Alleviating sample imbalance in water quality assessment using the VAE-WGAN-GP model.

Water resources are essential for sustaining human life and promoting sustainable development. However, rapid urbanization and industrialization have resulted in a decline in freshwater availability. Effective prevention and control of water pollution are essential for ecological balance and human well-being. Water quality assessment is crucial for monitoring and managing water resources. Existing machine learning-based assessment methods tend to classify the results into the majority class, leading to inaccuracies in the outcomes due to the prevalent issue of imbalanced class sample distribution in practical scenarios. To tackle the issue, we propose a novel approach that utilizes the VAE-WGAN-GP model. The VAE-WGAN-GP model combines the encoding and decoding mechanisms of VAE with the adversarial learning of GAN. It generates synthetic samples that closely resemble real samples, effectively compensating data of the scarcity category in water quality evaluation. Our contributions include (1) introducing a deep generative model to alleviate the issue of imbalanced category samples in water quality assessment, (2) demonstrating the faster convergence speed and improved potential distribution learning ability of the proposed VAE-WGAN-GP model, (3) introducing the compensation degree concept and conducting comprehensive compensation experiments, resulting in a 9.7% increase in the accuracy of water quality assessment for multi-classification imbalance samples.

Scorpion venom heat-resistant peptide alleviates mitochondrial dynamics imbalance induced by PM2.5 exposure by downregulating the PGC-1α/SIRT3 signaling pathway.

Background: Epidemiological inquiry reveals that neuroinflammation and mitochondrial dysfunction caused by PM2.5 exposure are associated with Alzheimer's disease. Nevertheless, the molecular mechanisms of mitochondrial dynamics and neuroinflammation induced by PM2.5 exposure remain elusive. In this study, our objective was to explore the impact of PM2.5 on mitochondrial dynamics and neuroinflammation, while also examining the reparative potential of scorpion venom heat-resistant synthetic peptide (SVHRSP). Methods: Western blot and quantitative reverse transcription polymerase chain reaction (RT-qPCR) were employed to ascertain the protein and gene levels of IL-1ß, IL-6, and TNF-α in BV2 cells. The concentration of IL-6 in the supernatant of the BV2 cell culture was measured by enzyme-linked immunosorbent assay. For the assessment of mitochondrial homeostasis, western blot, RT-qPCR, and cellular immunohistochemistry methods were utilized to investigate the protein and gene levels of DRP1 and MFN-2 in HT22 cells. In the context of signal pathway analyses, western blot, RT-qPCR, and immunofluorescence techniques were employed to detect the protein and gene expressions of PGC-1α and SIRT3 in HT22 cells, respectively. Following the transfection with siPGC-1αRNA, downstream proteins of PGC-1α/SIRT3 pathway in HT22 cells were investigated by Western blot and RT-qPCR. Results: The experimental findings demonstrated that exposure to PM2.5 exacerbated neuroinflammation, resulting in elevated levels of IL-1ß, IL-6, and TNF-α. Furthermore, it perturbed mitochondrial dynamics, as evidenced by increased DRP1 expression and decreased MFN-2 expression. Additionally, dysfunction was observed in the PGC-1α/SIRT3 signal pathway. However, intervention with SVHRSP ameliorated the cellular damage induced by PM2.5 exposure. Conclusions: SVHRSP alleviated neuroinflammation and mitochondrial dynamics imbalance induced by PM2.5 exposure by downregulating the PGC-1α/SIRT3 signaling pathway.

CircCDR1as mediates PM2.5-induced lung cancer progression by binding to SRSF1.

