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Summary: Approaches for detecting micro(nano)plastics (MNPs) released from intravenous infusion products (IVIPs) are vital for evaluating the safety of both IVIPs and their derived MNPs on human health, yet current understanding is limited. Here, we present a protocol for detecting polyvinyl chloride (PVC) MNPs by combining Raman spectroscopy, scanning electron microscopy equipped with energy-dispersive X-ray spectroscopy (SEM-EDS), and pyrolysis-gas chromatography-mass spectrometry (Py-GC-MS). We describe steps for collecting, pretreating, and measuring PVC MNPs released from IVIPs.For complete details on the use and execution of this protocol, please refer to Li et al.1 : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics.

The wide application of nanomaterials and plastic products generates a substantial number of nanoparticulate pollutants in the environment. Nanoparticulate pollutants are quite different from their bulk counterparts because of their unique physicochemical properties, which may pose a threat to environmental organisms and human beings. To accurately predict the environmental risks of nanoparticulate pollutants, great efforts have been devoted to developing reliable methods to define their occurrence and track their fate and transformation in the environment. Herein, we summarized representative studies on the preconcentration, separation, formation, and transformation of nanoparticulate pollutants in environmental samples. Finally, some perspectives on future research directions are proposed.

Summary: Understanding the pathways of human exposure to micro(nano)plastics (MNPs) is crucial for assessing their health impacts. Intravenous infusion can induce MNPs direct entry into the human blood, posing serious risks on human health, but remains unclear. Herein, we developed comprehensive analytical methods to detect polyvinyl chloride (PVC) MNPs down to 20 nm, and found about 0.52 μg equal to 105–1011 particles of PVC-MNPs released from intravenous infusion products (IVIPs) during each intravenous infusion of 250 mL injection. The released amounts of MNPs from IVIPs were dependent on the plastic materials, and the injection volume and composition. These findings indicated that the released MNPs should be directly introduced into the human blood circulatory system, causing serious impacts on human health. Our study reveals a previously ignored but important pathway of human exposure to MNPs, and calls for further research on the potential risks of these MNPs on human health.

Cadmium (Cd), as a type of heavy metal, can increase the incidence of many diseases, even in low concentrations. In this study, tobermorite was hydrothermally synthesized and then applied to adsorb Cd2+ from an aqueous solution. The physicochemical characteristics of the synthesized tobermorite were detected, and the results indicated that the well-crystallized tobermorite had a lot of mesopores and a large specific surface area of 140.92 m2/g. It acquired a pH self-adjustment ability via spontaneously releasing Ca2+ and OH- into the aqueous solution. The effects of different factors on Cd2+ removal were investigated. For Cd2+, the removal efficiency could reach 99.71% and the maximum adsorption capacity was 39.18 mg/g using tobermorite. The adsorption data was best fitted with the pseudo-second-order kinetic and Langmuir isotherm models. In addition, there was no strict limit on the solution pH in Cd2+ adsorption because the tobermorite could adjust the solution pH to an alkaline atmosphere spontaneously. The efficient removal of Cd2+ using tobermorite was a result of surface complexation and ion exchange.

Previous studies have indicated that the preformed martensite has a significant effect on the subsequent bainite transformation of nanobainite bearing steel, but its effects on the microstructure and mechanical properties are still unclear. In this paper, the effects of preformed martensite and its volume fraction on microstructure and mechanical properties of nanobainite bearing steel were investigated by using scanning electron microscope, transmission electron microscope, X-ray diffractometer and wear resistance experiments. It was demonstrated that the introduction of preformed martensite can refine bainitic microstructure and increase the volume fraction of retained austenite, but reduces the mechanical stability of retained austenite. When the volume fraction of preformed martensite is less than 20%, the hardness and wear resistance of nanobainite bearing steel gradually increases with the increase in the volume fraction of preformed martensite, but the toughness of steel decreases gradually. When the volume fraction of preformed martensite reaches 25%, the properties of nanobainite bearing steel, especially the wear resistance, obviously deteriorate. The optimized volume fraction of preformed martensite is ~10%–15% by comprehensive comparison the mechanical properties of nanobainite bearing steel.

Abstract Background Radiation-induced lung fibrosis (RILF) is a severe and life-threatening complication of thoracic radiotherapy. Cell death is the key issue in RILF. Ferroptosis is a form programmed cell death implicated in the pathologies of inflammation. This study aimed to investigate the role of ferroptosis in RILF, and the effectiveness and the potential underlying mechanism of ferroptosis inhibitor on RILF. Methods Immunofluorescence, western blot and RT-PCR assays were performed to examine the ferroptosis maker glutathione peroxidase 4 (GPX4) in a mice RILF model. The lung tissue sections were stained with hematoxylin and eosin (H&E), Masson trichrome staining and Sirius-Red staining to evaluate the histopathological changes in RILF mice. Reactive oxygen species (ROS) and hydroxyproline (HYP) in lungs were measured by the relevant kits. The serum levels of inflammatory cytokines (TNF-α, IL-6, IL-10, and TGF-β1) were measured with Elisa. The protein and mRNA levels of GPX4, nuclear factor (erythroid-derived 2)-like 2 (Nrf2), hemeoxygenase-1 (HO1) and quinone oxidoreductase 1 (NQO1) in lungs were examined by western blot and RT-PCR. Results GPX4 levels of the irradiated lungs were significantly down-regulated than the groups with no irradiation, and the ferroptosis inhibitor, liproxstatin-1, increased GPX4 levels significantly in RILF mice. Treatment with liproxstatin-1 lowered the Szapiel and Ashcroft scores significantly, down-regulated the levels of ROS and HYP in lungs and reduced the serum inflammatory cytokines levels in RILF mice. The protein and the mRNA levels of Nrf2, HO1 and NQO1 were up-regulated by liproxsratin-1 in RILF. Conclusions Our data suggested that ferroptosis played a critical role in RILF, ferroptosis inhibitor liproxstatin-1 alleviated RILF via down-regulation of TGF-β1 by the activation of Nrf2 pathway. The effectiveness of ferroptosis inhibition on RILF provides a novel therapeutic target for RILF.

