The value of single biomarkers in the diagnosis of silicosis: A meta-analysis.

This study aims to establish a scientific foundation for early detection and diagnosis of silicosis by conducting meta-analysis on the role of single biomarkers in independent diagnosis. The combined sensitivity (Sen), specificity (Spe), positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic score, and diagnostic odds ratio (DOR) were 0.84 (95% confidence interval (CI): 0.77-0.90), 0.83 (95% CI: 0.78-0.88), 5.08 (95% CI: 3.92-6.59), 0.19 (95% CI: 0.13-0.27), 3.31 (95% CI: 2.88-3.74) and 27.29 (95% CI: 17.77-41.91), respectively. The area under the curve (AUC) was 0.90 (95% CI: 0.88-0.93). The Fagan plot shows a positive posterior probability of 82% and a negative posterior probability of 15%. This study establishes an academic basis for the swift identification, mitigation, and control of silicosis through scientific approaches. The assessed biomarkers offer precision and dependability in silicosis diagnosis, opening novel paths for early detection and intervention, thereby mitigating the disease burden associated with silicosis.

Silica nanoparticles induce ferroptosis of HUVECs by triggering NCOA4-mediated ferritinophagy.

Silica nanoparticles (SiNPs) have been widely used in electronics, chemistry, and biomedicine. Human exposure to SiNPs and possible health effects have attracted much attention. The potential cardiovascular toxicity of SiNPs and their related mechanisms are still unclear. Therefore, in this study, we investigated the toxic effects of SiNPs on human umbilical vein endothelial cells (HUVECs). We found that SiNPs could induce HUVECs ferroptosis. The results showed that the level of intracellular divalent iron and lipid peroxidation increased, and mitochondrial cristae decreased. In addition, the pretreatment of the iron chelator deferoxamine mesylate (DFO) could alleviate the ferroptosis of cells. Interestingly, pretreatment of 3-methyladenine (3-MA), an autophagy/PI3K inhibitor could partially inhibit autophagy and reduce ferroptosis, which indicated that autophagy played an important role in cell ferroptosis. Additionally, after knocking down nuclear receptor coactivator 4 (NCOA4), Ferritin Heavy Chain 1 (FTH1) expression was up-regulated, and the levels of divalent iron and lipid peroxidation decreased, which suggested that NCOA4 mediated the ferroptosis of HUVECs induced by SiNPs. In conclusion, this study shows that SiNPs can induce cardiovascular toxicity in which there is ferroptosis. NCOA4-mediated ferritinophagy and resultant ferroptosis by SiNPs may play an important role. This study provides a new theoretical strategy for the treatment and prevention of cardiovascular diseases in the future.

Involvement of the JNK/HO­1/FTH1 signaling pathway in nanoplastic­induced inflammation and ferroptosis of BV2 microglia cells.

Nanoplastics (NPs) are a newly discovered type of environmental pollutant. The potential for neurotoxicity caused by NPs and their mechanisms are unclear. The present study aimed to determine the molecular mechanism underlying neurotoxicity induced by NPs. Microglia (BV2) cells were used for in vitro studies, and it was found that NPs invaded cells, activated inflammasomes, induced the release of significant quantities of inflammatory factors by detection of inflammatory response­associated proteins through Western blot and ELISA. By detection of FITC, SOD, GSH, cellular iron level, and ferroptosis­related proteins, it was found that NPs compromised the anti­oxidative mechanisms of cells, increased intracellular lipid peroxidation and Fe2+ concentration and triggered inflammatory reactions and ferroptosis. Pretreatment with reactive oxygen species (ROS) inhibitor N­acetylcysteine (NAC) alleviated induction of inflammatory reactions and ferroptosis of cells. In addition, inhibiting expression of c­Jun N­terminal kinase (JNK) increased expression of heme oxygenase (HO­1), resulting in decreased ferroptosis, indicating that the JNK/HO­1 signaling pathway was involved in NP­induced effects on ferroptosis in BV2 cells. In conclusion, NPs could induce inflammatory responses and ferroptosis in BV2 cells. JNK/HO­1 mediated ferroptosis may serve an important role in the toxicity of microglia induced by NPs. This study provided novel evidence for the toxic effects of NPs and highlighted a theoretical mechanistic basis for safe prevention and treatment of plastic pollution­induced neurotoxicity.

