Objective To investigate the effect of 8 Hz infrasound on the expression of brain derived neurotrophic factor(BDNF)in the rat hippocampus.Methods Forty-eight Sprague-Dawley rats were randomly divided into groups to be exposed to 90,100 and 130 dB infrasound,and a control group(n=12).All the animals in the infrasound exposure groups were exposed to 8 Hz infrasound at the planned intensity for 2 hours daily for 4 weeks.The rats of the control group were treated identically except that the infrasound amplitude was 0 dB.The animals were sacrificed and their brains were examined at the end of the 4-week infrasound exposure.Western blotting was used to detect the expression of BDNF protein,and in situ hybridization(ISH)was used to observe the distribution of BDNF mBNA in the hippocampus.Results Eight Hz infrasound induced down-regulation of BDNF protein in the hippocampus,with volume-dependent characteristics.ISH showed that BDNF mRNA was distributed widely in the hippocampus.After exposed to infrasound,BDNF mRNA in the hippocampus decreased,especially in the dental gyrus.Conclusion Eight Hz infrasound can down-regulate the expression of BDNF in the hippocampus,especially in the dental gyrus.

Objective To explore the distribution and characteristics of initial PSA and PSA velocity in men younger than years without prostate cancer. Methods PSA in men younger than 50 years without prostate cancer from January 2001 to November 2009 were retrieved retrospectively from our computer center. PSA velocity was calculated if their PSA was measured twice or more. The distributions of initial PSA and PSA velocity were analyzed. The correlations between initial PSA, initial PSA age, and PSA velo-city were also analyzed. Kaplan-meier and log-rank tests were used to estimate the significant difference at the risk of PSA≥ 2.5 ng/ml after initial PSA measurement, stratified by median initial PSA (0.6 ng/ml). Results A total of 4206 men without prostate cancer were included. The median initial PSA value in these men was 0.6 ng/ml. Of these men, 1026 (24.4%), 177 (4.2%), and 90 (2.1%) had an initial PSA≥1.0, ≥2.5, and ≥4.0 ng/ml, respectively. A total of 417 men had their PSA measured these men, 25 (6.0%), 13 (3.1%), and 8 (1.9%) had a PSA velocity≥0.35, ≥0.75, initial PSA age and initial PSA, initial PSA age and PSA velocity, and initial PSA and PSA velocity (correlation coefficient r=0.019, -0.015, and -0.006, respectively; P=0.218, 0.754, and 0.897, respectively). After a follow-up of up to 7.1 years from baseline PSA measurement, the risk of PSA≥2.5 ng/ml, stratified by median initial PSA (0.6 ng/ml) was significantly different (log-rank test, P＜0.001). Conclusions The median baseline PSA and PSA velocity in men younger than 50 years old without prostate cancer are 0.6 ng/ml and 0.03 cancer with an initial PSA higher than median (0.6 ng/ml) have a subsequently higher risk of PSA value ≥2.5 ng/ml.