Background and objective There exsits intimate relationship between infection with chlamydia pneumoniae (Cpn) and lung cancer incidence. But few studies have been reported about radiation-induced pulmonary lesion in lung cancer patients infected with Cpn. The aim of this study is to explore the correlation between cytokines related to radiation-induced pulmonary lesion and Cpn IgG positive in lung cancer patients. Methods A total of 69 patients with lung cancer received chest radiotherapy. Blood samples were collected and frozen before radiotherapy (pre-RT), middle radiotherapy (mid-RT) and after radiotherapy (post-RT). Cpn IgG and levels of IL-1β, SP-A, TGF-β, and TNF-α were measured by enzymelinked immunosorbent assay (ELISA). Results In the total of 69 patients, 21 patients were Cpn IgG positive, 48 patients negative. The positive rate was 30.43%. In mid-RT concentration of IL-1β in Cpn IgG positive and negative group were (35.82±10.09) ng/L and (30.01±6.46) ng/L, with statistically significant difference (P < 0.05). Pre-RT and post-RT concentrations of IL-1β in Cpn IgG positive and negative group had no statistically significant difference. Mid-RT concentrations of SP-A in Cpn IgG positive group and negative group were (641.78±106.81) ng/L and (100.86±61.4) ng/L respectively, with statistically significant difference (P < 0.05). Post-RT concentration of SP-A in Cpn IgG positive and negative group were (657.47±115.19) ng/L and (93.23±47.15) ng/L respectively, with statistically significant difference (P < 0.05). Concentrations of TNF-α in Cpn IgG positive and negative group had no statistically significant difference. Concentrations of TGF-β in Cpn IgG positive group were (710.67±358.16) pg/mL in pre-RT, (1,002.06±542.16) pg/mL in mid-RT, (2,125.16±1,522.29) pg/mL in post-RT; those in negative group were (867.77±412.48) pg/mL, (914.05±425.70) pg/mL, (1,073.36±896.01) pg/mL. Concentration of TGF-β in post-RT between Cpn IgG positive and negative group had statistically significant difference (P < 0.05). Conclusion Cpn IgG positive in lung cancer patients influenced levels of IL-1β, SP-A, TGF-β during chest radiotherapy. This might aggravate radiation-induced pulmonary lesion.

Fusion tags are commonly employed to enhance target protein expression, improve their folding and solubility, and reduce protein degradation in expression of recombinant proteins. Ubiquitin (Ub) and SUMO are highly conserved small proteins in eukaryotes, and frequently used as fusion tags in prokaryotic expression. ThiS, a smaller sulfur-carrier protein involved in thiamin synthesis, is conserved among most prokaryotic species. The structural similarity between ThiS and Ub provoked us into expecting that the former could be used as a fusion tag. Hence, ThiS was fused to insulin A and B chains, murine Ribonuclease Inhibitor (mRI) and EGFP, respectively. When induced in Escherichia coli, ThiS-fused insulin A and B chains were overexpressed in inclusion bodies, and to higher levels in comparison to the same proteins fused with Ub. On the contrast, ThiS fusion of mRI, an unstable protein, resulted in enhanced degradation that was not alleviated in protease-deficient strains. While the degradation of Ub- and SUMO-fused mRI was less and seemed protease-dependent. Enhanced degradation of mRI did not occur for the fusions with half-molecules of ThiS. When ThiS-tag was fused to the C-terminus of EGFP, higher expression, predominantly in inclusion bodies, was observed again. It was further found that ThiS fusion of EGFP significantly retarded its refolding process. These results indicated that prokaryotic ThiS is able to promote the expression of target proteins in E. coli, but enhanced degradation may occur in case of unstable targets. Unlike eukaryotic Ub-based tags usually increase the solubility and folding of proteins, ThiS fusion enhances the expression by augmenting the formation of inclusion bodies, probably through retardation of the folding of target proteins.

BACKGROUND: The radiation-induced lung injury is a common complication from radiotherapy in lung cancer. CpG ODN is TLR9 activator with potential immune modulatory effects and sensitization of radiotherapy in lung cancer. This study aimed to examine the effect of CpG ODN on acute radiation-induced lung injury in mice. METHODS AND RESULTS: The mouse model of radiation-induced lung injury was established by a single dose of 20 Gy X-rays exposure to the left lung. The results showed that the pneumonia score was lower in RT+CpG group than in RT group on 15th and 30th days. Compared with RT group, CpG ODN reduced the serum concentrations of MDA (P < 0.05) and increased the serum concentrations of SOD, GSH (P < 0.05). The serum concentration of TNF-α in RT+CpG group was lower on 15th and 30th days post-irradiation (P < 0.05). CONCLUSION: The study demonstrated that CpG ODN has preventive effects of acute radiation-induced lung injury in mice. Lung inflammatory reaction and oxidative stress are promoted in the initiation of radiation-induced pneumonia. CpG ODN may reduce the injury of reactive oxygen species and adjust the serum TNF-α concentration in the mice after irradiation, which reduces the generation of the inflammatory cytokines.