Objective To investigate the expression of ferritinophagy-related gene ELAV-like RNA binding protein 1(ELAVL1)in multiple myeloma(MM)and elucidate its diagnostic and prognostic value for MM.Methods First,we analyzed ELAVL1 expression level in healthy controls and MM patients using data from the GEO and TCGA databases.Subsequently,bone marrow specimens were collected from 28 newly diagnosed MM patients and 20 healthy controls,and qRT-PCR was employed to validate ELAVL1 expression.The diagnostic and prognostic potential of ELAVL1 was assessed using ROC curve analysis and Kaplan-Meier survival curves.Additionally,univariate and multivariate COX regression analyses were performed to identify independent risk factors for MM prognosis.Finally,KEGG and GO enrichment analyses were performed using the DAVID online platform.Results The level of ELAVL1 expression was significantly higher in newly diagnosed MM patients and refractory/relapsed MM patients than in the healthy controls(P＜0.001).Moreover,ELAVL1 expression was positively correlated with the International Staging System(ISS)stage of MM(P＜0.01).Furthermore,qRT-PCR validation confirmed that ELAVL1 expression was elevated in the 28 newly diagnosed MM patients compared to the 20 healthy controls(P＜0.001).ROC curve analysis demonstrated that ELAVL1 could effectively differentiate between newly diagnosed MM patients,healthy controls,and MGUS patients(P＜0.001 and P=0.000 2,respectively).Survival analysis revealed that high ELAVL1 expression was associated with shorter progression-free survival(P=0.0141)and overall survival(P=0.008 0).Univariate and multivariate COX regression analyses identified high ELAVL1 expression as an independent risk factor for poor MM prognosis(P=0.005 0).KEGG analysis suggested that ELAVL1 might be involved in the Hippo and MAPK signaling pathways.Conclusion High ELAVL1 expression in MM may serve as a biomarker for diagnosis and poor prognosis.ELAVL1 may promote MM initiation and progression via the Hippo and MAPK signaling pathways.

Objective To investigate the effects of the culture supernatant of Faecalibacterium prausnitzii(F.prausnitzii)on intestinal barrier function and liver fibrosis progression in mice.Methods A total of 24 male C57BL/6 mice were randomly assigned to three groups:normal control group(Control),liver fibrosis model group(Model),and model mice+F.prausnitzii supernatant group(Model+S).Hepatic fibrosis was induced by intraperitoneal injection of carbon tetrachloride in both the Model group and the Model+S group over a period of 10 weeks.Following a 2-week modeling period,the mice in the Model+S group were subjected to an 8-week treatment with bacterial supernatant.The colon and liver were analyzed for pathological morphology using HE staining.Additionally,impairment of intestinal barrier function was assessed by periodic acid schiff staining,ELISA,and fluorescein isothiocyanate-dextran(FITC-Dextran)fluorescent probe.Changes in the gut microbiota structure were analyzed with 16S rDNA sequencing.The degree of liver fibrosis was assessed using sirius red staining,and the expression levels of markers associated with intestinal barrier function,liver fibrosis,and inflammation were measured using qPCR and ELISA.Results Compared with the Model group,the severity of intestinal damage and the expressions of pro-inflammatory factors in the Model+S group were decreased.Additionally,there was a significant increase in the expressions of multiple genes related to intestinal barrier function,as well as a decrease in the concentration of FITC-Dextran in peripheral blood and lipopolysaccharide in the liver(all P＜0.05),and there was an improvement in the composition of the gut microbiota.Furthermore,while the liver function and extent of liver fibrosis in the Model+S group did not show any significant differences compared to the Model group,there was a noticeable decrease in the infiltration of inflammatory cells within the liver.Additionally,the expressions of pro-inflammatory factors such as Tlr4,Il-6 and Tnf-α,and the concentration of IL-6 in the liver was significantly decreased(all P＜0.05).Conclusion The F.prausnitzii supernatant exhibits the potential to enhance intestinal barrier function and rectify gut microbiota imbalance in mice with liver fibrosis,thus reducing hepatic inflammation.However,it does not exert any significant effect on the progression of liver fibrosis.

