Search

In marine applications, the scaled wind turbine model (SWTM) based aerodynamic testing apparatus is regarded as one of the most effective approaches to predict the aerodynamic performance of offshore floating wind turbines (OFWTs). To fully disclose the aerodynamics of OFWTs, such kind of apparatus should meet two design requirements: (1) accurate representation of the aerodynamic characteristics of reference wind turbines and (2) reasonable reproduction of the environmental factors from real-world wind-wave-coupled field. Baring with these considerations, the authors propose a cost-effective SWTM-based aerodynamic testing apparatus, which consists of an innovative SWTM, a wind-wave simulator (WWS) and a data acquisition and analyses system. The proposed SWTM is featured by a double-deck tower, which satisfies the requirements of similarity in geometry, stiffness and mass, and a set of redesigned blades. The proposed WWS is capable of simulating both the time-varying inflow wind and the wave-induced platform motions through a wind field generator and a motion simulator. Based on the developed apparatus, a series of aerodynamic tests are conducted to validate the effectiveness of the apparatus design. In addition, the coupling effects of inflow wind and platform motions on the aerodynamics of OFWT are further revealed through experimental tests.

This paper investigates the payment scheme and forecast information sharing issues in the express delivery logistics with the high-speed railway. The HSR carriers need to coordinate the transportation capacity between passenger and freight. It is widely recognized that the advance payment scheme (APS) using as deposit is a beneficial way for the HSR carriers to make decisions on the transportation capacity preserved for express delivery. However, the express service providers, who possess private forecast information of express delivery demand, may share inaccurate information with the HSR carriers to acquire sufficient preserved transportation capacity. This paper discusses what payment scheme is preferred by the HSR carrier, the express service provider through discussing the deposit decisions with or without forecast information sharing. We show that sharing demand forecast information can reduce the prereserved capacity and increase the profits of the HSR carrier. With the delayed payment scheme (DPS), the express service provider has no motivation to share the information; while with the APS, the HSR carrier can reasonably choose the deposit to encourage the express service provider to share the demand information. Our analysis also shows that the HSR carrier’s profits with the APS is restricted by the investment returns and the express service provider’s information sharing decisions. We also analyze the value range of the deposit, which is a proportion of the overall payment, that allows both the HSR carrier and the express service provider to prefer the APS, as well as to encourage the express service provider to share the demand information.

BackgroundWe previously found that occupational exposure to diesel engine exhaust (DEE) was associated with alterations to 19 biomarkers that potentially reflect the mechanisms of carcinogenesis. Whether DEE is associated with biological alterations at concentrations under existing or recommended occupational exposure limits (OELs) is unclear.MethodsIn a cross-sectional study of 54 factory workers exposed long-term to DEE and 55 unexposed controls, we reanalysed the 19 previously identified biomarkers. Multivariable linear regression was used to compare biomarker levels between DEE-exposed versus unexposed subjects and to assess elemental carbon (EC) exposure-response relationships, adjusted for age and smoking status. We analysed each biomarker at EC concentrations below the US Mine Safety and Health Administration (MSHA) OEL (<106 µg/m3), below the European Union (EU) OEL (<50 µg/m3) and below the American Conference of Governmental Industrial Hygienists (ACGIH) recommendation (<20 µg/m3).ResultsBelow the MSHA OEL, 17 biomarkers were altered between DEE-exposed workers and unexposed controls. Below the EU OEL, DEE-exposed workers had elevated lymphocytes (p=9E-03, false discovery rate (FDR)=0.04), CD4+ count (p=0.02, FDR=0.05), CD8+ count (p=5E-03, FDR=0.03) and miR-92a-3p (p=0.02, FDR=0.05), and nasal turbinate gene expression (first principal component: p=1E-06, FDR=2E-05), as well as decreased C-reactive protein (p=0.02, FDR=0.05), macrophage inflammatory protein-1β (p=0.04, FDR=0.09), miR-423-3p (p=0.04, FDR=0.09) and miR-122-5p (p=2E-03, FDR=0.02). Even at EC concentrations under the ACGIH recommendation, we found some evidence of exposure-response relationships for miR-423-3p (ptrend=0.01, FDR=0.19) and gene expression (ptrend=0.02, FDR=0.19).ConclusionsDEE exposure under existing or recommended OELs may be associated with biomarkers reflective of cancer-related processes, including inflammatory/immune response.