Research indicates that particulate matter with an aerodynamic equivalent diameter of less than or equal to 2.5 µm in ambient air may induce lung cancer progression. Circular RNAs are a special kind of endogenous noncoding RNA, and their functions are reflected in various diseases and physiological processes, but there are still few studies related to PM2.5-induced lung cancer. Here, we identified that circCDR1as was upregulated in lung cancer cells stimulated with PM2.5 and positively correlated with the malignant features of lung cancer. The lower expression of CircCDR1as reduced the adverse progression of lung cancer cells after PM2.5 treatment; the lower expression of circCDR1as impaired the growth size and metastatic ability of lung cancer cells in mouse tumour models. Mechanistically, circCDR1as specifically bound to serine/arginine-rich splicing Factor 1 (SRSF1) and affected the splicing of vascular endothelial growth factor-A (VEGFA) by SRSF1. Furthermore, circCDR1as affected SRSF1 function by regulating PARK2-mediated SRSF1 ubiquitination, protein production and degradation. CircCDR1as also affected C-myc and cyclin D1 expression by regulating SRSF1 and affecting the wnt/ß-catenin signalling pathway, ultimately promoting malignant behavior and inhibiting the apoptosis of lung cancer cells, thereby causing PM2.5-induced lung cancer development.

PM2.5 induced lung injury through upregulating ROS-dependent NLRP3 Inflammasome-Mediated Pyroptosis.

The main cause of air pollution is PM2.5, which directly causes lung injury through respiration. Oxidative stress and inflammation are considered to be the key mechanism of cell damage. Pyroptosis is a process of the programmed death of inflammatory cells and as a dangerous endogenous signal, it is widely involved in different inflammatory diseases. However, few studies have been conducted on PM2.5 exposure and cell pyroptosis. In this study, we aimed to investigate the effect of PM2.5 on apoptosis, pyroptosis and cell cycle arrest regulated by reactive oxygen species production. Balb/c mice were exposed to PM2.5 dynamically and verified by the RAW264.7 cells in vitro. The results showed the activation of NF-κB and NLRP3 inflammasome and the release of IL-1ß and reactive oxygen species were caused by exposure to PM2.5. The maturation of IL-1ß relied on Caspase-1, and the active Caspase-1 was related to cell pyroptosis. Oxidative stress, inflammation, apoptosis and pyroptosis all affected the cell cycle. This study describes a potentially important mechanism of PM2.5-induced lung damage that PM2.5 promotes lung injury via upregulating ROS-NLRP3-mediated the RAW264.7 cells pyroptosis.

Compound essential oils relieve oxidative stress caused by PM2 .5 exposure by inhibiting autophagy through the AMPK/mTOR pathway.

Fine particulate matter (PM2.5 ) potentially damages the respiratory system and causes respiratory diseases. Compound essential oils (CEOs) have been shown to alleviate the damage to the lung and macrophages caused by PM2.5 . However, the effect of PM2.5 exposure on the brain has rarely been investigated. When oxidative stress occurs in the brain, it readily causes neurological diseases. Autophagy is intimately involved in many physiological processes, especially processes important for the brain. Blocked or excessive autophagy causes a series of brain diseases, such as cerebral ischemia and stroke. This study investigated whether CEOs regulate excessive autophagy and reduce the oxidative stress caused by PM2.5 in the brain and BV2 microglial cells. PM2.5 increased the levels of ROS, Nox2, NF-κB and MDA while decreasing superoxide dismutase and HO-1 levels, which led to oxidative stress in the brain. The increased LC3 level and decreased P62 level suggested that PM2.5 exposure increased the level of autophagy. After exposure to PM2.5 , the levels of 5'-adenosine monophosphate-activated protein kinase (AMPK) increased, while the levels of mammalian target of rapamycin (mTOR) decreased, suggesting that PM2.5 might induce autophagy by activating the AMPK/mTOR pathway. In addition, CEOs alleviated oxidative stress and autophagy induced by PM2.5 . Therefore, we concluded that CEOs reduce oxidative stress induced by PM2.5 exposure by inhibiting autophagy via the AMPK/mTOR signaling pathway, and these findings provide new opportunities for the prevention of PM2.5 -induced brain diseases.

lncRNA Gm16410 Mediates PM2.5-Induced Macrophage Activation via PI3K/AKT Pathway.

