Objective:To explore the combined treatment rigimen of gonococcal prostatitis.　Methods:The combined treament of improving remedy of antibiotics was used by taking orally the Chinese medicine and herb medicine demibain in 54 cases of patient with gonococcal prostatitis. compared with controlled group.　Results:The curing rate of combined treatment group was 74.1%, being higher significantly than that of controlled group (P＜0.05).　Conclusion:The combined treatment is better than the controlled group in curing gonococcal prostatitis and preventing recurrence.

Objective To observe the effect of CYP4F2(rs2108622)polymorphism on the dose of warfarin in old patients(65 to 75 years old)who were treated with atrial fibrillation.Methods Sixty cases of old patients with atrial fibrillation were enrolled in the study.All the subjects had taken warfarin for 3 months,and the international normalized ratio(INR)maintained between 1.6 and 2.5.And the CYP4F2(rs2108622)variant were detected by PCR.Results The patients with CYP4F2(rs2108622)allele C/C scored significantly lower warfarin dose than patients with variant allele C/T and T/T (P < 0.05 ).Conclusion CYP4F2 (rs2108622)gene polymorphism have been related with warfarin dose in old patients.

Objective: To investigate the mechanism of miR-503 modulates radio-resistance of esophageal squamous cell carcinoma (ESCC) by targeting excision-repair cross-complementing 1 (ERCC1). Methods: The expression level of miR-503 in radio-resistant ESCC tumor tissues and KYSE140 and KYSE140R cells was detected by qPCR. The miR-503 mimic, miR-503 inhibitor or si-ERCC1 was transfected into KYSE140 and KYSE140R cells.After radiation treatment, the colony formation assay and CCK-8 assay were used to detect the proliferation of KYSE140R cells. Flow cytometry was used to detect apoptosis of KYSE140R cells. WB was used to detect changes in protein expression of ERCC1. Dual luciferase reporter gene assay was used to validate the targeting relationship between miR-503 and ERCC1. Results: The expression level of miR-503 was down-regulated in radio-resistant tissues and ESCC cell lines (all P<0.01). Over-expression of miR-503 significantly inhibited cell proliferation and promoted apoptosis of KYSE140R cells (all P<0.01). Dual-luciferase reporter assay validated that ERCC1 was a target gene of miR-503, and miR-503 negatively regulated the expression of ERCC1. Over-expression of miR-503 significantly down-regulated the expression of ERCC1 in KYSE140 and KYSE140R cells (both P<0.01), inhibited cell proliferation (both P<0.01), but significantly increased apoptosis rate (all P<0.01); knockdown of ERCC1 exhibited a similar effect, while knockdown of both ERCC1 and miR-503 reversed the above effects. Conclusion: Over-expression of miR-503 up-regulated the radio-sensitivity of KYSE140R cells by targeting ERCC1.