Identification of hub biomarkers and immune cell infiltration characteristics of polymyositis by bioinformatics analysis.

Background: Polymyositis (PM) is an acquirable muscle disease with proximal muscle involvement of the extremities as the main manifestation; it is a category of idiopathic inflammatory myopathy. This study aimed to identify the key biomarkers of PM, while elucidating PM-associated immune cell infiltration and immune-related pathways. Methods: The gene microarray data related to PM were downloaded from the Gene Expression Omnibus database. The analyses using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes, gene set enrichment analysis (GSEA), and protein-protein interaction (PPI) networks were performed on differentially expressed genes (DEGs). The hub genes of PM were identified using weighted gene co-expression network analysis (WGCNA) and least absolute shrinkage and selection operator (LASSO) algorithm, and the diagnostic accuracy of hub markers for PM was assessed using the receiver operating characteristic curve. In addition, the level of infiltration of 28 immune cells in PM and their interrelationship with hub genes were analyzed using single-sample GSEA. Results: A total of 420 DEGs were identified. The biological functions and signaling pathways closely associated with PM were inflammatory and immune processes. A series of four expression modules were obtained by WGCNA analysis, with the turquoise module having the highest correlation with PM; 196 crossover genes were obtained by combining DEGs. Subsequently, six hub genes were finally identified as the potential biomarkers of PM using LASSO algorithm and validation set verification analysis. In the immune cell infiltration analysis, the infiltration of T lymphocytes and subpopulations, dendritic cells, macrophages, and natural killer cells was more significant in the PM. Conclusion: We identified the hub genes closely related to PM using WGCNA combined with LASSO algorithm, which helped clarify the molecular mechanism of PM development and might have great significance for finding new immunotherapeutic targets, and disease prevention and treatment.

[Screening of the Reduction/Stabilization Reagent for Cr(â ¥) Contaminated Soil in a Planting Site and Reaction Process Monitoring].

There are lots of problems in the domestic remediation of Cr (Ⅵ) contaminated soil field,such as lack of the key processing parameters,poor long-term effect and so on.The Cr (Ⅵ) heavy polluted surface soil was sampled from an electroplating site in North-China,and then treated with five different reducing reagents.At the same time,the on-line ORP probes and interval sampling test were chosen to monitor the reaction process,and to explore the reaction rate and effect.The results showed that No.4 reagent had the highest Cr (Ⅵ) reduction effect,reaching up to 99.5%,and the minimum soil Cr (Ⅵ) concentration could reach 2.4 mg·kg-1.The No.1 and No.4 reagents had relatively faster reducing rates.There were obvious difference in ORP and pH monitoring values between different reductants,for example,the No.1 reagent kept the ORP value stable at around -400 mV.The No.4 reagent gradually increased the value from -200 mV to 100 mV since 30h,and then kept stable.According to the pH difference among different reductants,the No.4 reagent was the best and kept the pH value at around 7.Taking together the final effect and process key parameters,the No.4 reagent was the best.The scale-up experiment was operated with process monitoring,and the ORP and conductivity values showed that the reduction reaction took about 160 h.This work would provide theoretical basis for controlling the maintenance condition and reaction process in soil Cr (Ⅵ) remediation.

Ginkgolide B prevents cathepsin-mediated cell death following cerebral ischemia/reperfusion injury.

Ginkgolide B (GB) has been shown to exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanism by which GB prevents ischemic cell death remains unclear. Lysosomal proteases, including cathepsins B and L, have been implicated in ischemic cell death following reperfusion. Therefore, in the present study, we investigated the role of GB with respect to cathepsin-mediated cell death following I/R. Both the expression and enzymatic activity of cathepsins B and L were significantly increased in the ischemic cortex following cerebral I/R injury. We found that GB treatment markedly decreased the activity and expression of cathepsins B and L following I/R. Moreover, GB reduced necrotic and apoptotic cell death following I/R. These data strongly suggest that GB prevents cathepsin-mediated cell death following focal cerebral I/R injury, and they might provide new insights into the mechanism of the neuroprotective effects of GB.