Profile and inspirations of hospital value-based purchasing of MS-DRG in the United States / 中华医院管理杂志

Pay-for-performance(P4P) is the third stage of payment evolution in the United States. As of 2010, the Centers for Medicare and Medicaid Services launched a series of P4P programs, including hospital value-based purchasing(HVBP) program. This paper introduced the background and eligibility of HVBP in the United States, focusing on the contents and calculation methods of HVBP as references for the reform of payment methods in China.

Profile and inspirations of hospital value-based purchasing of MS-DRG in the United States / 中华医院管理杂志

Pay-for-performance(P4P) is the third stage of payment evolution in the United States. As of 2010, the Centers for Medicare and Medicaid Services launched a series of P4P programs, including hospital value-based purchasing(HVBP) program. This paper introduced the background and eligibility of HVBP in the United States, focusing on the contents and calculation methods of HVBP as references for the reform of payment methods in China.

Proteasome Inhibitor MG132 Inhibits Cell Proliferation and Induces Cell Apoptosis in Acute T Lymphoblastic Leukemia Cell Via FOXO3a/Puma Pathway / 中山大学学报(医学科学版)

[Objective]To explore the effect and the possible mechanism of the proteasome inhibitor MG132 on acute T lympho?blastic leukemia cells.[Methods]The influence of different concentrations of MG132 in the viability and proliferation of CCRF-CEM was measured by MTS. Apoptosis rates of CCRF-CEM treated by MG132 were determined by flow cytometry. After being exposed to MG132,the protein levels of FOXO3a in cytoplasm and nucleus were analyzed by Western blotting. qRT-PCR was applied to detect the mRNA of FOXO3a and Puma in cells treated by MG132. Then CCRF-CEM was stably transfected with antisense FOXO3a using Lentivirus infection. We further investigated the effects of MG132 in FOXO3a-shRNA cells and elucidated the mechanisms of FOXO3a and Puma.[Results]MG132 inhibits the proliferation of CCRF-CEM,but has no cytotoxicity in peripheral blood mononu?clear cells(PBMC). Cellular apoptosis was induced in cells treated with MG132. At mRNA level,MG132 had no influence on FOXO3a,but increased the expression of Puma. However,MG132 promoted the expression of both FOXO3a and Puma at protein level. Interestingly,the expression of FOXO3a increased very little in cytoplasm. In FOXO3a-shRNA cells the expression of FOXO3a and Puma decreased at protein level. FOXO3a's knockdown attenuated the proliferation inhibition mediated by MG132.[Conclusion]MG132 inhibits the proliferation and promotes to apoptosis of CCRF-CEM. One of the mechanism is that MG132 inhib? its the degradation of FOXO3a,and then activates FOXO3a/Puma pathway.

Research on the effect of Flavokawain B on the proliferation and apoptosis of acute T lymphoblastic leukemia cells / 中华实用儿科临床杂志

Objective To explore the effect of Flavokawain B on the proliferation and apoptosis of acute T lymphoblastic leukemia(T -ALL)cells and its preliminary mechanism.Methods After the T -ALL cell lines CEM-C7(sensitive to glucocorticoids)and MOLT -4(resistant to glucocorticoids)cells were treated with different concentrations of Flavokawain B,the influence of Flavokawain B on the growth rate and doubling time of CEM-C7 and MOLT -4 cells was observed by 3 -(4,5 -dimethylthiazol -2 -yl)-5 -(3 -carboxymethoxyphenyl)-2 -(4 -sulfophenyl)-2H -tetrazolium(MTS)assay,and apoptosis was analyzed by using flow cytometry.Furthermore,Wes-tern blot assay was used to detect the expressions of Bim,Bcl -2 and cleaved Caspase -9.At last,the expressions of Bim and Bcl -2 in clinical T -ALL patient samples were also detected by using Western blot assay.Results MTS as-say showed that Flavokawain B significantly inhibited the cellular proliferation of T -ALL cell lines in a dose and time dependent manner(P <0.01 ).Flow cytometry findings revealed that Flavokawain B significantly induced the apoptosis of T -ALL cells in a dose -dependent manner(P <0.001 ).Western blot results indicated that Flavokawain B in-creased the expression of Bim and cleaved Caspase -9,and decreased the expression of Bcl -2 in T -ALL cell lines, which increased Bim and decreased Bcl -2 in clinical T -ALL patients samples,both in a dose -dependent manner. Conclusions Flavokawain B can inhibit the proliferation and induce the apoptosis of T -ALL cells by up -regulating the expression of Bim and down -regulating the expression of Bcl -2 and activating Caspase -9,whether resistant to glu-cocorticoids or not.