Effect of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction in vivo

Acute myocardial infarction （AMI） is an acute cardiovascular emergency. This study was undertaken to assess the effect of tumor necrosis factor-a （TNF-a） on ventricular arrhythmias induced byAMI in rats in vivo. Two hundred and forty male Wistar rats were randomized into a sham- operation group, an AMI group, and a recombinant human tumor necrosis factor receptor：Fc fusion protein（rhTNFR：Fc） group. Acute anterior wall myocardial infarction was produced in the AMI group by ligating the left anterior descending coronary artery （LAD）, and there was no ligation but operation in the sham-operation group. The rhTNFR：Fc group was treated with rhTNFR：Fc（10 mg/kg）, a TNF-a antagonist, 24 hours before LAD ligation. The spontaneous and induced programmed electrical stimulation ventricular arrhythmias were recorded at baseline and 10 minutes, 20 minutes, 30 minutes, 60 minutes, 3 hours, 6 hours and 12 hours after ligation. At the same time the protein and mRNA expression levels of TNF-a among different groups were detected by histochemistry and real-time fluorescent quantitative PCR. Expression of TNF-a increased markedly from 10 minutes after infarction, peaked at 20-30 minutes, and returned to baseline gradually in the AMI group and rhTNFR：Fc group. The time- windows of spontaneous and induced ventricular arrhythmias were similar. Compared with the AMI group, the rhTNFR：Fc group showed a lesser expression of TNF-a protein and a lower incidence of ventricular arrhythmias （P〈0.05）. There was no obvious change in the sham-operation group. The expression of TNF-a induced by AMI could contribute to the onset of ventricular arrhythmias.

Prostate Volume Growth Rate Changes over Time:Results from Men 18 to 92 Years Old in a Longitudinal Community-based Study

Previous investigations have shown that changes in total prostate volume（TPV） are highly variable among aging men,and a considerable proportion of aging men have a stable or decreasing prostate size.Although there is an abundance of literature describing prostatic enlargement in association with benign prostatic hyperplasia,less is known about the appropriate age cut-off points for TPV growth rate.In this community-based cohort study,TPV was examined once a year in men who had consecutive health checkup,during a follow-up of 4 years.A total of 5058 men（age 18–92 years old） were included.We applied multiple regression analyses to estimate the correlation between TPV growth rate and age.Overall,3232（63.9%） men had prostate growth,and 1826（36.1%） had a stable or decreased TPV during the study period.The TPV growth rate was correlated negatively with baseline TPV（r= –0.32,P〈0.001）.Among 2620 men with baseline TPV 〈15 cm^3,the TPV growth rate increased with age（β=0.98,95% CI：0.77%–1.18%） only up to 53 years old.Among 2188 men with baseline TPV of 15–33.6 cm3,the TPV growth rate increased with age（β=0.84,95% CI,0.66%–1.01%） only up to 61 years old after adjusting for factors of hypertension,obesity,baseline TPV,diabetes mellitus and dyslipidemia.In this longitudinal study,the TPV growth rate increased negatively with baseline TPV,only extending to a certain age and not beyond.Further research is needed to identify the mechanism underlying such differences in prostate growth.