Research on the Medicine Price Reform of Urban Public Hospitals of Shaanxi / 中国卫生经济

Objective:To provide references for drugs zero-profit policy and the adjustment of the medical services price in urban public hospitals of Shaanxi.Methods:The method of weighted mean was used to calculate the rate of price adjustment before and after the medical service project.The price on drugs and medical services were processed by software batch change and manual changes separately.Chinese medical slices were in dependent managed.Results:The medical service price reform and drugs zero-profit poli-.cy come into effect in the city public hospitals,Shaanxi province,form 0:00 April 1st,2017.Before and after the reform of health,the medical work was steadily implemented.Conclusion:The successful implementation of drug zero-profit policy and medical service price reform provided references for other hospitals for medical service reform,which could present scientific references for other hospitals to improve the operation ability.

Apoptosis-inducing effect of carbazole alkaloid (HY-1) in human erythroleukemia K562 cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate apoptosis-inducing effect and its mechanisms of HY-1, a carbazole alkaloid, on human erythroleukemia K562 cells.</p><p><b>METHODS</b>Cell proliferation was detected by sulforhodamine B (SRB) assay after treated with HY-1 at indicated doses. Cell cycle analysis was performed by flow cytometry, mitochondria membrane voltage change was assessed by rhodamine 123 staining, annexin V-PI apoptosis detecting kit and DNA agarose gel electrophoresis were used to identify apoptosis-inducing effect of HY-1. The alterations of apoptosis-relating proteins were detected by Western blot.</p><p><b>RESULTS</b>The IC(50) of HY-1 in K562 cells was (29.05 +/- 0.90) micromol/L by SRB assay. HY-1 had significant apoptotic inducing effect on K562 cells in a dose- and time-dependent manner as verified by appearance of Sub-G(1) peak on histogram of flow cytometry analysis, reduction of mitochondria membrane voltage, appearance of double positive cell group in Annexin V-PI apoptosis detecting test, and remarkable DNA ladder. The expression of cytosolic cytochrome c was apparently increased. Pro-caspase-9, pro-caspase-3 and PARP were all cleaved to active segments. There was no change in the expression of caspase-8.</p><p><b>CONCLUSION</b>HY-1 exerts its anticancer activity through triggering apoptosis of K562 cells by mitochondria-activating pathways.</p>

Vitexicarpin, a flavonoid from Vitex trifolia L., induces apoptosis in K562 cells via mitochondria-controlled apoptotic pathway / 药学学报

<p><b>AIM</b>To investigate the inhibitory effect of vitexicarpin on the proliferation of human cancer cells and its mechanism of action.</p><p><b>METHODS</b>The inhibitory effect of vitexicarpin on the proliferation of human cancer cells was evaluated by the SRB method and its apoptosis-inducing effect was demonstrated by morphological observation under light microscope, flow cytometric analysis and agarose gel electrophoresis. The proteins related to apoptosis were examined by Western blotting analysis.</p><p><b>RESULTS</b>Vitexicarpin significantly inhibited the proliferation of human cancer cells, A2780, HCT-15, HT-1080 and K562, with the IC50 values of (19.1 +/- 2.4) micromol x L(-1) for A2780(48 h), (0.66 +/- 0.10) micromol x L(-1) for HCT-15(48 h), (0.44 +/- 0.06) micromol x L(-1) for HT-1080 (48 h) and (0.28 +/- 0.14) micromol x L(-1) for K562 (24 h). The cells treated with vitexicarpin showed characteristic morphology typical for apoptosis and gave dose-dependent sub-G0/G1 peak in the flow cytometric analysis and DNA ladder on agarose gel electrophoresis. In Western blotting analysis, the cleavage of PARP and caspase-3, the release of cytochrome c from mitochondria into the cytosol, the decrease of Bcl-2 expression level, and the down-regulation of the ratio of Bcl-2/Bax expression level were examined in the K562 cells treated with vitexicarpin.</p><p><b>CONCLUSION</b>Vitexicarpin induces apoptosis in K562 cells via mitochondria-controlled apoptotic pathway.</p>