姜黄素与羟基脲对K562细胞的体外联合作用

目的 了解姜黄素与羟基脲合用对人白血病Ｋ５６２细胞的体外作用。方法 采用ＭＴＴ法测定药物的体外杀伤作用,应用ＡＯ／ＥＢ荧光染料染色观察药物诱导细胞凋亡,金氏公式进行联合用药分析。结果 姜黄素５,１０ｕｇ／ｍｌ,羟基脲２５,５０ｕｇ／ｍｌ同时给药,对Ｋ５６２细胞可产生单纯相加的协同杀伤效果。姜黄素与羟基脲同时给药诱导Ｋ５６２细胞凋亡率高于羟基脲单独用药,低于姜黄素单独用药。结论 姜黄素与羟基脲同时联     

Severe idiopathic erythroblastic synartesis: successful treatment with the anti‐CD20 monoclonal antibody rituximab

Erythroblastic synartesis is a very rare disorder, considered to be caused by autoimmune mechanisms, leading to aggregation of erythroid precursor cells in the bone marrow and subsequently to acquired dyserythropoiesis with severe, transfusion‐dependent anemia. An association with lymphoproliferative or autoimmune diseases has been reported or strongly suggested in all six published cases. Here, we report a young patient with severe idiopathic erythroblastic synartesis without an underlying disease, who was successfully treated with rituximab, an anti‐CD20 monoclonal antibody. The patient received rituximab at a dose of 375 mg/m² once weekly for 4 wk after failure of both immunosuppressive therapies with corticosteroids and intravenous immunoglobulins. At a follow‐up of 30 months after treatment, the patient is still in continuous complete remission without any further treatment, suggesting that rituximab may induce prolonged remissions and eventually cure in this rare disease.     

ODC反义寡核苷酸对K562细胞凋亡及分化和相关基因表达的影响

目的：观察鸟氨酸脱羧酶反义寡核苷酸（ＯＤＣａｓＯＤＮ）引起鸟氨酸脱羧酶（ＯＤＣ）表达及活性的抑制对人红白血病Ｋ５６２细胞生长、凋亡的影响,为探索抑制多胺生物合成的抗癌新途径提供实验依据。方法：采用硫代修饰的ＯＤＣａｓＯＤＮ处理细胞,观察生长曲线,及用Ｇｉｅｍｓａ染色观察形态变化,ＲＮＡ斑点杂交检测基因表达,放射微量法测定ＯＤＣ活性。结果：ＯＤＣａｓＯＤＮ能抑制Ｋ５６２细胞生长、诱导凋亡,并证明了该细胞的ＯＤＣ、Ｂｃｌ２表达下降及ＯＤＣ活性受到抑制。结论：ＯＤＣａｓＯＤＮ能下调ＯＤＣ表达、降低其酶活性,引起ｂｃｌ２基因表达抑制,导致Ｋ５６２细胞生长抑制及凋亡诱导。     

应用RD-PCR方法制备K562细胞表达谱芯片基因探针

目的收集K562细胞表达谱芯片的基因片段。方法培养K562细胞,抽提其mRNA,反转录为cDNA,应用限制性显示PCR技术(RD-PCR)分离K562细胞不同组别的产物片段,分别行PCR扩增。结果制备了可用于基因芯片制作的基因探针片段。结论RD-PCR方法适合于基因芯片探针的收集。     

Idiopathic myelofibrosis terminating in erythroleukemia

A 55-year-old woman with a one-year history of idiopathic myelofibrosis progressed to erythroleukemia. This is the first reported occurrence of erythroleukemia progression from idiopathic myelofibrosis. Certain patterns of leukemia transformation from myeloproliferative disorders are favored: Myeloblastic or myelomonocytic. The rare incidence of erythroblastic transformation is discussed.     

