Background Previous studies suggested that inflammation was involved in chronic heart failure (CHF), but their sample sizes were small. Objective To summarise the clinical cytokine data systematically and emphasise the importance of proinflammatory cytokines in the pathogenesis of CHF, we conducted a meta-analysis of relevant literatures. Methods Articles about cytokines and CHF were searched in Pubmed, EMBASE, Cochrane Library, Chinese National Knowledge Infrastructure and Chinese Wanfang Database. The pooled effects were measured by weighted mean difference (MD) and 95% CI, which were calculated by RevMan 5.1 software. Results Finally, a total of 28 studies were included. Compared with normal control subjects, concentrations of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β and C reactive protein (CRP) in the peripheral blood in CHF patients are significantly increased. The overall MDs with 95% CIs for TNF-α, IL-6, CRP and IL-1β were 2.59 pg/ml (2.14∼3.05, p<0.00001), 5.49 pg/mL (4.68∼6.29, p<0.00001), 11.45 mg/dL (7.68∼15.23, p<0.00001) and 0.11 pg/mL (0.09∼0.14, p<0.00001). The mortality of elevated IL-6 group was significantly higher than control group (OR=6.73, 95% CI 2.39∼18.93, p=0.0003). Conclusions Concentrations of TNF-α, IL-6, IL-1β and CRP are significantly higher in CHF patients than in control subjects. Proinflammatory cytokines play an import role in the pathogenesis of CHF.

In this study, we hypothesized that the combination of hepatocyte growth factor (HGF) and insulin-like growth factor-1 (IGF-1) alters the expression of connexin 43 (Cx43) and results in a reduced frequency of induced ventricular arrhythmia in rats after myocardial infarction (MI) and explored the preliminary mechanisms involved. Cardiomyocytes were cultured in vitro in medium with PBS, HGF, IGF-1, GFs (HGF + IGF-1), HGF + p38 inhibitor, HGF + ERK inhibitor, IGF-1 + p38 inhibitor or IGF-1 + ERK inhibitor. The expression of Cx43 was tested by real-time PCR and Western blotting after 48 hours. MI was induced in 48 male Sprague-Dawley rats. The rats were randomly divided into four groups and received an injection of PBS, HGF, IGF-1 or GFs into the infarct border zone two weeks after MI. Six weeks after injection, the expression levels of Cx43 and programmed stimulation-induced ventricular arrhythmias were examined. In vitro, the expression of Cx43 mRNA and the Cx43 protein in cardiomyocytes was higher in the HGF, IGF-1, and GFs groups than in the PBS group. GFs had a combinatorial effect on the Cx43 mRNA level but not on the Cx43 protein level. There was a significant reduction in Cx43 mRNA and Cx43 protein levels in the IGF-1 + p38 inhibitor group and IGF-1 + ERK inhibitor group compared to the IGF-1 group. In vivo, programmed stimulation significantly decreased the frequency of ventricular arrhythmia in the GFs, HGF and IGF-1 groups, and this effect was accompanied by increased immunohistochemical staining for Cx43, myocardial Cx43 protein levels and Cx43 mRNA levels in the infarct border zone of the left ventricle compared with those in the PBS group. The combinatorial effect of GFs on Cx43 expression was only observed at the mRNA level. Both HGF and IGF-1 enhanced the expression of Cx43 and improved induced ventricular arrhythmia in rats with MI. Both synergistic and antagonistic effects of HGF and IGF-1 were not observed. In addition, IGF-1 may function through the MAPK/p38 and ERK1/2 signaling pathways to regulate Cx43 expression.

Atopic dermatitis (AD) is a prevalent inflammatory skin disease. Ample evidence has shown that non-coding RNAs play important roles in the progression of AD, however, the function of plasma microRNAs in AD is poorly understood. To identify key plasma microRNAs and explore their potential roles in AD. Plasma microRNAs from five children with AD and five control children were sequenced by microRNA sequencing (miRNA-seq) and five differentially expressed microRNAs were verified by RT-qPCR in 30 AD and 15 control children. The most differentially expressed microRNA, hsa-miR-194-5p, was selected for further analysis. Human epidermal keratinocytes were subjected to RNA sequencing following over-expression of hsa-miR-194-5p, and down-regulated genes were detected by RT-qPCR. The diagnostic potential of hsa-miR-194-5p in AD was evaluated based on receiver operating characteristic (ROC) curve analysis. Further hsa-miR-194-5p-regulated expression and gene-hsa-miR-194-5p interactions were evaluated by western blotting and luciferase assays, respectively. We identified 40 differentially expressed microRNAs, 26 up-regulated and 14 down-regulated, in children with AD compared with controls. Among the five verified plasma microRNAs, the most significant change was down-regulated hsa-miR-194-5p, which was shown to potentially serve as a biomarker for AD based on ROC analysis. Twenty-two down-regulated genes were observed following hsa-miR-194-5p over-expression, which were significantly associated with keratinocyte differentiation and establishment of the skin barrier. Moreover, HS3ST2 protein expression was down-regulated following over-expression of hsa-miR-194-5p, and the 3'-UTR of HS3ST2 was shown to bind to hsa-miR-194-5p. Hsa-miR-194-5p might be involved in the pathogenesis of AD by regulating HS3ST2 expression.

Background: Acute myeloid leukemia (AML) is a common hematological malignancy treated with regimens containing anthracycline, an agent with cardiotoxicity. However, the cardiac-specific mortality in AML patients receiving chemotherapy remains unknown.