Objective To measure the levels of neutrophil elastase (NE),citric acid and pH in prostatic fluid of patients with prostatitis type Ⅲ.Methods Fifty two patients with prostatitis type ⅢA,98 patients with prostatitis type Ⅲ B and 105 health subjects were enrolled in the study.The levels of NE,citric acid and pH in prostatic fluid were measured ; the expressed prostatic secretion (EPS) routine and bacterial culture were examined,and National Institutes of Health (NIH)-chronic prostatitis symptom index (NIH-CPSI) was evaluated.The data were analyzed by independent samples t-test.Results WBC count,NE and citric acid concentrations,pH in ⅢA group were (17.9 ±5.4)/HP,(898 ±704) μg/L and (14.5 ± 1.7) ng/L,7.60 ±0.43,respectively; those in ⅢB group were (3.9 ±2.2)/HP,(93 ±76) μg/L and (21.9 ±3.8) ng/L,6.71 ±0.25,respectively; those in control group were (3.6 ±2.2)/HP,(86 ±57) μg/L and (22.5 ± 3.9)ng/L,6.48 ± 0.51,respectively.There were significant differences in NE and citrate concentrations,pH value in EPS between Ⅲ A and Ⅲ B patients (t =8.22,16.64 and 13.88,all P ＜0.05),but no difference in NIH-CPSI (t =1.90,P 8 0.05).There were significant differences in WBC count,NE and citric acid concentrations,pH in EPS,NIH-CPSI score between Ⅲ A and control groups (t =18.92,8.47,26.53,18.37 and 32.47,all P ＜ 0.05).There were no differences in WBC count,NE and citric acid concentration and pH value in EPS between Ⅲ B group and control group (t =1.38,1.55,1.02 and 1.21,respectively,all P 80.05),but there was significant difference in NIH-CPSI score between two groups (t =49.46,P ＜ 0.05).In EPS,NE concentration and WBC count were positively correlated with NIH-CPSI (r =0.819 and 0.698,respectively,all P ＜0.01),and citric acid was negatively correlated (r =-0.625,P ＜ 0.01) ; citrate was negatively correlated with WBC count,CPSI and pH value (r =-0.728,-0.644 and-0.817,all P ＜ 0.01).Conclusions The results indicate that the measurements of NE,citric acid and pH in EPS are of significant clinical value in patients with prostatitis type ⅢA and Ⅲ B.

Hepatocellular carcinoma is one of the most common malignant tumors in the world,and its morbidity and mortality have been high.The current preferred treatment for hepatocellular carcinoma is surgical treatment and liver transplantation,but the 5-year survival rate is still low.Due to the insidious onset of hepatocellular carcinoma,most patients have no special manifestations at the initial stage.At the time of diagnosis,they are already in the terminal stage and lose the opportunity of surgery.The Hh pathway plays a key role in the development of tumors.The zinc finger protein GLi plays an important role in tumorigenesis as a key transcription factor in the Hh pathway.At the same time,zinc finger protein GLi can play a key role in the invasion and metastasis of hepatocellular carcinoma by inducing epithelial-mesenchymal transition.In addition,the zinc finger protein GLi also interacts with various tumor-related factors to affect the occurrence and development and treatment of hepatocellular carcinoma.This article reviews the role of zinc finger protein GLi in the development and treatment of hepatocellular carcinoma.

OBJECTIVE: To investigate the effect of down-regulation of pannexin 2 (Panx-2) channels on cisplatin-induced apoptosis in I-10 cells. METHODS: The expression of Panx-2 protein in testicular cancer cells was detected with Western blotting. The testicular cancer cell line I-10 was transfected with two short hairpin RNA (shRNA1 and shRNA2) Lipofectamine, the empty vector (NC group) or Lipofectamine2000 (blank control group), and the changes in the expression of Panx-2 was detected with Western blotting. The effects of transfection with a Panx-2 inhibitor on surviving fraction of the cells treated with cisplatin (16 μmol/L) for 24 h, 48 h and 72 h was assessed with MTT assay, and the clonogenic capacity of the cells was evaluated with colony-forming assay. At 8 h after incubation with 16 μmol/L cisplatin, AnnexinV/PI double staining was used to detect the early apoptosis of the cells. After 24 h of treatment with 16 μmol/L cisplatin, the cells were examined for expressions of caspase-3, Bcl-2 and Bax using Western blotting. RESULTS: The expression of Panx-2 was significantly increased in cisplatin-resistant I-10/DDP ( < 0.001) cells and Tcam-2/DDP ( < 0.01) cells as compared with I-10 cells and Tcam-2 cells. Transfection of I-10 cells with shRNA1 and shRNA2 resulted in significantly decreased Panx-2 expression ( < 0.05) and significantly reduced cell surviving fraction ( < 0.001). In the presence of cisplatin, the cells in NC group showed a higher clonogenic efficiency than those in shRNA1 and shRNA2 groups ( < 0.001). The early-stage apoptosis rate of the cells in shRNA1 and shRNA2 groups were significantly higher than that in NC group ( < 0.01). Panx-2 knockdown in I-10 cells significantly increased caspase-3 and Bax expressions ( < 0.05) and significantly decreased the expression of Bcl-2 ( < 0.01). CONCLUSIONS Down-regulation of Panx-2 channel enhances cisplatin-induced apoptosis in cultured testicular cancer cells.
Antineoplastic Agents ; Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin ; Connexins ; Down-Regulation ; Drug Resistance, Neoplasm ; Humans ; Male ; Testicular Neoplasms