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 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.

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 examine the effects of the MEK inhibitor on human pancreatic cancer cells, and to explore the molecular mechanisms. Methods Human pancreatic cancer cell lines CFPANC1, PANC1 and MiaPaCa2 were treated with MEK inhibitor PD98059 or DMSO, the sensitivity was analyzed by an MTT assay, and cell cycle distribution was evaluated by flow cytometry( FCM), The transcriptional level and protein expression of tumor suppressor genes were detected by real-time RT-PCR and western blot respectively. DNA methyltransferase (Dnmt)1, 3a and 3b were also assayed by western blot, The methylation status of the promoter of the p16INK4A gene was assayed by methylation-specific PCR (MSP). Results PD98059 inhibited to various degrees the growth of three pancreatic cancer cell lines, accompanied by G0-G1 cell cycle arrest. PD98059 up-regulated the expression of p16INK4a, p21WAF1, p27KIP1 mRNA, demethylated the hypermethylation status of p16INK4a gene promoter, and decreased Dnmtl and Dnmt3b in CFPANC1 and PANC1 cell lines. PD98059 only increased the expression of p27KIP1, while the changes of p16INK4a, p21WAF1 and Dnmt were less marked in MiaPaCa2 cell line. Conclusions MEK inhibitor PD98059 down-regulate the activation of Dnmt and up-regulate tumor supress genes, along with the inhibition of cell proliferation and cell cycle progression.

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 explore the effect of vascular endothelial growth factor antisense oligonucleotides(AS-VEGF)on HL60 cell and HL60/VCR multidrug resistance cell and analyze the function of P-gp and the expression of related multidrug resistance genes including Bcl-2,Mcl-1,MDR1,MRP,GST?,TopoⅡ? and TopoⅡ?.Methods A vector AS-VEGF which expressed in eukaryotic cell was established,then transfected the vector into HL60 and HL60/VCR by limposome transfection technology,observed and drew the growth curve by Tapanlan taining,RT-PCR was used to detect the expression of Bcl-2,Mcl-1,MDR1,MRP,GST?,TopoⅡ? and TopoⅡ? in mRNA level after transfected 24 h and 48 h.Western Blot was used to detect the expression of P-gp in proteinum level after transfected 24 h and 48 h.Results The growth of HL60 and HL60/VCR was inhibited by AS-VEGF(1.25 mmol/L).Between HL60 and HL60/VCR,AS-VEGF decreased the expression of MDR1,MRP,GST? and TopoⅡ? but could not influence the expression of Bcl-2,Mcl-1 and TopoⅡ?,and the expression of P-gp was also obviously decreased in 48 h compared with that in 24 h.Conclusions AS-VEGF can inhibite the growth of HL60 and HL60/VCR and reverse multidrug resistance by changing cell microenvironment and the cell membrane correlated protein transportating channel,reduce the cell disintoxicating and the self-repair ability.

In 2012, a new SARS-like coronavirus emerged in the Middle East, namely the Middle East respiratory syndrome coronavirus (MERS-CoV). It has caused outbreaks with high mortality. During infection of target cell, MERS-CoV S protein S1 subunit binds to the cellular receptor (DPP4), and its S2 subunit HR1 and HR2 regions intact with each other to form a stable six-helix bundle to mediate the fusion between virus and target cell membranes. Hence, blocking the process of six-helix bundle formation can effectively inhibit MERS-CoV entry into the target cells. This review focuses on the recent advance in the development of peptidic entry inhibitors targeting the MERS-CoV S2 subunit.
Antiviral Agents ; pharmacology ; Coronavirus Infections ; drug therapy ; Dipeptidyl Peptidase 4 ; metabolism ; Drug Design ; Humans ; Middle East Respiratory Syndrome Coronavirus ; drug effects ; physiology ; Peptides ; pharmacology ; Spike Glycoprotein, Coronavirus ; metabolism ; Virus Internalization ; drug effects

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Child ; Child, Preschool ; DNA, Neoplasm ; genetics ; Female ; Gene Rearrangement, B-Lymphocyte, Heavy Chain ; Humans ; Immunoglobulin Heavy Chains ; genetics ; Infant ; Lymphoma, B-Cell ; diagnosis ; genetics ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; genetics ; Male ; Middle Aged ; Paraffin Embedding ; Polymerase Chain Reaction ; Young Adult