Prediction of radiative properties of spherical microalgae considering internal heterogeneity and optical constants of various components.

Most of the current predictions of the radiative properties of microalgae use the homogeneous sphere approximation based on the Mie scattering theory, and the refractive indices of the model were regarded as fixed values. Using the recently measured optical constants of various microalgae components, we propose a spherical heterogeneous model for spherical microalgae. The optical constants of the heterogeneous model were characterized by the measured optical constants of microalgae components for the first time. The radiative properties of the heterogeneous sphere were calculated using the T-matrix method and were well verified by measurements. It shows that the internal microstructure has a more significant effect on scattering cross-section and scattering phase function than absorption cross-section. Compared with the traditional homogeneous models selected with fixed values as refractive index, the calculation accuracy of scattering cross-section of the heterogeneous model improved by 15%-150%. The scattering phase function of the heterogeneous sphere approximation agreed better with measurements than the homogeneous models due to the more detailed description of the internal microstructure. It can be concluded that considering the internal microstructure of microalgae and characterizing the microstructure of the model by the optical constants of the microalgae components helps to reduce the error caused by the simplification of the actual cell.

Efficacy of Alveolar Type II Epithelial Cell Transplantation for Pulmonary Fibrosis: A Meta-Analysis.

Background: Cell transplantation is a promising therapeutic strategy for pulmonary fibrosis. In order to clarify the alveolar type II epithelial cell potential utility in the treatment of lung disease, we conducted a meta-analysis, to evaluate alveolar type II epithelial cells in animal models of lung injury and pulmonary fibrosis. Methods: This review followed the recommendations from the PRISMA statements, Comprehensive retrieval method was used to search Embase, PubMed, Cochrane, Chinese Knowledge Infrastructure, VIP and Wanfang databases. A total of 7 studies and 286 model rats were included. Two researchers independently screened the identified studies, based on inclusion and exclusion criteria. All analyses were conducted using Review Manager V.5.3 software. The combined standard mean difference (SMD) and 95% confidence interval (CI) of data from the included studies were calculated using fixed or random-effects models. Results: The analysis of three outcome indexes showed that the heterogeneity of the oxygen saturation group was high (I2=85%), the lung weight group (I2=64%) was close to moderate heterogeneity, and the lung hydroxyproline content group (I2=0) was not heterogeneous. Conclusion: Meta-analysis showed that transplantation of alveolar type II epithelial cells has beneficial effects, and no obvious adverse reactions. Alveolar type II epithelial cell transplantation can significantly reduce the intervention group and lung hydroxyproline content weight, improve the blood oxygen saturation, lung histo-pathology showed significant improvement in pulmonary fibrosis.

Protective Effect of Panax Notoginseng Saponins on Apolipoprotein-E-deficient Atherosclerosis-prone Mice.

