Objective:The main objective of this study is to analyze the development trend of China's private healthcare providers since the issue of Document No. 58 by the General Office of the State Council in the year 2010. It intends to evaluate the effectiveness of the policy on encouragement and guidance to private healthcare. Methods:(1) Using the statistical data collected from national and provincial healthcare yearbook, we made a comparative a-nalysis on seven indicators regarding the development of private healthcare providers, including the number of health-care providers, the number of beds, the number of healthcare professionals, annual outpatient diagnose-and-treat per-son-times, annual inpatient hospitalization person-times, bed utilization rate and average length of stay for two periods of time (i. e. 2006—2010 and 2011—2015). (2) A field study was conducted to six selected provinces. In these provinces, essential information of the related policy was collected, held stakeholder interviews and focus group dis-cussions among hospital management team and medical workers and visits to several typical private providers were made to understand the policy effectiveness and existing problems. The study also tried to find the key factors for a successful private healthcare provider in China. Results:(1) The results show that since the issue of Document No. 58 in the year 2010 , the number of China's private healthcare providers has greatly increased while the scale and service capabilities of private providers still need to be improved. (2) As per the results again, a great difference ex-ists between provinces in terms of private healthcare provider development during 2010 to 2015 . Conclusion:A posi-tive impact of government regulation on the development of private healthcare providers was noticed. However, China's private healthcare providers are still facing many invisible obstacles and challenges. The government needs to put more focus on building a cross-department coordination and supporting regulation system to advance the sustain-able development of private healthcare providers. Moreover, the government needs to cautiously promote the Public-Private-Partnership ( PPP) to improve the effective allocation of resources in the healthcare market and provide essen-tial support to private healthcare providers in solving the problems they meet during their development process.

OBJECTIVE:To develop a HPLC method for determination of tinidazole and chlorhexidine acetate in co-tinidazole gargle.METHODS:Tinidazole and chlorhexidine acetate in co-tinidazole gargle were determined by RP-HPLC with metronidazole as the internal standard.ODS was adopted as stationary phase and acetonitrile-water(35∶65)as mobile phase.The detector was operated at UV254nm.RESULTS:The calibration curve of tinidazole was linear within the concen?tration range of(0.01～0.10)mg/ml(r=0.9999);The calibration curve of chlorhexidine acetate was linear within the con?centration range of(0.01～0.10)mg/ml(r=0.9997).The average recoveries of tinidazole and chlorhexidine were(97.06～102.02)%and(97.21～103.40)%,respectively.The within-day coefficients of variance were(0.20～1.26)%and(0.71～1.11)%,respectively.The between-days coefficients of variance were(0.50～2.06)%and(0.80～2.17)%,respective?ly.CONCLUSION:The method is suitable for determination of preparations containing tinidazole and chlorhexidine acetate.

BACKGROUND: Gene promoter methylation is a major epigenetic change in cancers, which plays critical roles in carcinogenesis. As a crucial regulator in the early stages of B-cell differentiation and embryonic neurodevelopment, the paired box 5 (PAX5) gene is downregulated by methylation in several kinds of tumors and the role of this downregulation in esophageal squamous cell carcinoma (ESCC) pathogenesis remains unclear. METHODS: To elucidate the role of PAX5 in ESCC, eight ESCC cell lines, 51 primary ESCC tissue samples, and eight normal esophageal mucosa samples were studied and The Cancer Genome Atlas (TCGA) was queried. PAX5 expression was examined by reverse transcription-polymerase chain reaction and western blotting. Cell apoptosis, proliferation, and chemosensitivity were detected by flow cytometry, colony formation assays, and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assays in ESCC cell lines with PAX5 overexpression or silencing. Tumor xenograft models were established for in vivo verification. RESULTS: PAX5 methylation was found in 37.3% (19/51) of primary ESCC samples, which was significantly associated with age (P = 0.007) and tumor-node-metastasis stage (P = 0.014). TCGA data analysis indicated that PAX5 expression was inversely correlated with promoter region methylation (r = -0.189, P = 0.011 for cg00464519 and r = -0.228, P = 0.002 for cg02538199). Restoration of PAX5 expression suppressed cell proliferation, promoted apoptosis, and inhibited tumor growth of ESCC cell lines, which was verified in xenografted mice. Ectopic PAX5 expression significantly increased p53 reporter luciferase activity and increased p53 messenger RNA and protein levels. A direct interaction of PAX5 with the p53 promoter region was confirmed by chromatin immunoprecipitation assays. Re-expression of PAX5 sensitized ESCC cell lines KYSE150 and KYSE30 to fluorouracil and docetaxel. Silencing of PAX5 induced resistance of KYSE450 cells to these drugs. CONCLUSIONS As a tumor suppressor gene regulated by promoter region methylation in human ESCC, PAX5 inhibits proliferation, promotes apoptosis, and induces activation of p53 signaling. PAX5 may serve as a chemosensitive marker of ESCC.
Animals ; Carcinoma, Squamous Cell/genetics* ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Epithelial Cells/metabolism* ; Esophageal Neoplasms/genetics* ; Esophageal Squamous Cell Carcinoma/genetics* ; Gene Expression Regulation, Neoplastic ; Humans ; Mice ; PAX5 Transcription Factor/genetics* ; Tumor Suppressor Protein p53/genetics* ; Xenograft Model Antitumor Assays