Effects of Arsenic Disulfide Combined with Itraconazole on Proli- feration and Apoptosis and Hedgehog Pathway of Diffuse Large B-Cell Lymphoma Cells / 中国实验血液学杂志

OBJECTIVE@#To investigate the effect of arsenic disulfide (AS@*METHODS@#The human DLBCL cell OCI-LY3 was treated with different concentrations of AS@*RESULTS@#The DLBCL cell viability was decreased significantly at 24, 48 or 72 h as cultured with itraconazole. Along with the increasing of itraconazole concentration, the DLBCL cell viability was significantly reduced as compared with that in control group, and the results showed statistically significant(r=-0.690，r=-0.639, r=-0.833, r=-0.808, r=-0.578). The inhibitory and apoptosis rates of the cells were significantly increased as compared with those of the single drug-treated group after treated by the combination of itraconazole and AS@*CONCLUSION@#Itraconazole can inhibit proliferation of DLBCL cells in a concentration-and time-dependent manner. In addition, the combination of AS

Regional comparison and implications of China's long-term care insurance system / 中国卫生政策研究

This paper attempts to review the long-term care insurance policies which have been issued in 13 national pilot cities such as Qingdao and Haidian district,Beijing. The paper investigates the problems and challen-ges China's long-term care insurance system faces with,and put forward the construction of long-term care insurance system. The preliminary thinking on some issues, such as the relationship between welfare and marketization when the long-term care insurance has been put into practice on a trial basis,the relationship between long-term care insur-ance and medical insurance,and the specific implementation plan of the long-term insurance. According to the issued documents issued by pilot regions,it was found that there are not only differences but also similarities among the pilot cities in who are insured,who pays the insurance fee,what might be covered,what the levels of insurance are,and what kind of service will be provided. Although the long term care insurance system has been initially established in these cities, the specific implementation remains to be demonstrated, e. g. supervision and management, nursing service provision. In addition,local governments need to continuously expand the benefit range of long-term care in-surance to ensure long-term success,do good coordination and connection of long-term care insurance and pension in-surance,and reasonably allocate the medical insurance,pension,and health care resources.

Effects of Quercetin on Chronic Myeloid Leukemia Cell Line Resistant to Imatinib and Its Mechanism / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To explore the growth inhibitory effect of quercetin on imatinib-resistant chronic myeloid leukemia cell lines and to clarify its involved mechanisms.</p><p><b>METHODS</b>The cell viability was detected by trypan blue Staining, percentage of apoptotic cells and cell cycle distribution were detected by flow cytometry, the protein expression was detected by Western blot.</p><p><b>RESULTS</b>Both inhibitory effect of proliferation and apoptosis-inducing effect were similar between the imatinib-resistant and -sensitive cell lines treated with 25 µmol/L quercetin for 24 hours and with arrest of cell cycle at G/M phase. Quercetin could not change the expression of BCR-ABL. The expression of γ-H2AX was markedly enhanced and the phosphorylation of JNK up-regulated by quercetin in both imatinib-resistant and imatinib-sensitive cell lines.</p><p><b>CONCLUSION</b>The growth of imatinib-resistant cells can be inhibited by quercetin, and the apoptosis of cells can be induced by quercetin, which may be related to cell cycle arrest in G/M. The DNA damage and up-regulation of p-JNK may be involved in these processes.</p>

Mechanism of apoptosis synergistically induced by bortezomib combined with cytarabine in U937 cell line / 中国实验血液学杂志

This study was aimed to further explore the apoptosis-inducing effect of bortezomib combined with cytarabine (Ara-C) on U937 cell line. Proliferation and apoptosis in U937 cells treated with bortezomib and/or Ara-C were assessed by cell count. Cell cycle distribution and reactive oxygen species (ROS) production level were measured by using flow cytometry. Cell signaling pathway related to apoptosis was analyzed by Western blot. The results showed that 10 nmol/L bortezomib combined with 50 nmol/L Ara-C significantly inhibited U937 cell proliferation. These two drug combination synergistically induced apoptosis in U937 cells, significantly increased cellular ROS level, and up-regulated the expression of phosphorylated form of JNK and P38 and down-regulated phosphorylation of ERK. It is concluded that the apoptosis of U937 cells synergistically induced by bortezomib combined with low concentration Ara-C is possibly associated with up-regulation of phosphorylated form of JNK, P38 and down-regulation of phosphorylation of ERK induced by increase of ROS, resulting in decrease of mitochondrial potential.

Effect of bortezomib and low concentration cytarabine on apoptosis in U937 cell line / 中国实验血液学杂志

This study was aimed to explore the effect of bortezomib and low concentration cytarabine (Ara-C) on proliferation and apoptosis in U937 cell line and its mechanism. The proliferation and apoptosis of U937 cells treated with bortezomib (10 nmol/L) and(or) Ara-C (50 nmol/L) were observed by cell count, cell morphology, flow cytometry and Western blot. The results showed that bortezomib and Ara-C alone inhibited U937 cell proliferation. The inhibitory effect was enhanced by combination of these two drugs, the inhibitory rates of U937 cell proliferation were (55.00 ± 2.81)% and (70.02 ± 3.33)% after treatment for 24 h and 48 h, respectively. Bortezomib and Ara-C synergistically induced apoptosis and decreased mitochondrial membrane potential in U937 cells. The percentage of Rhodamin123 positive cells was (38.70 ± 1.54)%. Bortezomib and Ara-C also synergistically induced activation of caspase-9, caspase-8 and caspase-3. It is concluded that the bortezomib and low concentration Ara-C synergistically induced apoptosis in U937 cells, mainly through mitochondrial pathway, and possibly through death receptor pathway.