Objective: To investigate the expression of metastatic suppressor Kangai 1 (KAI1) expression in the primary gallbladder carcinoma and its clinical significance. Methods: The clinical stages of 35 primary gallbladder carcinoma patients were determined according to the TNM criteria of International Union Against Cancer (UICC). Histopathologic changes and the expressions of KAI1 were detected by H-E and immunohistochemical methods, respectively. All the patients were followed up for 3 years. Results: It was found that 1 patient had carcinoma in situ (0 stage), 13 had early carcinoma (I-II stage), and 21 had intermediate or advanced carcinoma (III-IV stage). Histopathologic grading showed that 14 patients had well-differentiated carcinomas, 10 had moderately differentiated ones, and 11 had poorly differentiated ones. Immunohistochemical results revealed that 60.00% (21/35) of the patients were positive of KAI1, with the positive rate being 92.31% (12/13) in early carcinoma (I-II stage) and 42.86% (9/21) in intermediate and advanced carcinoma (III-IV stage), and the former was significantly higher than the latter (Pexact=0.00 476). The positive rate of KAI1 protein was negatively correlated with the clinical staging of patients (Ptrend=0.004) and positively correlated with histopathologic grading (Ptrend=0.001). The positive rate of KAI1 protein in well differentiated carcinoma was 92.86% (13/14), in moderately differentiated carcinoma was 60.00% (6/10), and in poorly differentiated carcinoma was 18.18% (2/11)(Pexact=0.000 475 between the 3 groups). The positive rate of KAI1 protein was 89.47% (17/ 19) in 19 survival patients and 25.00% (4/16) in 16 death cases. Obvious significance of the expression of KAI1 protein was found between the 2 groups (P=0.001). Conclusion: The positive rate of KAI1 is negatively correlated with the clinical staging but positively correlated with the histopathologic grading in patients with primary gallbladder carcinoma. The high expression of KAI1 genes may indicate a better prognosis of gallbladder carcinoma.

This paper reviews the development of appropriate health technology policy from 1992 to 2012 in Zhejiang province.The evolvement of recent twenty years is classified into several stages and each is analysed and evaluated.This study provides reference for the establishment of appropriate health technology policy and the transformation of science and technology policy across the country.

Objective To explore the method for differentiation induction of leukemia cells into dendritic cells(DC) by A23187 in vitro. Methods Chronic myeloid leukemia K562 cells were cultured with A23187 or cytokine to induce differentiation and form DC. The morphologic features of cells were observed under inverted microscope, the changes of DC surface marks were determined by flow cytometry and RT-PCR, the ability to stimulate lymphocyte proliferation was tested by MTT colorimetry. Results Under the condition of the does (385 ng/ml) of A23187 for four days, some of K562 cells were found in typical dendritic appearance.The expression of DC markers CD1a,CD83 ,HLA-DR,CD86 and CD80 was 6.65 ±2.70,7.37 ±2.40,6.24 ±4.29, 21.60 ± 3.84, 18.52 ± 4.48 repectively, and increased obviously compared with the negative control group(2.80 ±0.52,1.85 ±0.56,2.25 ±0.47,6.69 ±0.83,9.96 ±3.53). The differences had statistical significance (P < 0.05). K562 cells derived from DC acquired the ability to stimulate lymphocyte proliferation.Conclusion A23187 can induce the leukemia cells differenntiation into activated DC-like cells rapidly.

To enhance the capacity for extending and applying appropriate health technologies in rural areas in China,this paper proposes a supportive policy system that incoperates macro,average and microlevels. Thepolicysystemfocusesonorientation, incentives, regulationsand standardization,and its objectives and measures of each level are described.The policy system will contribute to the sustainable development rural health work.

Objective: To explore the cause and the strategy for air quantity signaling in old patients using mechanic air. Method: Summary and analysis of the causes for air quantity signaling in 187 cases of old patients using respiratory machine. Results: One hundred fifty-one cases showed low-limited air quantity signaling per minute whereas 36 cases presented high-limited air quantity signaling per minute. Conclusion: Judging and removing the obstacle in respiratory machine on time and accurately are the key point raising both the survival rate of severe patients and the successful rate of mechanic air.

The need analysis of information resource for appropriate health technologies is important for the related information transmission channel and promotion of those technologies at primary level.This paper introduces the current status of the information resource construction of appropriate health technologies in China,and analyzes the needs and means of transmission in terms of users,holders and spreader,taking Zhejiang as an example.Methods of literature review,questionnaire survey,interview,and symposium were employed.