[This corrects the article DOI: 10.1016/j.apsb.2022.05.019.].

Allergic rhinitis (AR) is a chronic non-specific inflammatory disease of the nasal mucosa caused by abnormal activation of the immune system, with alterations in macrophage polarization playing a crucial role in its occurrence and development. Non-coding RNA has been found to play a key role in the polarization of macrophages. This study aims to explore the latest developments in research on the role of non-coding RNA-regulated macrophage polarization in the pathogenesis of AR, with the goal of identifying new approaches and potential targets for the diagnosis and treatment of AR.
Humans ; Rhinitis, Allergic/immunology* ; Macrophages/metabolism* ; RNA, Untranslated/genetics* ; Animals ; Macrophage Activation/genetics* ; Cell Polarity/genetics*

Objective To investigate the effects of the culture supernatant of Faecalibacterium prausnitzii(F.prausnitzii)on intestinal barrier function and liver fibrosis progression in mice.Methods A total of 24 male C57BL/6 mice were randomly assigned to three groups:normal control group(Control),liver fibrosis model group(Model),and model mice+F.prausnitzii supernatant group(Model+S).Hepatic fibrosis was induced by intraperitoneal injection of carbon tetrachloride in both the Model group and the Model+S group over a period of 10 weeks.Following a 2-week modeling period,the mice in the Model+S group were subjected to an 8-week treatment with bacterial supernatant.The colon and liver were analyzed for pathological morphology using HE staining.Additionally,impairment of intestinal barrier function was assessed by periodic acid schiff staining,ELISA,and fluorescein isothiocyanate-dextran(FITC-Dextran)fluorescent probe.Changes in the gut microbiota structure were analyzed with 16S rDNA sequencing.The degree of liver fibrosis was assessed using sirius red staining,and the expression levels of markers associated with intestinal barrier function,liver fibrosis,and inflammation were measured using qPCR and ELISA.Results Compared with the Model group,the severity of intestinal damage and the expressions of pro-inflammatory factors in the Model+S group were decreased.Additionally,there was a significant increase in the expressions of multiple genes related to intestinal barrier function,as well as a decrease in the concentration of FITC-Dextran in peripheral blood and lipopolysaccharide in the liver(all P＜0.05),and there was an improvement in the composition of the gut microbiota.Furthermore,while the liver function and extent of liver fibrosis in the Model+S group did not show any significant differences compared to the Model group,there was a noticeable decrease in the infiltration of inflammatory cells within the liver.Additionally,the expressions of pro-inflammatory factors such as Tlr4,Il-6 and Tnf-α,and the concentration of IL-6 in the liver was significantly decreased(all P＜0.05).Conclusion The F.prausnitzii supernatant exhibits the potential to enhance intestinal barrier function and rectify gut microbiota imbalance in mice with liver fibrosis,thus reducing hepatic inflammation.However,it does not exert any significant effect on the progression of liver fibrosis.

