Histological changes of the prostate and acute urinary retention in patients with benign prostatic hyperplasia / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the roles of prostatic infarction, prostatic inflammation and the type of prostatic hyperplasia in acute urinary retention (AUR) in patients with benign prostatic hyperplasia (BPH).</p><p><b>METHODS</b>We retrospectively analyzed 102 cases of BPH, 49 complicated by AUR and the other 53 without AUR. We compared the incidences of prostatic infarction and prostatic inflammation, the types of prostatic hyperplasia, the patients' age, the level of prostate specific antigen (PSA), the prostate volume, and international prostate symptom score (IPSS) between the AUR and non-AUR groups.</p><p><b>RESULTS</b>The PSA level was significantly increased in the AUR group as compared with the non-AUR group (P < 0.05). There were no statistically significant differences between the two groups in the mean age, prostate volume and IPSS (P > 0.05). The type of prostatic hyperplasia showed no correlation with AUR. The incidence rate of AUR was 5.620 and 2.326 times higher in the BPH patients with prostatic infarction and prostatic inflammation respectively than in those without (P < 0.05).</p><p><b>CONCLUSION</b>Prostatic infarction and prostatic inflammation are important risk factors of AUR in BPH patients.</p>

Effects of insulin on the distribution of actins in vascular smooth muscle cells in the process of proliferation via mitogen-activated protein kinase in vitro / 生理学报

Proliferation of vascular smooth muscle cells (VSMCs) is often accompanied by changes in intracellular actin distribution. The changes are controlled by the signal transduction pathways of protein kinase C/mitogenic activated protein kinase (PKC-MAPK), but the mechanism is unclear. In order to study the effect of insulin on the intracellular signal transduction (PKC-MAPK) probably involved in the modulation of proliferation and redistribution of actins in the VSMCs, the DNA synthesis, MAPK activities and its gene expression, and the redistribution of intracellular actins were investigated in the isolated VSMCs of SHR pretreated with PKC inhibitor and/or insulin, respectively. We found that insulin treatment resulted in proliferation of the VSMCs and an increase in [(3)H] TdR incorporation. Meanwhile, the activities and expression of MAPK increased significantly compared to the control group. These effects of insulin were blocked by PKC inhibitor. In addition, insulin caused a redistribution of the intracellular actins in VSMCs, which was also inhibited by PKC inhibitor. It is, therefore, suggested that these effects of insulin on VSMCs proliferation and distribution of the intracellular actins may be mediated by the MAPK signal transduction pathway.