired food intake<3 times/week, the people whose fired food intake ≥3 times/week had a 2. 954-folds increased lung cancer risk(95% CI 2. 065-4. 226). Compare with the people whose smoked food intake<3 times/week, the people whose smoked food intake ≥3 times/week had a 6. 774-folds increased lung cancer risk(95% CI 3. 309-13. 866). The result of combined effect demonstrated that compare with the non-smoking drinker whose food intake score was 0, the smoking drinker whose food intake score was 1 had a 2. 108-folds increased lung cancer risk(95% CI 1. 551-2. 865); compare with the non-smoking drinker whose food intake score was 0, the smoking drinker whose food intake score ≥2 had a 2. 191-folds increased lung cancer risk(95% CI 1. 377-3. 484). The result of interaction analysis demenstrated that intake of two or three kinds of risky food(≥1 time/week) increased the risk of lung cancer(OR = 1. 309, 95% CI 1. 010-1. 696) and it was more dangerous to smokers and drinkers. As for smokers, intake of two or three kinds of risky food was associated with an increased risk of lung cancer in an exposure-response manner(Ptrend<0. 001)., Conclusion: The intake of fried food and smoked food are independent risk factors of lung cancer. In addition, the pickled food, fried food and smoked food have combined effects on smoking and alcohol drinking, and the risk of lung cancer increases when the risk factors are present. The intake of the three kinds of risky food increases the risk of lung cancer in smokers.