Objective We performed experiments using Neuregulin-1β (NRG-1β) treatment to determine a mechanism for the protective role derived from its beneficial effects by remodeling gap junctions (GJs) during heart failure (HF). Methods Rat models of HF were established by aortocaval fistula. Forty-eight rats were divided randomly into the HF (HF, n = 16), NRG-1β treatment (NRG, n = 16), and sham operation (S, n = 16) group. The rats in the NRG group were administered NRG-1β (10 μg/kg per day) for 7 days via the tail vein, whereas the other groups were injected with the same doses of saline. Twelve weeks after operation, Connexin 43 (Cx43) expression in single myocytes obtained from the left ventricle was determined by immunocytochemistry. Total protein was extracted from frozen left ventricular tissues for immunoblotting assay, and the ultrastructure of myocytes was observed by transmission electron microscopy. Results Compared with the HF group, the cardiac function of rats in the NRG group was markedly improved, irregular distribution and deceased Cx43 expression were relieved. The ultrastructure of myocytes was seriously damaged in HF rats, and NRG-1β reduced these pathological damages. Conclusions Short-term NRG-1β treatment can rescue pump failure in experimental models of volume overload-induced HF, which is related to the recovery of GJs structure and the improvement of Cx43 expression.

Objective: To evaluate the short-term clinical efficacy and adverse events of volumetric modulated arc therapy (VMAT) in the treatment of locally advanced non-small cell lung cancer (NSCLC). Methods: From January to December 2016, 58 patients (47 male and 11 female) with unresectable locally advanced NSCLC received concurrent or sequential chemoradiotherapy. The radiation dose was ranged from 38 Gy to 66 Gy. The radiation dose was equal or higher than 56 Gy in 53 patients (92%). The median radiotherapy fraction was 30, 1.8 Gy to 3.0 Gy for each fraction. Twenty-eight patients (48%) received concurrent chemoradiotherapy. Results: The median follow-up time was 9 months. The 1-year overall survival (OS) rate was 84% and the 1-year progression-free survival (PFS) rate was 48%.Eleven patients (19%) suffered from symptomatic radiation pneumonitis and one of them died of radiation pneumonitis. Within 6 months after radiotherapy, 31 patients (53%) developed asymptomatic local pulmonary fibrosis on CT images. Seventeen patients (29%) suffered from grade Ⅱ esophagitis. Ten cases (17%) had ≥ grade Ⅲ adverse events and 9 of them presented with leucopenia. Conclusions VMAT yields high short-term clinical efficacy and tolerable adverse events in the treatment of locally advanced NSCLC, which does not increase the risk of pneumonitis.

Objective: To investigate the effect of icariin (ICA) on the bisphenol A (BPA)-enhanced proliferation function of thyroid carcinoma cell B-CPAP and underlying mechanism. Methods: The proliferation of Gastric B-CPAP cell line was evaluated by cell counting kit-8 (CCK-8). Apoptosis and ROS expression in B-CPAP cells were detected by flow cytometry. The expression of superoxide dismutase (SOD) and malondialdehyde (MDA) in B-CPAP cells were measured by individual assay kits. The expressions of Bcl-2 and γ-HA2X were detected by Western blot. SPSS 18.0 software was used to analyze the data. Results: B-CPAP cell activity was promoted by treatment with 3×10^-7mol/L BPA for 48 h, with significant difference in absorbance between BPA and control groups (1.089±0.053 vs 0.935±0.010, P<0.05). The cell activities of BPA+ ICA₂₅, BPA+ ICA₅₀, BPA+ ICA₁₀₀ and BPA+ ICA₂₀₀ groups was 0.780±0.036, 1.007±0.050, 0.958±0.033 and 0.625±0.064, respectively (all P<0.01). The proliferation of B-CPAP cells treated with BPA for 72 hours showed a similar trend to 48 hours. There was no significant difference between all treatment groups in 24 hours. The apoptosis rate was (19.272±0.186)% in BPA-treated cells, and was (22.412±0.238)% in control cells (P<0.05). The apoptosis rates of BPA+ ICA₅₀ and BPA+ ICA₂₀₀ groups were (23.688±0.412)% and (30.270±0.696)%, respectively (P<0.01). The intracellular accumulation of ROS in BPA, BPA+ ICA₅₀, and BPA+ ICA₂₀₀ groups were 806±21, 1 772±37, 2 041±16, respectively (P<0.01). The expressions of anti-apoptotic protein Bcl-2 in control, BPA, BPA+ ICA₅₀, BPA+ ICA₂₀₀ groups were 7 120±151, 9 801±286, 5 902±171 and 4 203±216, respectively (P<0.01). Conclusion BPA can promote the proliferation of thyroid carcinoma B-CPAP cells and decrease the apoptosis of cells, and this effect can be inhibited by ICA. The possible mechanism is to induce high expression of intracellular ROS and inhibit the expression of antioxidase system, leading to cell oxidative damage, thereby inducing apoptosis.

【Objective】 To explore the effect of bisoprolol on ICa，Lin volume overload combined with pressure overload heart failure in rabbits. 【Methods】 Totally 82 male New Zealand rabbits （2.5-3.0 kg） were randomly divided into three groups： SO （sham group）， HF （heart failure group）， and BF （heart failure with bisoprolol treatment group）. HF rabbits were duplicated by aortic valve insufficiency procedure combined with abdominal aorta constriction procedure. Real-time PCR and Western blot analysis were performed to detect the expression of ICa，L in left ventricular myocytes. Left ventricular myocytes were isolated； then the cell membrane capacitance， the current density， activation and inactivation of ICa，L were recorded by whole cell patch clamp. 【Results】 ① Bisoprolol could improve the heart function of heart failure rabbits according to the measurement of echocardiography and BNP. ② The expressions of ICa，L mRNA and protein decreased significantly in heart failing rabbits （P<0.01）， but remained unaltered after chronic bisoprolol treatment （P>0.05）. ③ Membrane capacitance was larger in heart failing groups than in sham group （P<0.01）. ICa，L current density decreased greatly in HF group （P<0.01）. Bisoprolol treatment could not change Cm or ICa，L density （P>0.05）. V1/2 of activation curve negative shift enlarged window currents in heart failure groups. Bisoprolol treatment caused window currents to decrease. 【Conclusion】 Bisoprolol could reverse the heart function of heart failure rabbits and also affect the function of ICa，L.