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Background: Osteoarthritis is a chronic degenerative joint disease, and increasing evidences suggest that the pathogenic mechanism involves immune system and inflammation. Aims: The aim of current study was to uncover hub genes linked to immune infiltration in osteoarthritis synovial tissue using comprehensive bioinformatics analysis and experimental confirmation. Methods: Multiple microarray datasets (GSE55457, GSE55235, GSE12021 and GSE1919) for osteoarthritis in Gene Expression Omnibus database were downloaded for analysis. Differentially expressed genes (DEGs) were identified using Limma package in R software, and immune infiltration was evaluated by CIBERSORT algorithm. Then weighted gene co-expression network analysis (WGCNA) was performed to uncover immune infiltration-associated gene modules. Protein–protein interaction (PPI) network was constructed to select the hub genes, and the tissue distribution of these genes was analyzed using BioGPS database. Finally, the expression pattern of these genes was confirmed by RT-qPCR using clinical samples. Results: Totally 181 DEGs between osteoarthritis and normal control were screened. Macrophages, mast cells, memory CD4 T cells and B cells accounted for the majority of immune cell composition in synovial tissue. Osteoarthritis synovial showed high abundance of infiltrating resting mast cells, B cells memory and plasma cells. WGCNA screened 93 DEGs related to osteoarthritis immune infiltration. These genes were involved in TNF signaling pathway, IL-17 signaling pathway, response to steroid hormone, glucocorticoid and corticosteroid. Ten hub genes including MYC, JUN, DUSP1, NFKBIA, VEGFA, ATF3, IL-6, PTGS2, IL1B and SOCS3 were selected by using PPI network. Among them, four genes (MYC, JUN, DUSP1 and NFKBIA) specifically expressed in immune system were identified and clinical samples revealed consistent change of these four genes in synovial tissue retrieved from patients with osteoarthritis. Conclusion: A 4-gene-based diagnostic model was developed, which had well predictive performance in osteoarthritis. MYC, JUN, DUSP1 and NFKBIA might be biomarkers and potential therapeutic targets in osteoarthritis. [ABSTRACT FROM AUTHOR]

A Mediterranean-style diet (MED) can promote people lengthen the span of life and avoid atherosclerotic cardiovascular disease (ASCVD) in primary prevention. Metabolic syndrome (MetS) can significantly reduce life expectancy and increase the risk of ASCVD. However, few studies have focused on the role of the Mediterranean diet in patients with MetS. Participants in the National Health and Nutrition Examination Survey (NHANES) with MetS (N = 8301) from 2007 to 2018 were examined. A 9-point evaluation scorewas used to measure the degree of adherence to the MED diet. In order to compare the various levels of adherence to the MED diet and the effects of the specific MED diet components on all-cause and cardiovascular mortality, Cox regression models were utilized. Among the 8301 participants with MetS, about 13.0% (1080 of 8301) died after a median follow-up of 6.3 years. In this study, participants with MetS with adherence to high-quality and moderate-quality Mediterranean diet were significantly associated with lower all-cause mortality as well as cardiovascular mortality during the follow-up period. Futhermore, in joint analysis of the Mediterranean diet and sedentary behavior or depression, we found that high-quality or moderate-quality Mediterranean diet could attenuate, even reverse the adverse effects of sedentary behavior and depression on all-cause and cardiovascular mortality in participants with MetS. Among the components of the MED diet, greater intakes of vegetables, legumes, nuts and high MUFA/SFA ratio were significantly associated with lower all-cause mortality and greater vegetables intake was significantly associated with lower cardiovascular mortality, while more red/processed meat intake was significantly associated with higher cardiovascular mortality in participants with MetS. [ABSTRACT FROM AUTHOR]

Background: There is a bidirectional effect between sleep disorders and Mediterranean diet (MED), but the joint effect of MED and sleep disorders on mortality is unclear. The aim of this study was to investigate whether there is a synergistic effect of adherence to MED and sleep disorders on all-cause and cause-specific mortality. Methods: The study included 23,212 individuals in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. A 9-point evaluation score, alternative Mediterranean diet (aMED) index was used to assess adherence to MED. Sleep disorder and hours of sleep were assessed by structured questionnaires. Cox regression models were used to assess the relationship between sleep disorders, aMED and all-cause mortality, cause-specific mortality (cardiovascular-related death, cancer-related death). The interaction effect of sleep disorders with aMED on mortality was further assessed. Results: Results showed that participants with lower aMED and presence of sleep disorders had significantly higher risk of all-cause mortality and cardiovascular-related mortality (HR, 2.16, 95% CI, 1.49–3.13, P < 0.0001; HR, 2.68, 95% CI, 1.58–4.54, P = 0.0003). A significant interaction effect was found between aMED and sleep disorders on cardiovascular mortality (p for interaction = 0.033). No significant interaction existed between aMED and sleep disorders on all-cause mortality (p for interaction = 0.184) and cancer-related mortality (p for interaction = 0.955). Conclusions: Poorer adherence to MED and sleep disorders synergistically increased long-term all-cause mortality and cardiovascular mortality in NHANES population. [ABSTRACT FROM AUTHOR]