BACKGROUND: It is widely recognized that atherosclerosis (AS) is related to vascular inflammation. Panax notoginseng saponins (PNS) extracted from the roots of Panax notoginseng have been shown to possess anti-inflammatory activity. It is widely used in the clinical treatment of cardiovascular and cerebrovascular diseases, but the protective effect of PNS on atherosclerosis is not fully understood. This study was designed to test the effects of PNS administration in apolipoprotein (apo)-E-deficient (ApoE-/-) mice on the activation of NF-κB p65, IL-1ß, IL-6, TNF-α and Calpain1 proteins. METHODS: 24 ApoE-/- mice fed with high-fat diet for 8 weeks to create the AS model. PNS, dissolved in three distilled water, was administered orally to two treatment groups at dosages of 60 mg/kg/d/mice and 180 mg/kg/d/mice. After 8 weeks, peripheral blood was collected for assessing the levels of TG, TC, LDL-C and HDL-C in serum by Biochemical Analyzer. HE staining was used to observe pathomorphological changes in the aortic root. Oil Red O staining was used to observe the lipid deposition in the aortic root. ELISA kits were used to assess the levels of IL-1ß and TNF-α in serum. The expression levels of NF-κB p65, IL-1ß, IL-6, TNF-α, and Calpain1 proteins in the aortic root were identified by Western blot. RESULTS: After PNS administration for 8 weeks, the levels of TG, TC, LDL-C, IL-1ß and TNF-α were decreased, the level of HDL-C was increased in apoE-/- mice. The arrangement of the tissue of aortic root tended to be normal, the cell morphology was restored, and the lipid depositions were reduced in apoE-/- mice treated with PNS. Moreover, PNS inhibited the expression levels of NF-κB p65, IL-6, IL-1ß, TNF-α and Calpain1 proteins of aortic root tissues in apoE-/- mice. CONCLUSION: PNS may inhibit the progression of atherosclerotic lesions via their anti-inflammatory biological property. PNS suppress the NF-κB signaling pathway and inhibits the expression of pro-inflammatory factors such as NF-κB p65, IL-6, IL-1ß, TNF-α and Calpain1 proteins in aortic root tissues of apoE-/- mice.

Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice.

Microplastics (MPs) are new environmental pollutants and have received widespread attention in recent years, but the toxicity of the MPs remains to be fully elucidated. To explore the effect of MPs on hepatotoxicity in mice and unravel the mechanism of pyroptosis and ferroptosis in the process of liver injury, we treated mice with 5.0 µm polypropylene microplastics (MPs) at 0.1, 0.5 and 1 mg/mL for 4 weeks. Results revealed that MPs could damage liver structure and function with broken and reduced mitochondrial cristae, as well as increased levels of aspartate minotransferase (AST), alanine aminotransferase (ALT), AST/ALT, alkaline phosphatase (ALP) and lactate dehydrogenase (LDH). Treatment with MPs resulted in pyroptosis as evidenced by increasing expressions of interleukin IL-1ß, IL-18. Additionally, MPs were shown to induce the NOD-like receptor protein 3 (NLRP3) inflammasomes and apoptosis associated speck-like protein (ASC) containing a caspase recruitment domain activation in liver tissue, enabling activation of Caspase-1-dependent signaling pathway induced by inflammatory stimuli resulting from oxidative stress. In addition, the increase of malondialdehyde (MDA) and decrease of glutathione (GSH) and superoxide dismutase (SOD) in the liver indicated that MPs could induce oxidative damage. Moreover, MPs induced lipid peroxidation in the liver of mice could activate the expression of ferroptosis related proteins, including iron metabolism, such as transferrin receptor (TFRC) was active but ferritin heavy chain 1 (FTH1) was inhibited; amino acid metabolism, such as XCT system and glutathione peroxidase 4 (GPX4) were inhibited; lipid metabolism, such as acyl-CoA synthetase long-chain family member 4 (ACSL4) was inhibited. Collectively, these findings evidenced that pyroptosis and ferroptosis occurred in MPs-induced liver injury accompanied by intense oxidative stress and inflammation.

Properties of Iron Bacteria Biofouling on Ni-P-rGO Coating under Flowing Conditions.

Biofouling on heat exchange devices can decrease heat transfer efficiency, corrode materials, and even lead safety accidents. Most heat exchange devices are made of carbon steel, which produces biofouling easily. In this paper, nickel-phosphorus-reduced graphene oxide (Ni-P-rGO) coating was prepared on carbon steel by electroless plating as a kind of advanced material to study the properties of iron bacteria biofouling under flowing conditions. The coating was analyzed via scanning electron microscopy and Raman spectroscopy. The properties of iron bacteria biofouling on carbon steel and Ni-P-rGO coating were then compared under flowing conditions. Compared with carbon steel, the asymptotic value of fouling resistance on the Ni-P-rGO coating significantly decreased. Additionally, the induction period and the time of reaching the asymptotic value greatly increased. The inhibition properties of biofouling of advanced materials Ni-P-rGO coating under different temperatures, flow velocities, and initial concentrations was also studied.