Prostate volume growth rate changes over time: Results from men 18 to 92 years old in a longitudinal community-based study / 华中科技大学学报（医学）（英德文版）

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, 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 cm, 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.

Role of ubiquitin ligase Ring2 in DNA damage induced by benzoapyrene / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the role of ubiquitin ligase Ring2 in the DNA damage induced by benzo[a]pyrene (B[a]P).</p><p><b>METHODS</b>The expression of Ring2 in human bronchial epithelial (16HBE) cells was inhibited by small interfering RNA (siRNA) to obtain siRNA-Ring2 16HBE cells. The siRNA-Ring2 16HBE cells, as well as normal 16HBE cells, were exposed to B[a]P (0, 1, 2, 4, 8, 16, and 32 µmol/L) for 24 h; other siRNA-Ring2 16HBE cells and normal 16HBE cells were exposed to B [a]P (16 µmol/L) for 0, 1, 2, 4, 8, 12, and 24 h. The levels of DNA damage were evaluated by alkaline single cell gel electrophoresis assay.</p><p><b>RESULTS</b>After being treated with siRNA for 36 h, the siRNA-Ring2 16HBE cells showed a 72% decrease in Ring2 expression compared with normal 16HBE cells. The analysis of covariance showed that whether to be treated with siRNA and concentration of B[a]P had impacts on Olive tail moment (OTM) (P = 0.032 and P < 0.001); the adjusted mean of OTM was significantly higher in siRNA-Ring2 16HBE cells than in normal 16HBE cells. Whether to be treated with siRNA and B[a]P exposure time had impacts on OTM (P = 0.031 and P < 0.001); the adjusted mean of OTM was significantly higher in siRNA-Ring2 16HBE cells than in normal 16HBE cells.</p><p><b>CONCLUSION</b>The DNA of 16HBE cells with decreased Ring2 expression has increased susceptibility to B[a]P, which may be due to reduced H2A monoubiquitination following decrease in Ring2 expression.</p>

Effect of necrostatin-1 on apoptosis induced by aluminum and its mechanism / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effect of necrostatin (Nec-1) on apoptosis induced by aluminum (Al), and approach the mechanism.</p><p><b>METHODS</b>Neural cell death model was made by 4 mmol/L Al treated neuroblastoma cells (SH-SY5Y). Cell viabilities were detected at different concentrations of Al and/or Nec-1. Hoechst 33342/PI double staining was used to observe apoptosis and (or) necrosis that were quantified by flow cytometry using Annexin V/PI double staining. Apoptotic pathway was tested by activities of Caspase-3, Caspase-8 and Caspase-9. In addition, the expression of NF-kappa B and Cyt-c was measured by immunocytochemistry.</p><p><b>RESULTS</b>Cell viabilities were significantly decreased with the increasing concentrations of Al (P < 0.05), which could be significantly upregulated by 60 micromol/L Nec-1 (P < 0.05) and were correlated with the concentrations of Nec-1 (P < 0.05, P < 0.01). Apoptosis and necrosis were observed under fluorescent microscope and quantified by flow cytometry, which suggested an increasing trend of apoptotic and necrotic rates (P < 0.05, P < 0.01). Whereas, Nec-1 could not only decrease the necrotic rate but also apoptotic rate as well (P < 0.05, P < 0.01). Data of Nec-1 on caspases activities showed that Nec-1 could not affect Caspase-9 activity (P > 0.05) and Cty-c protein expression as well (P > 0.05). However, Nec-1 could reduce Caspase-8 activity significantly (P < 0.05, P < 0.01) and increase NF-kappa B protein expression (P < 0.05, P < 0.01) and finally decrease Caspase-3 activity (P < 0.05).</p><p><b>CONCLUSION</b>Nec-1 could reduce cell apoptosis induced by Al, through Caspase-8 pathway, and up-regulate the expression of NF-kappa B protein.</p>

Role of necroptosis in aluminum induced SH-SY5Y cell death / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study whether necroptosis exists or not in neural cell death induced by aluminum.</p><p><b>METHODS</b>SH-SY5Y cells were treated with 4 mmol/L AlCl(3) x 6H(2)O The cell viability was determined with CCK-8 kit after treated with Nec-1 at different dosages (0, 30, 60, 90 micromol/L). Mitochondria membrane potential (MMP), content of reactive oxygen species (ROS), and apoptotic rate/necrotic rates were measured with cytometry.</p><p><b>RESULTS</b>Nec-1 ameliorated the necrotic-like cell morphology, the cell viability were 0.28 +/- 0.05, 0.58 +/- 0.03, 0.68 +/- 0.04, and 1.03 +/- 0.17, there were significant differences between the Nec-1 treated groups and that of controls (t values were 3.25, 3.36, 4.56; P < 0.05). After Nec-1 treatment, the necrotic rates were 16.46% +/- 0.54%, 10.40% +/- 0.64%, 5.43% +/- 0.68%, and 6.28% +/- 0.35%, there were significant differences between the Nec-1 treated cells and that of controls (t values were 3.62, 7.32, 6.96; P < 0.05); while the apoptotic rates were 8.68 +/- 0.36, 7.66 +/- 0.53, 5.68 +/- 0.41, and 4.13 +/- 0.41, there was no significant difference among the groups (F = 6.33, P = 0.11). Cytometry had shown the increased cell MMPs after Nec-1 treatment, which were 67.54 +/- 6.36, 49.42 +/- 5.96, 84.79 +/- 6.86, and 95.51 +/- 7.01, there were significant differences as comparing MMPs of the middle and high dosage of Nec-1 treated cells with those of controls (t values were 3.21, 4.01; P < 0.05); while ROS contents in the Nec-1 treated SH-SY5Y cells were 54.07 +/- 3.32, 52.79 +/- 2.36, 54.68 +/- 1.91, and 59.23 +/- 2.96, there was no significant difference among the groups (F = 5.26, P = 0.19).</p><p><b>CONCLUSION</b>Nec-1, as a specific inhibitor of necroptosis, might effectively block the cell death pathway induced by aluminum, it indicates that necroptosis should be one of the major causes of the SH-SY5Y cell toxicity induced by aluminum, and necroptosis also plays an important role in aluminum induced SH-SY5Y cell death.</p>