Objective To detect the synergetic effect and mechanism of arsenic trioxide(As2O3)and Trichostatin A(TSA)during inducing apoptosis of HL-60 cells.Methods MTT method was used to test the proliferation of HL-60 cells.Cell cycle and apoptosis were detected by FCM.Semi-quantitative RT-PCR was used to detect the mRNA expression of Bax and Bcl-2 in the cells treated by As2O3 and(or)TSA.Results As2O3 combined with TSA could inhibit proliferation and induce cell cycle arrest at G0 and G1.The percent of apoptosis induced by combination of As2O3 and TSA was obviously higher than that of either As2O3 or TSA.Bax gene expression was increased,while Bcl-2 gene expression was decreased,Bax/Bel-2 ratio was up-regulated.Conclusion Synergetic effect by As2O3 and TSA is remarkable in inducing apoptosis of HL-60 cells.Cell cycte arrest and Bax/Bcl-2 ratio play an important role in apoptosis of HL-60 cells induced by As2O3,TSA or their combination.

Objective To study effect and mechanism of fungus polysaccharide PSM-a of Polyporus sp.M05 on S180 bearing mice. Methods MTT method was used to detect the inhibiting role of PSM-a on S180 cells proliferation in vitro. S180 mice model was established,and was administered by gavage. Tumor volume was detected, and the ratio of tumor to mile weight and inhibiting tumor rate. The activity of NK and LAK cells on the target cells was analyzed by MTT colorimetric assay ;HE stain was used to detect the necrosis of tumor cells. Results PSM-a could inhibit S180 cells grouth in vitro. PSM-a could decrease the tumor weight and increase the ratio of tumor volume and mice weight; Tumor inhibiting rate reached 80% and above when treated with 250 μg/nml PSM-a. PSM-a could increase the activity of NK and LAK cells, and necrosis happened. Conclusion PSM-a could significantly inhibit the growth of S180 cells, and the mechanism bnay be related with the increased killing activity of immunne cells to tumor cells.

Objective To investigate the effect of TGF-β1/SMAD signaling pathway on K562 cells growth inhibition caused by HMBA. Methods After establishing the in vitro differentiation model with HMBA on K562 cells, the MTT assay was used to detect the proliferation of K562 cells, the cell cycle profile was detected by flow cytometry, and the mRNA expression of TGF-β1, SMAD3, SMAD4 and EVI1 was measured by RT-PCR assay. Results HMBA could inhibit the proliferation and promote the differentiation of K562 cells obviously, which was time and concentration-dependent, and the 72 h corresponding IC50, was about 2 mmol/L. Within 72 h, flow cytometry assay indicated that the ration of G0-G1 phase cells was up-regulated, and the results of RT-PCR showed that relative mRNA expression of TGF-β1, SMAD3 and SMAD4 at mRNA level was increased gradually while that of EVI1 was decreased gradually. Conclusion HMBA can inhibit K562 cells proliferation through TGF-β1/SMAD signaling pathway.

Objective To detect the proliferation inhibition and apoptosis of HL-60 cell induced by APS-1 and APS-2 isolated from Polyporus sp. M05 and to investigate its mechanism. Methods The proliferation inhibition was detected by living cells count method,and chosed proper concentration.Flow cytometry with propidium iodide staining was used to detect cell apoptosis. Semi-quantitative RT-PCR was used to detect the expression of apoptosis related gene. Results APS-1 and APS-2 could significantly inhibit the proliferation of HL-60 cells on a time and dose dependent manner. Apoptosis ratio increased to 47. 9% and 26. 8% after HL-60 cells were exposed to APS-1 and APS-2 respectively for 48 h,and the differences had statistical significance (P <0.01). After being induced by APS-1,mRNA of Bax,Fas,Caspase-3 was upregulated. And after being induced by APS-2,mRNA of Bax,Caspase-3 was upregulated,while Fas mRNA did not change. Conclusion APS-1 and APS-2 can inhibit the proliferation and induce apoptosis of HL-60 cells. Mechanism of HL-60 cell apoptosis induced by APS-1 is related to both mitochondrial pathway and Fas signaling pathway,while apoptosis induced by APS-2 is only related to mitochondrial pathway.