H-2半相合小鼠EL9611红白血病模型的建立

①目的　探讨建立EL96 1 1红白血病F1小鼠模型的可行性 ,并为研究移植物抗白血病 (GVL)效应提供模型。②方法　将 1 0 4～ 1 0 7个EL96 1 1细胞分别接种F1小鼠 ,观察生存时间 ,对濒死小鼠取肝、脾和骨髓做病理检查。接种F1小鼠腹腔注射环磷酰胺和阿糖胞苷 (剂量分别是 5 0mg·kg-1 ·d-1 和 6 0mg·kg-1 ·d-1 ) ,连用 6d ,观察化疗敏感性。51 Cr释放实验测定T细胞对EL96 1 1的细胞毒作用。③结果　F1小鼠接种 1 0 4～ 1 0 7个EL96 1 1细胞后均发病 ,EL96 1 1细胞接种量与小鼠生存时间呈负相关 (r =- 0 .91 ,P <0 .0 1 )。肝、脾和骨髓是EL96 1 1细胞常见浸润部位。接种F1小鼠对环磷酰胺和阿糖胞苷灵敏度分别为 2 35 %和 1 97%。T细胞对EL96 1 1细胞的杀伤作用明显高于对照。④结论　接种 1 0 4～ 1 0 7个EL96 1 1细胞可建立EL96 1 1 F1小鼠红白血病模型 ;T细胞对EL96 1 1细胞有较强细胞毒效应     

急性红白血病55例染色体特征和预后分析

目的探讨急性红白血病（M6）染色体特征和预后因素。方法回顾性分析55例患者染色体核型特征,采用病例对照方法,分为原发组和骨髓增生异常综合征（MDS）转化组;染色体核型异常组和正常组,并分析各组异基因造血干细胞移植（all-HSCT）治疗和（或）化疗疗效及生存预后因素。结果45例经染色体检查,18例正常,染色体异常检出率为60．0％（27／45）,其中复杂异常17例,简单异常10例,10例可见亚二倍体或超二倍体明显增多,18．5％（5／27）5号染色体受累,25．9％（7／27）7号或8号染色体受累。55例患者完全缓解（CR）率63．6％;MDS转化组CR率（42．8％）显著低于原发组（85．2％）,P〈0．05;染色体核型异常组CR率（37．0％）显著低于正常组（83．3％）,P〈0．01。生存预后因素：随访中位时间30（3—79）个月,染色体核型异常组和MDS转化M6患者生存期（OS）和无病生存期（DFS）,移植治疗者较化疗者显著延长（P〈0．01）。16例患者行all-HSCT治疗,其中9例为染色体核型异常MDS转化M6患者,4例为未缓解患者;移植后11例DFS 28个月,2年生存率68．7％（11／16）。结论染色体核型异常和（或）MDS转化M6患者常规化疗疗效差、生存期短,预后差,all-HSCT治疗显著延长生存期,改善预后,染色体核型异常和（或）MDS转化M6患者,宜早期all-HSCT治疗。     

Placental gene expression patterns of epidermal growth factor in intrauterine growth restriction

Objective

In this study, we compared human placental gene expression patterns of epidermal growth factor (EGF) in pregnancies with intrauterine growth restriction (IUGR) vs. normal pregnancies as control.

Study design

Gene expression of EGF was determined from human placental samples collected from all pregnancies presenting with IUGR at our institution during the study period January 1, 2010–January 1, 2011. Multiple clinical variables were also assessed including maternal age, gestational weight gain, increase of BMI during pregnancy and fetal gender.

Results

A total of 241 samples were obtained (101 in the IUGR pregnancy group, 140 in the normal pregnancy group). EGF was found to be underexpressed in the IUGR group compared to normal pregnancy (Ln2^α: −1.54; p < 0.04). Within the IUGR group no fetal gender-dependent difference was seen in EGF gene expression (Ln2^α: 0.44; p < 0.06). Similarly, no significant difference in EGF expression was noted in cases with more vs. less severe forms of IUGR (Ln2^α: −0.08; p = 0.05). IUGR pregnancies were significantly more common in the maternal age group 35–44 years compared to other age groups. Gestational weight gain and gestational BMI increase were significantly lower in IUGR pregnancies compared to controls.

Conclusions

Placental expression of EGF was found to be reduced in IUGR pregnancies vs. normal pregnancies. This may partly explain the smaller placental size and placental dysfunction commonly seen with IUGR. An increased incidence of IUGR was observed with maternal age exceeding 35 years. The probability of IUGR correlated with lower gestational weight gain and lower BMI increase during pregnancy.