PM2.5 refers to atmospheric particulate matters with a diameter of less than 2.5 µm. The deposit of PM2.5 in lung cells can cause oxidative stress, leading to changes in macrophage polarity, which can subsequently cause pulmonary inflammation. Long-chain non-coding RNA (lncRNA) is a class of transcripts that regulate biological processes through multiple mechanisms. However, the role of lncRNA in PM2.5-induced lung inflammation has not been established. In this study, the biological effects and associated mechanism of lncRNA in PM2.5-induced change in macrophage polarity were investigated. The lncRNA-mediated PM2.5-induced macrophage inflammation and lung inflammation-associated injury were also determined. Mice were exposed to chronic levels of PM2.5, and changes in the expression of lncRNA in the lung were measured by lncRNA microarray. lncRNAs that showed significant changes in expression in response to PM2.5 were identified. lncRNA showing the biggest change was subjected to further analysis to determine its functional roles and mechanisms with respect to macrophage activation. The result showed that a significant reduction in expression of one lncRNA, identified as lncGm16410, was observed in the lung of mice and RAW264.7 cells following exposure to PM2.5. lncGm16410 suppressed PM2.5-induced macrophage activation via the SRC protein-mediated PI3K/AKT signaling pathway. PM2.5 promoted lung inflammation by downregulating the expression of lncGm16410, enhancing the activation of macrophages. Thus, lncGm16410 might provide new insight into the prevention of PM2.5 injury.

Protective effect of scorpion venom heat-resistant synthetic peptide against PM2.5-induced microglial polarization via TLR4-mediated autophagy activating PI3K/AKT/NF-κB signaling pathway.

There is growing evidence that fine particulate matter (PM2.5) is a considerable risk factor for neurodegenerative diseases. Scorpion venom heat-resistant synthetic peptide (SVHRSP) plays a neuroprotective effect by promoting neurogenesis and neuron axon growth. In this study, SVHRSP inhibited the level of TLR4, autophagy and PM2.5-induced microglia M1 polarization, thereby promoting Phosphorylation of PI3K and AKT, inhibiting the expression of NF-κB. Moreover, SVHRSP suppressed the cytotoxic factors and increased the cytoprotective factor. This research demonstrates that SVHRSP relieves PM2.5-induced microglial polarization via TLR4-mediated autophagy activating PI3K/AKT/NF-κB signaling pathway, which provides new insights for the treatment of PM2.5-induced neurodegenerative diseases.

LncRNA Gm16410 regulates PM2.5-induced lung Endothelial-Mesenchymal Transition via the TGF-ß1/Smad3/p-Smad3 pathway.

Exposure to PM2.5 can cause serious harm to the respiratory system. Until now, although many toxicological studies have shown that pulmonary fibrosis can be caused by long-term PM2.5 exposure, there is no evidence that Endothelial-Mesenchymal Transition (EndMT) can trigger the process of pulmonary fibrosis after exposure. LncRNAs are a class of non-coding RNAs detected in mammalian cells. Nevertheless, researchers have not found whether lncRNAs participate in PM2.5 induced EndMT during pathophysiological duration. The Balb/c mouse model was exposed to PM2.5 for 4 months by dynamic intoxication. The levels of specific endothelial and mesenchymal markers were evaluated by molecular biology experiments to elucidate the mechanisms of EndMT induced by PM2.5 in lung tissues. LncRNA microarray analysis of the established mouse model of PM2.5 exposure was performed. Based on a bioinformatics analysis and RT-qPCR analysis, lncRNA Gm16410 attracted our attention. The change of lncRNA Gm16410 in mouse pulmonary vascular endothelial cells (MHCs) exposed to PM2.5 was verified, and the mechanism of lncRNA Gm16410 in EndMT was discussed. The changes of cell function were evaluated by cell migration and proliferation experiments. The molecular biology experiments proved that PM2.5 induced EndMT by activating the TGF-ß1/Smad3/p-Smad3 pathway in vitro. The relationship of EndMT and lncRNA Gm16410 was verified in mouse lung tissues and MHC cells by PM2.5 exposure. The involvement of lncRNA Gm16410 in PM2.5-induced EndMT highlights the potential of lncRNA to promote pulmonary fibrosis under environmental pollution.