Spontaneous Epstein-Barr virus transformed B-cell line sharing the identical immunoglobulin gene rearrangement with acute myeloid leukemia

Mononuclear cells from a 44-year-old patient with acute myeloid leukemia (AML) gave rise to a spontaneous permanent cell line cultured in suspension. The cell line was shown to be positive for Epstein-Barr virus nuclear antigen (EBNA). As expected, its composite phenotype was of B-cell type with B-cell antigens (CD 20, CD 21) and with monoclonal surface IgM of kappa type, but without detectable IgM secretion. Surprisingly, identical monoclonal rearrangements of the immunoglobulin heavy chain (JH) sequences could be demonstrated in the uncultured bone marrow AML cells and in the cell line that also had kappa light chain gene rearrangement. This is the first case to our knowledge of an EBNA positive B-cell line with identical monoclonal Ig heavy chain rearrangement as detected in myeloblastic leukemia cells.     

A comparative study of the iron-clearing properties of desferrithiocin analogues with desferrioxamine B in a Cebus monkey model

A comparative study of the iron-clearing properties of subcutaneously administered desferrioxamine B (DFO) with those of orally administered desferrithiocin sodium salt (1), desmethyl desferrithiocin (2), desazadesmethyl desferrithiocin sodium salt (3), desazadesmethyl desferrithiocin pivaloyloxymethyl ester (4), and desazadesmethyl-5,5- dimethyl desferrithiocin (5) in an iron-loaded Cebus monkey model and a non-iron overloaded bile duct-cannulated rat model is presented. All six drugs, which performed well in rodent studies, demonstrated increased efficiency in the Cebus monkey model. When administered to rodents at a daily dosage of 384 mumol/kg over a period of 10 days, drug 1 demonstrated severe renal toxicity. whereas drugs 3, 4, and 5 exhibited severe gastrointestinal (GI) toxicity. Under the same experimental protocol, drug 2 did not show significant toxic side effects. In addition, to further evaluate the iron-clearing properties of analogue 2, a dose-response study was performed in the primates that showed that iron excretion increased in a dose-dependent fashion.     

Polymorphonuclear leukocyte dysregulation during the systemic inflammatory response syndrome

Altered polymorphonuclear leukocyte (PMN) function is thought to contribute to organ dysfunction during the systemic inflammatory response syndrome (SIRS). To test this hypothesis, we evaluated whole blood PMN function adherent to fibronectin or laminin in patients with mild or severe acute pancreatitis as a paradigm for sirs. Whole-blood PMN intracellular H2O2 production, expression of CD32w (Fc gamma R II), CD16 (Fc gamma R III), and phagocytosis were performed using dichlorofluorescein diacetate, fluorescein isothiocyanate-labeled anti- CD32w, CD16, and serum-opsonized fluorescent microspheres. Group I (n x 7) represents normal control individuals; group II (n x 11) represents patients with mild acute pancreatitis. Group III (n x 15) represents critically ill patients with severe acute pancreatitis. Adherence of PMN from groups I and II to matrix proteins resulted in a 5% to 20% increase in each PMN function assayed whereas adherence of PMN from group III to matrix proteins resulted in 50% to 75% increases in each PMN function assayed. Pertussis toxin, pentoxifylline, and dibutyryl cyclic adenosine monophosphate (cAMP) each reduced group I-II H2O2 production and phagocytosis. Pentoxifylline and dibutyryl cAMP but not pertussis toxin reduced group III H2O2 production. Both intracellular H2O2 and phagocytosis assays from group III but not groups I-II showed exaggerated upregulation when exposed to NaF (4 mmol/L). Anti- interleukin-6 reduced the increase in intracellular H2O2 production in group III patients and significantly altered the exaggerated oxidative response to NaF. Longitudinal studies of group III whole-blood PMN showed persistent upregulation of intracellular H2O2 production in those patients whose hospital courses were complicated by multiple system organ failure. These results demonstrate abnormal whole blood PMN function during the systemic inflammatory response syndrome in the presence of fibronectin, or laminin and that this is mediated in part via a pertussis toxin insensitive altered guanosine triphosphate- binding protein.     

Bone matrix degradation by the plasminogen activation system. Possible mechanism of bone destruction in arthritis

The observed increase in urokinase-type plasminogen activator (u-PA) and its receptor (u-PAR) in synovial tissue of patients with rheumatoid arthritis (RA) suggests pathophysiological involvement of the plasminogen activation (PA) system in inflammatory joint disease. In the present study, we investigated the capacity of the PA system to degrade non-mineralized and mineralized bone-like matrix in vitro as a model for bone destruction. Transfected mouse LB6 cell lines, that expressed either human u-PA or u-PAR, were cultured separately and simultaneously on radiolabelled bone matrix in the presence of plasminogen. Osteoblast-like murine calvarial MC3T3-E1 cells were used to produce a well-characterized, highly organized bone-like matrix, that could be mineralized in the presence of beta-glycerol phosphate. Bone matrix degradation was followed by the release of radioactivity in the culture medium. u-PA-producing cells, in contrast to u-PAR- producing cells, degraded both non-mineralized and mineralized bone matrix. This effect could be inhibited by anti-u-PA antibodies, as well as by tranexamic acid and by aprotinin, indicating that the degrading activity is u-PA mediated and plasmin dependent. Co-cultivation of a small portion of u-PA-producing cells with u-PAR-expressing cells resulted in a marked increase in degradation activity. Reduction of this potentiating effect by suramin or the amino-terminal fragment of u- PA, both competitive inhibitors of u-PA receptor binding, shows that this synergistic effect is due to binding of u-PA to u-PAR. u-PAR must be cell associated, as binding of u-PA to a soluble u-PAR prevented this enhancement. The capability of the PA system to degrade bone matrix in vitro, and the previously demonstrated increased expression of u-PA and u-PAR in synovial tissue of patients with RA, further support a role for the PA system in the development of bone erosions.      

