白血病的

Objective: To induce and differentiate into dendritic cells from leukemic cells of patients with chronic myeloid leukemia.

目的：将慢性髓性白血病患者的白血病细胞体外诱导分化成为树突状细胞。

Linalool could eliminate cells of quiescence effectively, suggesting that it maybe kill leukemia stem cells.

芳樟醇能够杀伤处于静止期的白血病细胞，提示其可能对白血病干细胞具有杀伤作用，值得进一步研究。

Phylogenetic analysis of the long terminal repeatand env gene of htlv-1 gave a phylogenetic classification of htlv-1 genotypes into five major molecular subtypes: cosmopolitan, japanese, west african, central african, and melanesian. in order to understand the major genotype of htlv-1 prevalent in china, htlv-1 env gene was amplified by pcr and sequenced from peripheral blood lymphocyts of three htlv-1 carriers in the putian region of fujian province.

根据基因组及血清学反应可将其分为人t淋巴细胞白血病病毒1型（htlv-1）和2型（htlv-2），两型病毒基因组同源性大于60％。htlv-1主要侵染t淋巴细胞，可引起成人t细胞白血病、热带下肢痉挛性瘫痪或htlv-1相关脊髓病，并且在多种自身免疫病患者体内也发现了该病毒的存在。

To investigate the ability of ADA isozyme expression to discriminatebetweem lymphoid and nonlymphoid cell types in acute leukemia,the gelfiltration with FPLC system was used as micromethod for ADA isozymeanalysis.

为进一步阐明白血病细胞ADA同工酶生化性质，探讨制备ADA同工酶抗体的可能性，我们采用分子筛FPLC和阴离子交换FPLC系统二步法分离纯化健康人血清、单个核细胞和急性粒单核细胞白血病细胞ADA同工酶，获得部分纯化ADA1和ADA2，ADA1纯化71.62倍，活力62.2u/mg pr，ADA2纯化37倍，活力42.8u/mg pr，ADA总回收率44%，2步FPLC层析法酶活力回收率分别为68.4%和81.5%。

Results It found that apoptosis was induced in leukemia cells and bcl-2 expression down-regulated by realgar.

结果 雄黄可诱导白血病细胞发生典型的凋亡，同时雄黄可使白血病细胞bcl-2蛋白表达呈时间依赖性下降。

In the study, there were 11 mortalities, including five patients who died during therapy and six who later died as a result of relapse or refractoriness of the leukemia.

在回顾中一共有十一位病患死亡，包括五位病人死於治疗霉菌疗程中，六位死於后续的白血病复发或顽固型白血病。

Cytogenetical evolution was always associated with disease progression in subacute myeloid leukemia patients.

亚急性髓性白血病在病程中出现核型演进时，均伴有病情进展，多为进展到显著的白血病阶段。

In addition, DNA methylation profiles segregated patients with CEBPA aberrations from other subtypes of leukemia, defined four epigenetically distinct forms of AML with NPM1 mutations, and showed that established AML1-ETO, CBFb-MYH11, and PML-RARA leukemia entities are associated with specific methylation profiles.

此外，根据DNA甲基化的不同可将CEBPA基因畸变与其他亚型的白血病区分开来，并定义出四个不同表型的伴NPM1基因突变的急性髓系白血病，并且表明AML1-ETO， CBFb-MYH11，和 PML-RARA 三种白血病类型与特定的甲基化有关。

The transforming growth factor-β superfamily, a large group of highly conserved growth factors including TGF-βs, activins and BMPs, regulate a wide variety of cellular functions such as proliferation, differentiation, apoptosis and migration. Signals from these growth factors are transduced by a group of Smad proteins. To date, there are nine vertebrate Smads, including the receptor-activated Smads , Smadsl-3, 5 and 8, the common mediator Smad4 and Smad4β, and the inhibitory Smads, Smad6 and 7. Signaling is initiated when the ligand induces assembly of a heteromeric complex of type Ⅱ and type Ⅰ TGFβ receptors. Then R-Smads are directly phosphorylated by activated type I TGF-β receptors.

在多种SMADS中，SMAD5令我们产生兴趣，基于三个原因：1、Smad5基因敲除胚胎中发现卵黄囊的异位造血以及CFU-GM祖细胞数目增加，表明SMAD5可能是早期造血发育的负向调控基因。；2、应用反义核酸封闭Smad5可以逆转TGF-β对祖细胞增殖的抑制效应，表明它可能介导TGF-β信号转导，后者的异常，包括某些SMADS的功能异常，和白血病紧密相关；3、Smad5基因定位在人染色体5q21，此区域的缺失和急性髓系白血病和骨髓增生异常综合症相关，因此，Smad5被怀疑为白血病抑制基因。

Our results indicate that 1 NSC606985, at nanomolar level, can effectively induce apoptosis in AML cells NB4 and U937 and significantly inhibit the proliferation without cell death in breakpoint cluster region–Abelson murine leukemia kinase-carrying leukemic K562 cells; 2 At such low concentrations, this agent also significantly inhibits the clonogenic activity of hematopoietic progenitors from patients with AML; 3 For apoptosis induction, NSC606985 rapidly induces the proteolytic activation of protein kinase Cδ with loss of mitochondrial transmembrane potential and caspase-3 activation; 4 Co-treatment with rottlerin, a PKCδ-specific inhibitor, completely blocks NSC606985-induced mitochondrial m loss and caspase-3 activation, while the

结果显示：(1)纳摩尔浓度的NSC606985即可有效诱导AML细胞系NB4和U937细胞凋亡并显著抑制含有bcr-abl融合蛋白激酶的K562细胞的增殖；(2)低浓度的NSC606985也显著抑制来自AML病人骨髓的新鲜白血病细胞的克隆形成能力；(3)除了迅速诱导线粒体跨膜电位的崩塌及Caspase-3的活化外，NSC60698也导致蛋白激酶Cδ的水解激活；(4)PKCδ特异的抑制剂rottlerin能够完全抑制NSC606985诱导的线粒体跨膜电位的崩塌和Caspase-3的活化，而Caspase-3特异的抑制剂z-DEVD-fmk仅能部分削弱PKCδ的活化及细胞的凋亡；(5)以移植PML-RARα转基因小鼠产生的白血病细胞建立的模型研究了该化合物对白血病可能的治疗作用。

For a big chunk of credit-card losses; the number of filings (and thus charge-off rates) would be rising again, whether

年美国个人破产法的一个改动使得破产登记急速下降，而后引起了信用卡大规模的亏损。

Eph. 4:23 And that you be renewed in the spirit of your mind

弗四23 而在你们心思的灵里得以更新