Objective: To investigate the quality of life of patients with chronic prostatitis. Methods: Two hundred patients were included and tested with WHOQOL-100 . Results: Compared with normal controls, the following aspects had no significant difference, including energy and fatigue, appearance and status, working activity, daily life and environment. There were significant difference to controls in other 6 fields and 20 aspects. The major factors that do harm to QOL include satisfaction on life, income and depression. Conclusion: It should deserve the clinician's attention that the QOL of patients with chronic prostatitis is greatly lower than that of the normal controls.

Objective To evaluate the efficacy and safety of use of platelet membrane glycoprotein (GP) Ⅱ b/Ⅲ a inhibitor tirofiban for percutaneous coronary interventional (PCI) in elderly patients with acute ST segment elevation myocardial infarction (STEMI).Methods A total of 120 elderly patients who suffered from STEMI and underwent PCI were selected from July 2007 to November 2009.The patients were randomly assigned to control group, standard-dose tirofiban group and low-dose tirofiban group.We observed coronary blood reflow, the bleeding complication, coagulation factor(TF,vWF) and cell adhesion molecular(sICAM-1 and sVCAM-1).Results Total 116 patients accomplished this study (control group: 38 cases; standard-dose group: 39 cases; low-dose: 39 cases).The percentages of TIMI 3 flow after PCI were higher in the two tirofiban groups than in control group (P<0.05).The incidences of bleeding complications in both tirofiban groups (12.8%,5.1%) were higher than that in control group (2.6%, P<0.05).The concentration of TF, vWF,sICAM-1 and sVCAM-1 were lower in both tirofiban groups than in control group(P< 0.05).Conclusions GP Ⅱ b/Ⅲ a inhibitor tirofiban can benefit the elderly patients with STEMI referred for PCI therapy, low-dose tirofiban may offer almost the same level of efficacy as standard-dose, with less associated bleeding.

Objective To explore the therapeutic potential and mechanism of stem cells mobilized by granulocyte colony-stimulating factor (G-CSF) and AMD3100 to repair global cerebral ischemia injuries in a rat model of cardiac arrest (CA) and cardiopulmonary resuscitation (CPR).Methods Cardiac arrest was induced by asphyxia.Fifty-six SD rats were randomly assigned into four groups:G-CSF group,G-CSF + AMD3100 group,CPR control group and sham operated group.The animals were sacrificed at 3d and 6d after CPR respectively.The neurological status and morphological changes of damaged cerebrum,the apoptosis of nerve cells and vascular endothelial growth factor (VEGF) expressed in brain tissue and capillary density in hippocampus and temporal lobe cortex were measured and analyzed by means of neurological deficit score (NDS),adhesive tape removal test (TRT),ELISA,MRI and immunofluorescence.Results NDS in G-CSF + AMD3100 group (61.4 ± 10.7) was significantly higher than that in CPR control group (49.9 ± 10.4) at 3 d after CPR (P ＜0.05).And less time consumption for TRT found in G-CSF + AMD3100 group (85.5 ±28.9) s rather than was in CPR control group (148.1 ± 23.8) s and G-CSF group (118.5 ± 30.4) s (P ＜ 0.05).The severity of cerebral injury assessed by MRI was significantly milder at both 3 d and 6 d in the two stem cell mobilization groups.The apoptosis rate of nerve cells in G-CSF + AMD3100 group (0.23 ± 0.06) was significantly lower than that in G-CSF group (0.34 ±0.08) at 3 d after CPR,and that in both stem cell mobilization groups was lower than that in CPR control group (0.44 ± 0.09) (P ＜ 0.05).At 3 d and 6 d after CPR,the levels of VEGF in brain tissue were (106.2 ±23.3) pg/mL and (79.9 ± 18.4) pg/mL in G-CSF + AMD3100 group,and were (50.6 ± 13.7) pg/mL and (73.9 ± 16.6) pg/mL in G-CSF group,which were both significantly higher than that in CPR control group (23.1 ± 10.2) pg/mL and (36.2 ± 12.8) pg/mL (P ＜0.05).At 3 d after CPR,the cerebral capillary density (351.8 ±67.9) branches in every high power field (A/HPF) was significantly higher in G-CSF + AMD3100 group than that (301.4 ± 77.3) A/HPF in G-CSF group and (250.4 ± 48.0) A/HPF in CPR control group (P ＜ 0.05).The cerebral capillary density in G-CSF group elevated to (348.4 ±76.7) A/HPF at 6 d after CPR which was significantly higher than that at 3 d (P ＜0.05),and there was no difference between that at 3 d and 6 d in G-CSF + AMD3100 group.Conclusions The mobilization stem cells improve the impaired neurological function.The increased expression of VEGF in brain tissue,the neo-vascularization promoted by the mobilized stem cells and the inhibition of nerve cell apoptosis may be associated with the protective effects of the stem cell mobilization.

Objective To explore the role of miR-221 in the injury induced by hydrogen peroxide (H2O2) in rat myocardial cells (H9c2).Methods The viability of H9c2 cell induced by cell different concentrations of H2O2 was determined by MTT.The expression of miR-221 was detected by RT-PCR method.The miR-221 inhibitor and negative control were transferred into H9c2 cells by Lipofectamine 2000, then the cells were divided into normal control group, model control group (H2O2 group), negative control group (H2O2+ negative control group), inhibition group (H2O2+miR-221 inhibitor group).The cell viability was measured by MTT assay.Cell apoptosis was detected by acridine orange staining method.The expression of Bcl-2, Bax, phosphatase and tensin homolog deleted on chromosome ten (PTEN, p-protein kinase B (AKT) were assayed by Western Blot.Results 0,25,50,100,200,400 μmol/L H2O2 inhibited H9c2 cell activity gradually, of which 200 mol/L inhibition of cell viability moderate, so as a subsequent induction dose.Compared with normal control group, cell viability was decreased (P < 0.01), cell apoptotic rat was increased (P < 0.01), the expression of Bax and PTEN was upregulated (P < 0.01), the expression of Bcl-2 and p-AKT was downregulated (P < 0.01) in model control group and negative control group.Compared with model control group and negative control group, inhibition group proves the contrary.Conclusions Down-expression of miR-221 could significantly inhibit oxidative stress damage in H9c2 cells, which related to regulation of PTEN/AKT signal pathway.