Objective To assess the feasibility and efficacy of robot-assisted laparoscopic simple prostatectomy (RALSP) for the treatment of benign prostatic hyperplasia (BPH) with large prostate.Methods From January 2014 to July 2015,16 patients with large prostate (≥80 ml) were treated by RALSP.The average patient's age was 69 years.The prostate volume was (98.3 ± 12.9) ml,preoperative residual urine was (78.0 ± 24.8) ml,the average IPSS was (22.9 ± 5.9),the average QOL was (4.8 ±1.5) and the average Qmax was (8.9 ± 3.7) ml/s,respectively.All patients agreed to accept RASP.The pre-operative and three months post-operative IPSS,QOL,residual urine and Qmax were compared and analyzed.Results All 16 patients underwent the surgeries uneventfully.The average operation time was (92.5 ± 15.5) minutes,the estimated blood loss was (125.5 ±25.5) ml,drainage time was (4.6 ±0.8)days,catheterization time was (7.9 ± 1.2) days and postoperative hospital stay was (5.1 ± 1.1) days.Three months after surgery,patient's IPSS was (11.8 ± 3.1),QOL was (1.6 ± 0.9),the average residual urine was (12.3 ± 2.6) ml and Qmax was (29.4 ± 11.6) ml/s,respectively.All the parameters significantly improved compared with the preoperative data (P ＜ 0.05).Conclusions Robot-assisted laparoscopic simple prostatectomy is a safe and effective method for the treatment of BPH patients with prostate volume larger than 80 ml.

ObjectiveTo investigate the effect of cSN50.1 on the proliferation， migration， invasion， and colony formation of HepG2 cells and its mechanism. MethodsHepG2 cells were divided into cSN50.1 0 μmol/L， cSN50.1 10 μmol/L， cSN50.1 30 μmol/L， cSN50.1 50 μmol/L， cSN50.1 70 μmol/L， and cSN50.1 90 μmol/L groups， and CCK－8 assay was used to investigate the effect of different concentrations of cSN50.1 on the proliferation of HepG2 cells and calculate half－maximal inhibitory concentration （IC₅₀）. HepG2 cells were divided into cSN50.1 0 μmol/L， cSN50.1 10 μmol/L， cSN50.1 30 μmol/L， and cSN50.1 50 μmol/L groups， and wound healing assay， Transwell assay， and colony－forming assay were used to investigate the effect of different concentrations of cSN50.1 on the migration， invasion， and colony formation of HepG2 cells. HepG2 cells were divided into Control group， SP600125 group （an inhibitor of the AP－1 signaling pathway）， and cSN50.1 group to investigate the influence of the AP－1 signaling pathway on the effect of cSN50.1 on hepatocellular carcinoma cells， and RT－PCR and Western Blot were used to measure the expression of CXCL5， TNF－α， and c－Jun protein in cytoplasm and nucleus. HepG2 cells were divided into Control group， PDTC group （an inhibitor of the NF－κB signaling pathway）， and cSN50.1 group to investigate the influence of the NF－κB signaling pathway on the effect of cSN50.1 on hepatocellular carcinoma cells， and RT－PCR and Western Blot were used to measure the expression of CXCL5， TNF－α， and NF－κB protein in cytoplasm and nucleus. A one－way analysis of variance was used for comparison between multiple groups， and the SNK－q test was used for further comparison between two groups. ResultsCompared with the 0 μmol/L group， the 10 μmol/L group had no significant changes in proliferation， migration， invasion， and colony formation abilities （P >0.05）； the 30 μmol/L group had no significant change in proliferation ability （P>0.05）， but with significant reductions in migration， invasion， and colony formation abilities （P<0.05）； the 50 μmol/L group had significant reductions in proliferation， migration， invasion， and colony formation abilities （all P<0.01）； the 70 μmol/L and 90 μmol/L groups had a significant reduction in cell proliferation ability （P<0.01）， but with a cell survival rate of below 50%. Compared with the Control group， the SP600125， PDTC， and cSN50.1 groups had significant reductions in the mRNA and protein expression levels of CXCL5 and TNF－α （all P<0.05）. Compared with the Control group， the SP600125 group， the PDTC group， and the cSN50.1 group had a significant reduction in nuclear protein of c－Jun and NF－κB expression （P<0.05）； the SP600125 group and the PDTC group had a significant reduction in cytoplasmic protein of c－Jun and NF－κB expression （P<0.05）； the cSN50.1 group had a significant increase in cytoplasmic protein of c－Jun and NF－κB expression （P<0.05）. ConclusionThis study shows that cSN50.1 can inhibit the malignant behavior of hepatocellular carcinoma cells and reduce the expression of CXCL5 and TNF－α by inhibiting the nuclear import of c－Jun and NF－κB in hepatocellular carcinoma cells.