PurposeRotenone is the most widely used neurotoxin for the making Parkinson disease (PD) animal model. The neurodegenerative disorder PD shows symptoms, such as slowness of movements, tremor at resting, rigidity, disturbance of gait, and instability of posture. We investigated whether treadmill running improves motor ability using rotenone-caused PD rats. The effect of treadmill running on PD was also assessed in relation with apoptosis of cerebellar Purkinje cells. MethodsTreadmill running was applied to the rats in the exercise groups for 30 minutes once a day for 4 weeks, starting 4 weeks after birth. We used rota-rod test for the determination of motor coordination and balance. In this experiment, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, immunohistochemistry for calbindin, glial fibrillary acidic protein (GFAP), Iba-1, and western blot analysis for Bax and Bcl-2 were performed. ResultsTreadmill running enhanced motor balance and coordination by preventing the loss of Purkinje cells in the cerebellar vermis. Treadmill running suppressed PD-induced expression of GFAP-positive reactive astrocytes and Iba-1-positive microglia, showing that treadmill running suppressed reactive astrogliosis and microglia activation. Treadmill running suppressed TUNEL-positive cell number and Bax expression and enhanced Bcl-2 expression, demonstrating that treadmill running inhibited the progress of apoptosis in the cerebellum of rotenone-induced PD rats. ConclusionsTreadmill running improved motor ability of the rotenone-induced PD rats by inhibiting apoptosis in the cerebellum. Apoptosis suppressing effect of treadmill running on rotenone-induced PD was achieved via suppression of reactive astrocyte and inhibition of microglial activation.

PurposeThe metabolic syndrome (MS) has been accepted as an important cause of benign prostatic hyperplasia (BPH) in old age. However, there are no studies of the influence of MS on prostate volume in relatively young adults. We evaluated the relationship between parameters of MS and prostate volume in men under 50 years of age who visited our health promotion center.Materials and MethodsA total of 968 men aged 30 to 49 years were enrolled from March 2009 to June 2010. Prostate volume by transrectal ultrasonography of the prostate, serum prostate-specific antigen, digital rectal examination, urinalysis, and MS-related parameters were investigated. We evaluated the correlations of prostate volume with MS and MS-related parameters.ResultsProstate volume was not significantly larger in the MS group (18.4 cc; range: 14.3-23.1 cc) than in the non-MS group (17.8 cc; range, 13.6-21.6 cc). The prostate volumes in subjects with abnormal fasting plasma glucose (FPG) (18.9 cc; range, 14.3-22.7 cc) and abnormal waist circumference (WC) (19.5 cc; range, 15.6-23.7 cc) were significantly larger than those of subjects with normal parameters (16.9 [range, 12.7-20.4] cc and 17.5 [range, 13.3-21.2] cc, respectively; p=0.001). The logistic regression analysis showed the FPG level and WC to have a significantly positive correlation with the prostate volume (odds ratios: 1.441 [95% CI: 1.303-1.643] and 2.305 [95% CI: 1.470-3.614], respectively).ConclusionsGroups with abnormal FPG and WC had larger prostate volumes than did normal groups. The abnormal FPG and WC could be more important factors than MS in prostate volume enlargement in relatively young adults.

BackgroundSpinal cord injury (SCI) deteriorates various physical functions, in particular, bladder problems occur as a result of damage to the spinal cord. Stem cell therapy for SCI has been focused as the new strategy to treat the injuries and to restore the lost functions. The oral mucosa cells are considered as the stem cells-like progenitor cells. In the present study, we investigated the effects of oral mucosa stem cells on the SCI-induced neurogenic bladder in relation with apoptotic neuronal cell death and cell proliferation.ResultsThe contraction pressure and the contraction time in the urinary bladder were increased after induction of SCI, in contrast, transplantation of the oral mucosa stem cells decreased the contraction pressure and the contraction time in the SCI-induced rats. Induction of SCI initiated apoptosis in the spinal cord tissues, whereas treatment with the oral mucosa stem cells suppressed the SCI-induced apoptosis. Disrupted spinal cord by SCI was improved by transplantation of the oral mucosa stem cells, and new tissues were increased around the damaged tissues. In addition, transplantation of the oral mucosa stem cells suppressed SCI-induced neuronal activation in the voiding centers.ConclusionsTransplantation of oral mucosa stem cells ameliorates the SCI-induced neurogenic bladder symptoms by inhibiting apoptosis and by enhancing cell proliferation. As the results, SCI-induced neuronal activation in the neuronal voiding centers was suppressed, showing the normalization of voiding function.