To evaluate the reforming effects of health service performance appraisal and distribution motivation system at our center,discuss some questions during the development and application of such an evaluation system and conduct comparative analysis of the policies and data before and after management pilot separation between revenue and expenditure.The performance evaluation system and distribution mechanism were established so as to boost the working efficiency of community health services and ensure their sustained and healthy developments.

Objective To study the effect of a recombinant adenovirus carrying p53 gene, B7 1 gene and GM CSF (BB 102) on the nude mice transferred with laryngeal carcinoma. Methods Nude mice model bearing laryngocarcinoma was established using human laryngeal squamous carcinoma cell line (Hep 2). Large amounts of recombinant adenovirus (BB 102) were injected into the tumor. Changes in carcinoma treated with recombinant BB 102 adenovirus were observed under light and electron microscopes. Results The difference between experimental and control groups was statistically significant. The morphology of cells infected with BB 102 was analyzed for evidence of apoptosis by transmission electron microscopy. It has been shown that wild type P53 protein can inhibit cell growth and induce apoptosis, while B7 1 and GM CSF have no such effects. Conclusions The results showed that recombinant adenovirus BB 102 has significant efficacy in suppressing tumor cell growth and in inducing their apoptosis, suggesting that BB 102 might be developed into a therapeutic agent in clinical therapy of laryngeal carcinoma

AIM:To prepare the sulfadiazine silver collagen sheeting for burn(SD-Ag sheeting) and determine the release rate of sulfadiazine silver METHODS:To prepare the SD-Ag sheeting by cross-linking method and to determine the release rate by uniform design RESULTS:The release rate of SD-Ag from SD-Ag sheeting was (22 38?0 036)% CONCLUSION:The preparation of SD-Ag sheeting by cross-linking method was convenient The determining method was accurate,rapid and simple for the quality control of the SD-Ag sheeting

Objective To study the effects of mifepristone on the expression of estrogen receptor(ER)? and progesterone receptor(PR) in the endometrium of patients with adenomyosis in different menstrual cycles. Methods Forty-seven patients with adenomyosis and 15 normal subjects were divided into 3 groups: mifepristone group(n=24),non-drug group(n=23) and control group(n=15).The expression of ER? and PR in eutopic,ectopic and normal endometrium in proliferative phase and secretory phase were detected by immunohistochemistry. Results In non-drug group,the expression of ER? and PR in ectopic endometrial glandular and stromal cells was significantly lower than that in eutopic and normal endometrium(P0.05).The expression of ER? and PR in both ectopic and eutopic endometrial glandular and stromal cells in mifepristone group was lower than that in the non-drug group(P

Objective To study whether the mechanism of mifepristone in treating adenomyosis is suppressing matrix metalloproteinase-9 and tissue inhibitors of metalloproteinase-1(MMP-9/TIMP-1). Methods Thirty-five patients in the mifepristone treated group(19 cases of adenomyosis) and the control group(16 cases of adenomyosis,non-drug treated) underwent hysterectomy.Endometrium was looked as eutopic endometrium and adenomyosis as ectopic endometrium.Expression of MMP-9 and TIMP-1 in eutopic and ectopic endometrium were measured by immunohistochemical techniques. Results The ectopic endometrium of the mifepristone treated group expressed lower level of MMP-9,higher level of TIMP-1 and lower ratio of MMP-9/TIMP-1 than the ectopic endometrium of the control group(P

OBJECTIVETo investigate the toxicological mechanism of microcystin-LR (MCLR) on L-02 cells.

METHODSL-02 cells was treated with MCLR at different concentrations and the subsequent changes such as cell proliferation (MTT assay), morphology, lactate dehydrogenase (LDH) leakage, apoptosis rate and apoptosis-related gene expression were examined.

RESULTSMTT assay showed that MCLR mildly inhibited the cell growth within the initial 24 h of treatment but enhanced the cell viability after that till 60 h in a time- and dose-dependent manner. LDH leakage underwent no marked changes in response to 48-hour MCLR treatment but increased upon prolonged treatment for 60 h, indicating the presence of oxidative damage. After a 48-h treatment with MCLR at 50 microg/ml, obvious apoptosis of L-02 cells occurred as manifested by cell rounding, detachment from the substrate, cell shrinkage and membrane blebbing. The apoptosis rates were rather low (between 22% and 29%) after treatment with MCLR at different concentrations for 36 h, and increased to as much as 80% after a 60-h treatment with 50 microg/ml MCLR. The expressions of p53 and bcl-2 increased in the cells after treatment with high-concentration MCLR, suggesting that MCLR up-regulated the expression levels of the two proteins.

CONCLUSIONMCLR can induce apoptosis and up-regulate p53 and bcl-2 expressions in human normal liver cell line L-02.

Apoptosis ; drug effects ; Cell Line ; Hepatocytes ; cytology ; Humans ; Microcystins ; toxicity ; Proto-Oncogene Proteins c-bcl-2 ; biosynthesis ; genetics ; Tumor Suppressor Protein p53 ; biosynthesis ; genetics

OBJECTIVETo investigate the effects of hydrocamptothecin on the expression of Wnt signaling pathway inhibitor DKK-1 in tumor cells.

METHODSHuman HepG2, Hep3B, LoVo and U251 cells were treated with the antitumor drug Hydrocamptothecin. DKK-1 mRNA expression in the cells was detected with RT-PCR, and beta-catenin expression was measured by fluorescence-activated cell sorting (FACS).

