Double-Network Luminescent Films Constructed Using Sulfur Quantum Dots and Lanthanide Complexes.

Although UV light-switchable luminescent films are of importance for application in soft optical devices and anticounterfeiting labels, there are still challenges in developing such films integrated with outstanding luminescent property, high self-healing efficiency, and simultaneously excellent mechanical strength. Herein, double-network (DN) luminescent films are designed and constructed via an intermolecular hydrogen bond crosslinking strategy of poly(ethylene glycol) (PEG) in sulfur quantum dots (S-QDs) and polyurethane (PU), where S-QDs ("stone" one) play dual roles of acting both as a soft segment to crosslink another segment PU ("bird" one) and also as the origin of a luminescence center ("bird" two) in films. In addition, lanthanide(III) complexes (LnCs, Ln═Eu3+, Tb3+) are employed as another emission source to embed in the films and switch the emission colors of DN films from the multicolor (red-yellow-green) of LnCs to the blue color of S-QDs by changing the ultraviolet excitation wavelength from 254 to 365 nm. It is worth noting that the crosslinking network strategy can effectively prevent S-QDs and LnCs from aggregating or leaking and enable both luminescence centers to homogeneously distribute, resulting in luminescent DN films possessing extraordinary UV light-switchable luminescence, improved mechanical property, and excellent self-healing ability. This work presents a viable method for the design and fabrication of luminescent films with multifunctional applications in flexible robotics, wearable devices, and dual-luminescent anticounterfeiting materials.

Identification of the hormetic dose-response and regulatory network of multiple metals co-exposure-related hypertension via integration of metallomics and adverse outcome pathways.

Environmental stressors, including heavy metals, can be associated with hypertension development. However, little information regarding the dose-response relationship and toxicity mechanisms of metal mixtures with hypertension development is currently available. Therefore, we recruited 940 participants from six factories in northeastern China and measured the urinary concentrations of 19 metals. Then, we used Bayesian kernel machine regression (BKMR) to explore associations between metals co-exposure and hypertension. The BKMR model indicated a hermetic dose-response relationship between eight urinary metals (Co, Cr, Ni, Cd, As, Fe, Zn, and Pb) and hypertension risk. Moreover, heterogeneous and non-linear association patterns were detected across different metals/metalloids concentrations. Next, for the first time, we analyzed data of chemicals containing specific metal elements in the Comparative Toxicogenomics Database (CTD) from a disease perspective and provided insights from various biological levels to explain heavy metal co-exposure-related hypertension. On the molecular scale, 43 chemical components and 112 potential target genes were detected for metal exposure-related hypertension. Further, the network topology analysis indicated that target genes such as insulin (INS, degree = 78), albumin (ALB, degree = 74), renin (REN, degree = 71), interleukin-6 (IL6, degree = 70), endothelin 1 (EDN1, degree = 70), and endothelial nitric oxide synthase (NOS3, degree = 69) have a strong correlation with heavy metals co-exposure. Finally, we used integrative analyses in the adverse outcome pathway (AOP) wiki to analyze the co-exposure of heavy metals and hypertension and support an integrated metallomics approach. We selected the AOP 149 as the framework and found that the molecular initiating events (MIEs) of hypertension stems from the oxidation of AA residues on critical peptides of the NO pathway. The NOS3 was particularly promising since its subunit has three metal ion cross-linking domains with Zn2+, Fe2+, and Ga3+, which might serve as a binding site for heavy metal ions.

Trends in global, regional and national incidence of pneumoconiosis caused by different aetiologies: an analysis from the Global Burden of Disease Study 2017.

OBJECTIVES: Pneumoconiosis remains a major global occupational health hazard and illness. Accurate data on the incidence of pneumoconiosis are critical for health resource planning and development of health policy. METHODS: We collected data for the period between 1990 and 2017 on the annual incident cases and the age-standardised incidence rates (ASIR) of pneumoconiosis aetiology from the Global Burden of Disease Study 2017. We calculated the average annual percentage changes of ASIR by sex, region and aetiology in order to determine the trends of pneumoconiosis. RESULTS: Globally, the number of pneumoconiosis cases increased by a measure of 66.0%, from 36 186 in 1990 to 60 055 in 2017. The overall ASIR decreased by an average of 0.6% per year in the same period. The number of pneumoconiosis cases increased across the five sociodemographic index regions, and there was a decrease in the ASIR from 1990 to 2017. The ASIR of silicosis, coal workers' pneumoconiosis and other pneumoconiosis decreased. In contrast, measures of the ASIR of asbestosis displayed an increasing trend. Patterns of the incidence of pneumoconiosis caused by different aetiologies were found to have been heterogeneous for analyses across regions and among countries. CONCLUSION: Incidence patterns of pneumoconiosis which were caused by different aetiologies varied considerably across regions and countries of the world. The patterns of incidence and temporal trends should facilitate the establishment of more effective and increasingly targeted methods for prevention of pneumoconiosis and reduce associated disease burden.