Objective To investigate the expression of ferritinophagy-related gene ELAV-like RNA binding protein 1(ELAVL1)in multiple myeloma(MM)and elucidate its diagnostic and prognostic value for MM.Methods First,we analyzed ELAVL1 expression level in healthy controls and MM patients using data from the GEO and TCGA databases.Subsequently,bone marrow specimens were collected from 28 newly diagnosed MM patients and 20 healthy controls,and qRT-PCR was employed to validate ELAVL1 expression.The diagnostic and prognostic potential of ELAVL1 was assessed using ROC curve analysis and Kaplan-Meier survival curves.Additionally,univariate and multivariate COX regression analyses were performed to identify independent risk factors for MM prognosis.Finally,KEGG and GO enrichment analyses were performed using the DAVID online platform.Results The level of ELAVL1 expression was significantly higher in newly diagnosed MM patients and refractory/relapsed MM patients than in the healthy controls(P＜0.001).Moreover,ELAVL1 expression was positively correlated with the International Staging System(ISS)stage of MM(P＜0.01).Furthermore,qRT-PCR validation confirmed that ELAVL1 expression was elevated in the 28 newly diagnosed MM patients compared to the 20 healthy controls(P＜0.001).ROC curve analysis demonstrated that ELAVL1 could effectively differentiate between newly diagnosed MM patients,healthy controls,and MGUS patients(P＜0.001 and P=0.000 2,respectively).Survival analysis revealed that high ELAVL1 expression was associated with shorter progression-free survival(P=0.0141)and overall survival(P=0.008 0).Univariate and multivariate COX regression analyses identified high ELAVL1 expression as an independent risk factor for poor MM prognosis(P=0.005 0).KEGG analysis suggested that ELAVL1 might be involved in the Hippo and MAPK signaling pathways.Conclusion High ELAVL1 expression in MM may serve as a biomarker for diagnosis and poor prognosis.ELAVL1 may promote MM initiation and progression via the Hippo and MAPK signaling pathways.

【Objective】 To investigate the expression of optineurin (OPTN) in multiple myeloma (MM) and explore the mechanism and clinical value of OPTN gene in the occurrence and development of MM. 【Methods】 In this study, three gene expression omnibus (GEO) data sets were used to analyze the expression level of OPTN in MM. Clinical bone marrow samples of MM patients were collected. qRT-PCR was used to further verify the expression of OPTN in MM patients. The Kaplan-Meier survival curve and receiver operating characteristic (ROC) curve were used to analyze the value of OPTN in the prognosis and diagnosis of MM. At the same time, MM transcriptome data were downloaded from the Cancer Genome Atlas (TCGA) database. According to the median boundary of OPTN mRNA expression level, the MM patients were divided into OPTN high- and low-expression groups. In order to investigate the possible molecular mechanisms of OPTN in MM, gene set enrichment analysis (GSEA) was made after the differentially expressed genes were filtered using the limma package of the R language. 【Results】 The expression level of OPTN was significantly lower in MM tissues than in normal tissues (P<0.05). OPTN expression level was significantly correlated with International Staging System (ISS) in MM patients (P<0.05). ROC results showed that the expression level of OPTN could distinguish between normal and MM patients. Survival analysis showed that the overall survival (OS) of patients with low OPTN expression was significantly lower than that of patients with high OPTN expression (P<0.05). GO, KEGG and GSEA enrichment analyses indicated that OPTN might affect apoptosis and autophagy, and regulate cellular immune response by regulating Nod-like receptors, NF-κB, TNF and RAS/MAPK pathways. 【Conclusion】 Low expression of OPTN in MM is associated with poor prognosis of patients, and thus may be an important potential biomarker for the diagnosis and treatment of MM.

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.

Electronic skin has shown great application potential in many fields such as healthcare monitoring and human-machine interaction due to their excellent sensing performance, mechanical properties and biocompatibility. This paper starts from the materials selection and structures design of electronic skin, and summarizes their different applications in the field of healthcare equipment, especially current development status of wearable sensors with different functions, as well as the application of electronic skin in virtual reality. The challenges of electronic skin in the field of wearable devices and healthcare, as well as our corresponding strategies, are discussed to provide a reference for further advancing the research of electronic skin.
Humans ; Wearable Electronic Devices ; Virtual Reality

Objective:To analyze the clinical features and genetic basis for a child featuring elevated creatine kinase (CK).Methods:Next-generation sequencing (muscular dystrophy-related gene panel) was carried out for the proband. Candidate variants were verified by Sanger sequencing of the child and his parents.Results:The child was found to harbor compound heterozygous variants of the FKTN gene, including a missense c. 536G>C (p.R179T) variant from his father and a non-frameshift c. 1299_1301delGTG (p.W434del) variant from his mother. Both variants were predicted to be pathogenic. Conclusion:The compound heterozygous variants of the FKTN gene probably underlay the disease in this child. Above finding has expanded the mutation spectrum of congenital muscular dystrophy.