This study aims to investigate the incidence of hepatitis B virus (HBV) reactivation in inflammatory arthritis (IA) patients with HBV infection using anti-tumor necrosis factor (TNF) agents and evaluate the efficacy of antiviral therapy in reducing the risk of viral reactivation in chronic HBV infection. IA patients using anti-TNF agents from six centers were enrolled. Their HBV infection conditions and ALT and HBV-DNA levels were monitored periodically. Among the six chronic hepatitis B patients, HBV reactivation was found in two patients without antivirus prophylaxis and no viral replication was detected in the other four patients with antivirus prophylaxis. In the 31 inactive carriers, the increase of viral load was detected in 6 of 22 (27.3 %) patients without antiviral prophylaxis, and there was no viral reactivation in the other 9 patients with antiviral prophylaxis. HBV reactivation was not found in the 50 patients with resolved HBV infection. It is suggested that anti-TNF therapy might increase the risk of HBV reactivation in patients with chronic HBV infection, and antiviral prophylaxis could effectively decrease the risk. Anti-TNF agents seem to be safe in patients with resolved HBV infection.

Gypenosides (GP) are the predominant components of Gynostemma pentaphyllum, a Chinese herb medicine that has been widely used for the treatment of chronic inflammation, hyperlipidemia, and cardiovascular disease. GP has been demonstrated to exert protective effects on the liver and brain against ischemia-reperfusion (I/R) injury, yet whether it is beneficial to the heart during myocardial I/R is unclear. In this study, we demonstrate that pre-treatment with GP dose-dependently limits infarct size, alleviates I/R-induced pathological changes in the myocardium, and preserves left ventricular function in a rat model of cardiac I/R injury. In addition, GP pre-treatment reduces oxidative stress and protects the intracellular antioxidant machinery in the myocardium. Further, we show that the cardioprotective effect of GP is associated with the preservation of mitochondrial function in the cardiomyocytes, as indicated by ATP level, enzymatic activities of complex I, II, and IV on the mitochondrial respiration chain, and the activity of citrate synthase in the citric acid cycle for energy generation. Moreover, GP maintains mitochondrial membrane integrity and inhibits the release of cytochrome c from the mitochondria to the cytosol. The cytoprotective effect of GP is further confirmed in vitro in H9c2 cardiomyoblast cell line with oxygen-glucose deprivation and reperfusion (OGD/R), and the results indicate that GP protects cell viability, reduces oxidative stress, and preserves mitochondrial function. In conclusion, our study suggests that GP may be of clinical value in cytoprotection during acute myocardial infarction and reperfusion.

Background: Patients with paroxysmal atrial fibrillation (AF) experience impaired quality of life (QoL) and psychological distress. Catheter ablation of AF can markedly improve QoL. However, the effect of catheter ablation of AF on psychological status is unknown. Hypothesis: Depression, anxiety, and QoL improve after catheter ablation in patients with paroxysmal AF. Methods: A total of 166 consecutive patients with symptomatic paroxysmal AF were examined. Eighty-two patients (55 men, mean age 55.9 ± 6.1 y) underwent catheter ablation and 84 patients (58 men, mean age 57.2 ± 5.4 years) received antiarrhythmic drug (AAD) therapy. The Self-Rating Depression Scale, Self-Rating Anxiety Scale, and Medical Outcomes Survey 36-item Short-Form questionnaires were completed by these patients at baseline, and at 3, 6, 9, and 12 months of follow-up. Results in the ablation group were compared with those of the AAD group. Results: In the ablation group, 42.7% of patients showed symptoms of depression and 37.8% showed symptoms of anxiety, which were similar to those in the AAD group. Both groups similarly displayed reduced physical and mental QoL. Catheter ablation was effective in reducing symptoms of depression and anxiety and improving QoL, and it was superior to AAD therapy (all P < 0.001). Multiple regression analysis demonstrated that catheter ablation, no AF recurrence, avoidance of warfarin use, higher baseline depression and anxiety scores, and lower baseline QoL scores contributed to improvement of depression, anxiety, and QoL, respectively. Conclusions: Catheter ablation is more effective for improving depression, anxiety, and QoL in patients with paroxysmal AF compared with AAD therapy.

Aim Dilated cardiomyopathy (DCM) is characterised by left ventricular dilation and associated with systolic dysfunction. Recent evidence has reported the high expression of latent transforming growth factor beta binding protein 2 (LTBP2) in heart diseases, which may play a role in regulating multiple biological functions of myocardial cells. Thus, this study set out to investigate the molecular mechanism and effects of LTBP2 in myocardial oxidative stress injury, fibrosis and remodelling in a rat model of DCM, with the involvement of NF‐κB signalling pathway. Methods The rat model of DCM was treated with si‐LTBP2 and/or activator of NF‐κB signalling pathway to examine the haemodynamic indexes, cardiac functions, oxidative stress injury, fibrosis and remodelling. Moreover, in vitro experiments were conducted to verify the regulatory role of LTBP2 and NF‐κB signalling pathway in DCM. Results LTBP2 was up‐regulated in DCM rats. After LTBP2 was knocked down, haemodynamic indexes, HW/BW ratio, collagen volume fraction (CVF) level, positive expression of LTBP2, levels of reactive oxygen species (ROS), malondialdehyde (MDA), interleukin‐6 (IL‐6), tumour necrosis factor‐alpha (TNF‐α), tumour necrosis factor beta 1 (TGF‐β1) and brain natriuretic peptide (BNP) were all decreased. Meanwhile, levels of LTBP2, Col‐I, Col‐III, p65 and p52 were also reduced, while HW, BW and levels of SOD and TAOC were increased. In contrast, activation of NF‐κB signalling pathway reversed effects of LTBP2 gene silencing. These findings were confirmed by in vivo experiments. Conclusions LTBP2 silencing can attenuate myocardial oxidative stress injury, myocardial fibrosis and myocardial remodelling in DCM rats by down‐regulating the NF‐κB signalling pathway.