BackgroundMillions of workers worldwide are exposed to diesel engine exhaust (DEE), a known genotoxic carcinogen. Alu retroelements are repetitive DNA sequences that can multiply and compromise genomic stability. There is some evidence linking altered Alu repeats to cancer and elevated mortality risks. However, whether Alu repeats are influenced by environmental pollutants is unexplored. In an occupational setting with high DEE exposure levels, we investigated associations with Alu repeat copy number.MethodsA cross-sectional study of 54 male DEE-exposed workers from an engine testing facility and a comparison group of 55 male unexposed controls was conducted in China. Personal air samples were assessed for elemental carbon, a DEE surrogate, using NIOSH Method 5040. Quantitative PCR (qPCR) was used to measure Alu repeat copy number relative to albumin (Alb) single-gene copy number in leucocyte DNA. The unitless Alu/Alb ratio reflects the average quantity of Alu repeats per cell. Linear regression models adjusted for age and smoking status were used to estimate relations between DEE-exposed workers versus unexposed controls, DEE tertiles (6.1–39.0, 39.1–54.5 and 54.6–107.7 µg/m3) and Alu/Alb ratio.ResultsDEE-exposed workers had a higher average Alu/Alb ratio than the unexposed controls (p=0.03). Further, we found a positive exposure–response relationship (p=0.02). The Alu/Alb ratio was highest among workers exposed to the top tertile of DEE versus the unexposed controls (1.12±0.08 SD vs 1.06±0.07 SD, p=0.01).ConclusionOur findings suggest that DEE exposure may contribute to genomic instability. Further investigations of environmental pollutants, Alu copy number and carcinogenesis are warranted.

ObjectivesTrichloroethylene (TCE) -induced hypersensitivity syndrome (TIHS) is a potentially life-threatening disease. Several genetic susceptibility biomarkers have been found to be associated with TIHS, and this systematic prospective study has been conducted to evaluate the utility of these genetic susceptibility biomarkers in preventing the disease.MethodsThe newly hired TCE-exposed workers were recruited from March 2009 to October 2010. HLA-B*13:01genotyping and 3-month follow-up procedure were conducted. All workers were monitored for adverse reaction by telephone interview every week. The workers with early symptoms of TIHS were asked to go to the hospital immediately for further examination, diagnosis and treatment. The medical expense record data of patients with TIHS were collected for cost-effectiveness analysis in 2018.ResultsAmong 1651 workers, 158 (9.57%) were found to carry the HLA-B*13:01allele and 16 (0.97%) were diagnosed with TIHS. HLA-B*13:01allele was significantly associated with an increased TIHS risk (relative risk=28.4, 95% CI 9.2 to 86.8). As a risk predictor of TIHS, HLA-B*13:01testing had a sensitivity of 75%, a specificity of 91.1% and an area under curve of 0.83 (95% CI 0.705 to 0.955), the positive and negative predictive values were 7.6% and 99.7%, respectively. The incidence of TIHS was significantly decreased in HLA-B*13:01non-carriers (0.27%) compared with all workers (0.97%, p=0.014). Cost-effectiveness analysis showed that HLA-B*13:01screening could produce an economic saving of $4604 per TIHS avoided.ConclusionsProspective HLA-B*13:01screening may significantly reduce the incidence of TIHS and could be a cost effective option for preventing the disease in TCE-exposed workers.