RESULTSDKK mRNA in Hep3B, HepG2, LoVo and U251 cells was significantly increased after hydrocamptothecin treatment for 24 h, and the percentage of beta-catenin-positive cells and fluorescence intensity for beta-catenin expression was lowered in the cells after the treatment.

CONCLUSIONHydrocamptothecin promotes mRNA expression of Wnt signaling pathway inhibitor DKK-1 in Hep3B, HepG2, LoVo and U251 cells.

Antineoplastic Agents, Phytogenic ; pharmacology ; Camptothecin ; analogs & derivatives ; pharmacology ; Cell Line, Tumor ; Colorectal Neoplasms ; genetics ; metabolism ; pathology ; Flow Cytometry ; Humans ; Intercellular Signaling Peptides and Proteins ; biosynthesis ; genetics ; Liver Neoplasms ; genetics ; metabolism ; pathology ; RNA, Messenger ; biosynthesis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; drug effects ; Wnt Proteins ; metabolism

BACKGROUNDMacrophage stimulating protein (MSP) is produced by human bone marrow endothelial cells. In this study, we sought to observe its effects on inducing the expansion of early hematopoietic progenitor cells which were cultured in a liquid culture system in the presence of the combination of stem cell factor (SCF), interleukin 3 (IL-3), interleukin 6 (IL-6), granulocyte macrophage-colony stimulating factor (GM-CSF), erythropoietin (EPO) (Cys) and MSP or of Cys and bone marrow endothelial cell conditioned medium (EC-CM).

METHODSHuman bone marrow CD34(+) cells were separated and cultured in a liquid culture system for 6 days. Granulocyte-macrophage colony forming unit (CFU-GM) and colony forming unit-granulocyte, erythrocyte, macrophage, megakaryocyte (CFU-GEMM) were employed to assay the effects of different treatment on the proliferation of hematopoeitic stem/progenitor cells. The nitroblue tetrazolium (NBT) reductive test and hoechest 33258 staining were employed to reflect the differentiation and apoptosis of the cells respectively.

RESULTSMSP inhibited the proliferation of CFU-GM and CFU-GEMM in semi-solid culture and the inhibitory effect on CFU-GEMM was stronger than on CFU-GM. MSP inhibited the differentiation of early hematopoietic progenitor cells induced by hematopoietic stimulators. Bone marrow (BM) CFU-GEMM was 2.3-fold or 1.7-fold increase or significantly decreased in either Cys + EC-CM, Cys + MSP or Cys compared with 0 hour control in liquid culture system after 6 days.

CONCLUSIONMSP, a hematopoietic inhibitor, inhibits the differentiation of early hematopoietic progenitor cells induced by hematopoietic stimulators and makes the early hematopoietic progenitor cells expand in a liquid culture system.

Antigens, CD34 ; analysis ; Apoptosis ; drug effects ; Cell Differentiation ; drug effects ; Cells, Cultured ; Chemokine CCL3 ; Chemokines, CC ; pharmacology ; Hematopoietic Stem Cells ; drug effects ; Hepatocyte Growth Factor ; pharmacology ; Humans ; Proto-Oncogene Proteins ; pharmacology

Taking the Maternal and Child Health Care Hospital of Zhenjiang as an example,the paper introduces its mobile medical insurance payment system based on the Internet payment platforms,describes the system architecture and the main functional modules including binding of social security card,diagnosis and treatment service,personal center and so on,and analyzes the existing problems and deficiencies.

OBJECTIVETo explore the molecular mechanism by which Biejiajian pills inhibit hepatocellular carcinoma in a nude mouse model bearing HepG2 cell xenograft.

METHODSThe inhibitory effect of Biejiajian pills on the growth of HepG2 cell xenograft in nude mice was observed. Immunohistochemical method was used to examine proliferating cell nuclear antigen (PCNA) expression in HepG2 cell xenograft, and TUNEL method was employed to detect the cell apoptosis; the expression levels of β-catenin and Tbx3 were measured by Western blotting.

RESULTSBiejiajian pills significantly suppressed the growth of HepG2 cell xenograft in nude mice. The tumor-bearing mice treated with a high and a moderate dose of Biejiajian pills showed significantly increased apoptosis rate of the tumor cells [(22.9±1.220)% and (14.7±0.50)%, respectively] compared with the control group [(5.5±0.90)%, P<0.05]. Treatment with Biejiajian pills significantly decreased the expressions of PNCA, β-catenin, and Tbx3 in the cell xenograft (P<0.05).

CONCLUSIONSBiejiajian pills can inhibit the growth of HepG2 cell xenograft in nude mice and promote tumor cell apoptosis possibly by inhibiting PNCA expression and the Wnt/β-catenin signaling pathway.

Animals ; Apoptosis ; Carcinoma, Hepatocellular ; drug therapy ; metabolism ; Cell Proliferation ; Drugs, Chinese Herbal ; pharmacology ; Hep G2 Cells ; Humans ; Liver Neoplasms ; drug therapy ; metabolism ; Mice ; Mice, Nude ; Proliferating Cell Nuclear Antigen ; metabolism ; T-Box Domain Proteins ; metabolism ; Wnt Signaling Pathway ; Xenograft Model Antitumor Assays ; beta Catenin ; metabolism