A novel biomarker for pleural effusion diagnosis: Interleukin-36γ in pleural fluid.

BACKGROUND: Numerous studies have described the critical importance of interleukin (IL) -36γ in host defense against lung infections, but it is unknown whether it plays a role in infectious pleural effusion (IPE). This study aimed to examine the levels of IL-36γ in pleural effusions of different etiologies and evaluate the diagnostic accuracy of IL-36γ in the differential diagnosis of IPE. METHODS: A total of 112 individuals was enrolled in this research. IL-36γ levels in pleural fluids of all 112 patients were measured by enzyme-linked immunosorbent assay (ELISA). We also characterized these markers' diagnostic values across various groups. RESULTS: Patients with tuberculous pleural effusion (TPE) and parapneumonic effusion (PPE) had exhibited markedly higher IL-36γ levels in their pleural fluid than the malignant pleural effusion (MPE) and transudative effusion patients. Furthermore, the IL-36γ concentrations in TPE patients were evidently higher than in uncomplicated parapneumonic effusion (UPPE) patients but significantly lower than in complicated parapneumonic effusion (CPPE)/empyema patients. Pleural fluid IL-36γ is a useful marker to differentiate TPE from UPPE, at a cut-off value for 657.5 pg/ml (area under the curve = 0.904, p < 0.0001) with 70.0% sensitivity and 95.7% specificity. CONCLUSIONS: The elevated IL-36γ in pleural effusion may be used as a novel biomarker for infectious pleural effusion diagnosis, particularly in patients with CPPE/empyema, and is a potentially promising biomarker to differentiate between TPE and UPPE.

hsa_circ_0115355 promotes pancreatic ß-cell function in patients with type 2 diabetes through the miR-145/SIRT1 axis.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a complex metabolic disease closely related to obesity, a growing global health problem. T2DM is characterized by decreased islet beta-cell mass and impaired insulin release from these cells, and this dysfunction is exacerbated by hyperglycemia (glucolipotoxicity). Circular RNAs (circRNAs) are abnormally expressed and play a regulatory role in T2DM. OBJECTIVE: This study aimed to evaluate the function and molecular mechanism of hsa_circ_0115355 in the progression of T2DM. METHODS: The regulatory effect of hsa_circ_0115355 on INS-1 cell function was assessed under glucolipotoxicity by MTT, flow cytometry analysis, and insulin secretion assay. Dual-luciferase experiments revealed a direct interaction of hsa_circ_0115355 with miR-145 and miR-145 with SIRT1. Furthermore, the regulatory role of the hsa_circ_0115355/miR-145/SIRT1 axis was verified by examining the function of INS-1. RESULTS: In this study, hsa_circ_0115355 was significantly underexpressed in both patients with T2DM and INS-1 cell lines. This study thus showed that hsa_circ_0115355 inhibits the occurrence and development of T2DM by regulating the expression of SIRT1 by adsorbing miR-145. CONCLUSION: The underexpression hsa_circ_0115355 is also a potential novel diagnostic marker and therapeutic target for T2DM.

Establishment and analysis of the lncRNA-miRNA-mRNA network based on competitive endogenous RNA identifies functional genes in heart failure.

Heart failure (HF), a common disease in adults, accounts for significantly global morbidity and mortality. Due to population aging, therapeutic progression in acute cardiovascular events, the prevalence of HF is increasing, in spite of the efficacy of multiple therapies for HF patients with decreased ejection fraction. Despite great progress in the underlying molecular mechanisms, it remains incompletely clear of the function of competing endogenous RNA (ceRNA) network in HF pathogenesis. Herein, we established an HF-related ceRNA network on the basis of differentially expressed long noncoding RNAs (lncRNAs), microRNAs (miRNAs) as well as mRNAs from GSE136547 and GSE124401 datasets. In brief, the ceRNA network composed of 58 mRNA nodes, 5 miRNA nodes, 82 lncRNA nodes as well as 252 edges. In addition, three lncRNAs (KCNQ1OT1, XIST and AC010336) with higher node degrees than other lncRNAs were chosen as hub nodes. At the same time, we have established five subnetwork of miR-17-5p, miR-20b-5p, miR-107, miR-125a-5p and miR-140-5p centered ceRNA. Pathway analysis revealed the enrichment of ceRNA network in cell cycle pathways. Collectively, our research sheds new lights on the essential functions of ceRNA network in HF development, which also suggests possible application of these hub nodes as diagnostic biomarkers as well as therapeutic targets.