This study assesses the effects of long-term exposure to ambient air pollutants on inflammatory response and lung function. We selected 390 male coke oven workers with exposure to polycyclic aromatic hydrocarbons (PAHs) and fine particulate matter (PM2.5) and 115 control workers. The average duration in the exposed group was 9.10 years. The total amount of PAHs was more enriched in PM2.5which collected from the coke oven workshops compared with the control areas. Correspondingly, the internal PAHs exposure indicated by urinary 1-hydroxypyrene (1-OHP) in the exposure group increased 25.7-fold compared to that of the control group. Moreover, the increasing level of urinary 1-OHP was associated with the decrease of forced expiratory volume in 1 s to forced vital capacity ratio (FEV1/FVC). In non-current smokers of exposure group, inverse correlation of 1-OHP with FEV1/FVC was also found. Particularly, an exposure duration-dependent decline in FEV1/FVC and mean forced expiratory flow between 25% and 75% of forced vital capacity (FEF25–75%) indicated that small airways were functionally obstructed. Furthermore, the increasing serum high-sensitivity C-reactive protein (hs-CRP) was correlated with the decline in pulmonary function in all subjects. These findings provide a clue that long-term exposure to PAHs-enriched PM2.5impairs pulmonary function in occupational population.

Diesel engine exhaust (DEE) is a predominant contributor to urban air pollution. The International Agency for Research on Cancer classified DEE as a group I carcinogen. Inflammatory response is considered to be associated with various health outcomes including carcinogenesis. However, human data linking inflammation with long-term DEE exposure are still lacking. In this study, a total of 137 diesel engine testing workers with an average exposure of 8.2 years and 108 unexposed controls were enrolled. Peripheral blood samples were collected from all subjects, and the association of DEE exposure with inflammatory biomarkers was analyzed. Overall, DEE exposed workers had a significant increase in the C-reactive protein (CRP) and a significant decrease in cytokines including interleukin (IL)-1β, IL-6, IL-8, and macrophage inflammatory protein (MIP)-1β compared to controls after adjusting for age, BMI, smoking status, and alcohol use, and findings were highly consistent when stratified by smoking status. In addition, exposure time dependent patterns for IL-6 and CRP were also found (Ptrend= 0.006 and 0.026, respectively); however, the levels of IL-1β and MIP-1β were significantly lower in subjects with a DEE working time of less than 10 years compared with the controls and then recovered to control levels in workers exposed for >10 years. There were no significant differences in blood cell counts and major lymphocyte subsets between exposed workers and the controls. Our results provide epidemiological evidence for the relationship between DEE exposure and immunotoxicity considering the important roles of cytokines in immunological processes.

Previous studies have shown an etiologic link between exposure to polycyclic aromatic hydrocarbons (PAHs) and lung cancer development. While the tumor suppressor gene RASSF1ais mostly silenced by DNA methylation in various tumors, it is unclear whether aberrant methylation of RASSF1ais involved in the process of PAH-induced biological consequences. To address this issue, 69 coke-oven workers (exposure group) and 46 steel rolling workers (control group) were recruited in this study. Bisulfite sequencing (BSP) was performed to examine the methylation status of RASSF1apromoter in peripheral blood lymphocytes (PBLs) from PAH-exposed and control workers. The DNA fragment examined lies across −282 bp to +638 bp from the transcription start site, containing 966 bp and 87 CpG sites across the RASSF1apromoter. Of the 87 CpG sites we analyzed, 5 were significantly hypermethylated in the PAH-exposed workers compared to the control (2.5% vs.0%, P< 0.001). We defined these 5 CpG sites as “Hot CpG sites”. The levels of methylation from Hot CpG sites were positively correlated with the concentration of urinary 1-OHP (β= 0.98, P= 0.001) and the frequency of cytokinesis-block micronucleus (CBMN) (β= 1.29, P= 0.019) in PBLs, indicating that PAH exposure induced CpG site-specific hypermethylation of RASSF1awas associated with the levels of internal exposure and the degree of DNA damage. Moreover, the Hot CpG site hypermethylation and the corresponding down-regulation of RASSF1aexpression were also found in COE (coke-oven emission)-treated human primary lymphocytes and HBE cells. Taken together, these observations revealed that RASSF1aHot CpG site hypermethylation could be a promising biomarker for the PAH exposure and DNA damage.

