Immune checkpoint inhibitors including programmed death-1 inhibitors are promising agents for many types of malignancies; however, it is still an off-label choice for type B3 thymoma. We reported for the first time a patient with type B3 thymoma developed fatal myocarditis and rhabdomyolysis after one dose of nivolumab administration. The results from myocardial and muscle biopsies revealed extensive myocyte damage, T-lymphocytic infiltration and strongly expression of PD-L1 which confirmed the nivolumab-related immune-related adverse events (irAEs). The blood tests showed elevated levels of serum AChR-binding antibody and inflammatory cytokines, in addition abnormal lymphocyte subsets were noted. Our report suggested that administration of nivolumab in type B3 thymoma could cause rare but fatal myocarditis and rhabdomyolysis, over-expressed AChR-binding antibody and inflammatory cytokines may be potential biomarkers for irAEs.

SIRT1 mRNAs are direct targets of miR-132. miR-132 controls lipogenesis and cholesterogenesis in HUVECs by inhibiting SIRT1 and SREBP-1c expression and their downstream regulated genes, including FASN and HMGCR. Inhibition of SIRT1 by miR-132 was associated with lipid metabolism-dependent pro-inflammatory processes in HUVECs. The newly identified miRNA, miR-132 represents a novel targeting mechanism for AS therapy.

Atherosclerosis is the major cause of myocardial infarction and stroke, which is a leading cause of morbidity and mortality in developed countries. During the pathological process of atherosclerosis, inflammation participates in all stages of atherosclerosis. Tumor necrosis factor-α (TNF-α), one of the most important inflammatory factor, induces apoptosis of endothelial cells, which play a central role in endothelial dysfunction. However, the underlying mechanism involved in long noncoding RNA (lncRNA) remains unclear. In the present study, we demonstrated the role of lncRNA highly upregulated in liver cancer (HULC) in TNF-α-induced apoptosis. HULC expression was decreased with TNF-α treatment. Restoring HULC expression rescued the apoptosis induced by TNF-α. HULC regulated TNF-α-induced apoptosis through regulation of miR-9 expression. Furthermore, RNA immunoprecipitation and RNA pull-down assays showed that HULC modulated miR-9 expression through association with DNA methyltransferases and suppression of miR-9 expression. HULC-miR-9 pathway may be a potential target for treating atherosclerosis.

Background: Several studies were published to assess the association between serum uric acid levels and atrial fibrillation risk, but no consistent results were reported. We performed a meta-analysis to evaluate the evidence of the association between hyperuricemia and atrial fibrillation risk. Material/Methods: Pubmed and Embase databases were searched for prospective cohort studies assessing the association between hyperuricemia and atrial fibrillation risk. Relative risks (RRs) with corresponding 95% confidence intervals (95%CIs) were pooled using random-effect of meta-analysis to assess the risk of atrial fibrillation in individuals with hyperuricemia. Results: Six cohort studies were finally included into the meta-analysis. Meta-analysis of those 6 studies showed that hyperuricemia was significantly associated with increased risk of atrial fibrillation (RR = 1.49, 95%CI 1.24-1.79, P < 0.001). Sensitivity analysis by omitting single study sequentially by turns did not have any obvious influence on the pooled risk estimates. There was no obvious risk of publication bias in the meta-analysis. Conclusions: Based on the currently available data, hyperuricemia is associated with increased risk of atrial fibrillation.

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B-lines were significantly correlated with the more established parameters of ADHF. The correlation between B-lines and E/e' was better, especially in the HFpEF group.

To assess whether global and regional myocardial strains from three-dimensional speckle tracking echocardiography (3D-STE) correlate with myocardial infarction size (MIS) detected by single photon emission computed tomography (SPECT). Fifty-seven patients with a history of ST-segment elevation myocardial infarction (MI) within 3-6 months were enrolled, alongside 24 healthy volunteers. Left ventricular (LV) global area strain, global longitudinal strain (GLS), global radial strain, global circumferential strain, left ventricular ejection fraction (LVEF) and wall motion score index (WMSI) were measured and compared with the corresponding SPECT-detected MISs. Patients were sub-grouped into massive MIS group (MIS ≥ 12%) and small MIS group (MIS < 12%). Myocardial strains of all the LV segments were compared with the corresponding MIS. Global myocardial strain parameters, LVEF and WMSI of the patients were significantly different from the control group (all P < 0.05) and correlated well with MISs, most significantly for GLS (r = 0.728, P < 0.01). Significant differences in myocardial strain parameters were found between the massive and small MIS groups (all P < 0.05). Receiver operating characteristic curve analysis indicated that GLS had a highest diagnostic value and when the cutoff was -13.8%, the area under the curve was 0.84, with the 70.6% sensitivity and 87.5% specificity. Significant differences of myocardial strain parameters were observed between segments with and without transmural MIs (P < 0.01). 3D-STE myocardial strain parameters evaluated LV global MIS, 3D GLS had the highest diagnostic value. It also preliminarily gauged the degree of ischemia and necrosis of regional myocardial segments.

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