The aryl hydrocarbon receptor (AhR) is an important nuclear receptor and mediates the biological consequences in response to environmental stimuli. However, the mechanism of AhR regulation in this process is still unclear. In this study, we attempt to identify which microRNAs (miRNAs) specifically modify the expression of AhR in A549 and HepG2 cells. miR-203 was predicted to target AhR by bioinformatic analysis. We performed a luciferase reporter assay and found miR-203 specifically binding to the mRNA 3′-UTR region of AhR, leading to the suppression of the expression of AhR at both the mRNA and protein levels. When exposed to TCDD or BaP, the expression of miR-203 could be induced and resulted in a reduction of AhR expression. The ectopic expression of miR-203 in A549 and HepG2 cells attenuated the activation of AhR induced by TCDD and subsequently suppressed its downstream regulated genes including cytochrome P450 1A1, 1A2 (CYP1A1, CYP1A2), and NADPH dehydrogenase 1 (NQO1). Moreover, overexpression of miR-203 affects the inducible enzyme activity of CYP1A1 by TCDD induction and the cytotoxicity induced by BaP. Taken together, we identify a novel miRNA that negatively regulates the expression of AhR, demonstrating that epigenetic modifications play a critical role in the metabolic activation of environmental chemicals.

An aryl hydrocarbon receptor (AhR) is a transcription factor mediating the responses to polycyclic aromatic hydrocarbon (PAH) compounds. To investigate the epigenetic mechanism involved in the regulation of AhR, we treated human bronchial epithelial cells (16HBE) with benzo(a)pyrene (BaP) and found a transcriptional suppression of AhR in a dose- and time-dependent manner. Suppression of AhR significantly attenuated the extent of BaP-induced CYP1A1 expression and the cell growth arrest, and conferred 16HBE cells insensitive to DNA damage. In addition, we found that the mRNA level of AhR was elevated more than twice in 16HBE cells treated with histone deacetylase inhibitor trichostatin A (TSA), indicating that AhR expression might be regulated viahistone modification. Moreover, we showed that BaP or 3-MC treatment led to a reduction of acetylation at residues H3K9, H3K18 and H3K27, suggesting that histone modifications are associated with chemical exposure. Using chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR), we further demonstrate that the reduction of histones H3K18ac and H3K27ac is correlated with the decreased binding affinity with the AhR promoter in HBE cells treated with BaP or 3-MC. In addition, we identified that specific regions located at the transcriptional start site (TSS) of the AhR gene were responsible for H3K18ac- and H3K27ac-related transcriptional activity of the AhR promoter. Taken together, we identified that two specific histone modifications, H3K18ac and H3K27ac, were involved in regulation of the transcriptional activation of AhR, which might contribute to BaP-induced toxicity and the response to DNA damage.

We report the application of modified pulse-coupled neural network (PCNN) models as an image processing tool to improve the quality of digital halftoning. Four factors including weight matrice, internal activity computation, type of error diffusion and linking coefficient were researched and optimized in terms of the PSNR metric and visual inspection on halftoning simulations. Experimental results show that the optimized PCNN model is able to yield satisfying halftoning outputs, which has better quality than that obtained by using the traditional order dither algorithm. Moreover, because of the utilization of random function in the modified PCNN model, simulated images generated from that PCNN model eliminate the periodic visual defect that the order dither innately has and therefore can potentially get rid of moiré pattern if used for printing color image. This research, on the one hand, provides a new way to do digital halftoning, on the other hand, expands the application field of the PCNN method.

Compared with the T-cell potential of particulate matter (PM) in animal studies, comprehensive evaluation on the impairments of T-cell response and exposure–response from PM and its components in human population is limited. There were 768 participants in this study. We measured environmental PM and its polycyclic aromatic hydrocarbons (PAHs) and metals and urinary metabolite levels of PAHs and metals among population. T lymphocyte and its subpopulation (CD4+T cells and CD8+T cells) and the expressions of T-bet, GATA3, RORγt, and FoxP3were measured. We explored the exposure–response of PM compositions by principal component analysis and mode of action by mediation analysis. There was a significant decreasing trend for T lymphocytes and the levels of T-betand GATA3with increased PM levels. Generally, there was a negative correlation between PM, urinary 1-hydroxypyrene, urinary metals, and the levels of T-betand GATA3expression. Additionally, CD4+T lymphocytes were found to mediate the associations of PM2.5with T-betexpression. PM and its bound PAHs and metals could induce immune impairments by altering the T lymphocytes and genes of T-betand GATA3.