青少年田径运动员个性人格因素特征的测定

目的:测定青少年田径运动员的人格因素特征,为田径运动员的选材、培养和使用提供必要的心理依据。方法:于2005-10/11从中国矿业大学、徐州师范大学、徐州市第三中学、徐州云龙山体校4所学校的田径运动员中随机抽取116名为调查对象。同时随机抽取同一年龄段的134名普通学生作为对照。采用卡氏十六种人格因素表、双重个性因素的推导公式、十六种人格因素测验应用公式进行调查。其中卡氏十六种人格因素表标准分为1～10分,<4.5分为低分,4.5～6.5分为中间分,>6.5分为高分。得分越高,其特征为乐群外向、聪慧、富有才识、情绪稳定、好强固执、轻松兴奋、有恒负责、冒险敢为、敏感、感情用事、怀疑刚愎、幻想、狂放不羁、精明能干、世故、忧虑抑郁、烦恼多端、自由、批评激进、自主、当机立断、知己知彼、自律谨严、紧张困扰。结果:发放问卷250份,回收有效问卷219份。其中田径运动员108名,男55名,女53名。普通高中生111名,男55名,女56名。①男田径运动员乐群性、有恒性、忧虑性、自律性、紧张性5项因素得分高于普通男生,差异有显著性(6.891±1.802,5.418±1.536;6.455±1.951,4.980±1.484;6.000±1.633,5.382±1.604;6.964±1.598,5.691±1.998;5.818±1.657,5.036±1.677,P<0.05～0.01)。②男田径运动员在怯懦与果断型一项因素得分低于普通男生,差异显著(5.004±1.418,5.880±1.327,P<0.01)。③男田径运动员在专业有成就者的个性因素、在新环境中有成长能力个性因素得分高于普通男生(61.100±6.705,54.945±9.296;24.001±3.093,21.273±4.030),男田径运动员在创造能力个性因素得分低于普通男生(4.709±1.729,5.655±1.828),差异均有显著性(P<0.01)。④女田径运动员与普通女生有恒性、敏感性、幻想性、实验性、自律性5项因素评分比较,差异显著(6.453±1.475,4.554±1.726;5.736±1.595,6.357±1.645;5.434±1.896,6.554±1.525;4.792±1.524,5.911±1.478;6.924±1.639,5.289±1.692,P<0.05～0.01)。⑤女田径运动员在怯懦与果断型一项得分低于普通女生,差异有显著性(4.630±1.547,6.254±1.682,P<0.05～0.001)。⑥女田径运动员在专业有成就者的个性因素、在新环境中有成长能力个性因素得分高于普通女生(57.906±8.349,52.464±9.332;23.793±3.953,20.250±4.010),女田径运动员在创造能力个性因素得分低于普通女生(5.094±1.656,5.875±1.849),差异均有显著性(P<0.05～0.01)。结论:男、女田径运动员在有恒性、自律性、专业有成就者的个性因素、在新环境中有成长能力个性因素上存在相似优点,男性外向、热情、乐群,与他人相处时合作与适应新环境能力较强,女性除这些良好特征外,表现更显持稳、保守、传统、务实、理智、重现实。男、女田径运动员同时也存在轻度紧张、烦恼不安,都对教练员依赖性大、顺从性高,缺乏创新精神。     

贫困县小学生睡眠状况调查

目的:了解贫困地区小学生睡眠状况,探讨提高农村儿童睡眠质量的有效措施。方法:于2005-10在吉林省的国家级贫困县应用澳大利亚悉尼大学儿童睡眠中心临床问卷的中国修订版(内容涉及儿童个人情况、睡眠状况、家庭居住环境,父母睡眠状况、吸烟状况,以及父母职业及受教育程度、家庭成员之间的关系等),采用二阶段整群随机抽样法,对750名小学生的睡眠状况进行调查分析,统计分析近1年内儿童在未患重大疾病时的睡眠状况,包括全天睡眠时间分布状况、睡眠障碍发病率及其相关影响因素,根据美国精神障碍诊断统计手册中儿童睡眠障碍的诊断标准,将每周出现1～3次单一或几种睡眠障碍相关症状,定为存在睡眠问题。结果:共发放问卷750份,回收有效问卷691份,回收率为92.1%。6岁和13岁组人数较少予以去除,实际纳入分析者669名。其中男生300名,女生369名;汉族361名,朝鲜族288名,其他民族20名;7岁组96名,8岁组93名,9岁组94名,10岁组122名,11岁组128名,12岁组136名。①贫困县小学生全天睡眠时间均值为(9.62±1.12)h,汉族小学生全天平均睡眠时间比朝鲜族学生长[(9.75±1.23),(9.48±0.90)h,P<0.01]。各年龄组学生全天睡眠时间差异无统计学意义(F=0.169,P>0.05)。②睡眠障碍总时点发病率为27.40%。低年级组小学生(一～四年级)睡眠障碍发病率高于高年级组(五～六年级)(31.80%,24.15%,P<0.05),男生睡眠障碍发病率高于女生(35.35%,20.95%,P<0.01)。③睡眠障碍症状发病率前5位依次为:睡眠不安(8.4%),睡眠姿势异常(8.3%)、张口呼吸(6.1%),梦呓(5.2%);打鼾(4.3%)。④调查结果经单因素相关分析及多重逐步回归分析显示抚养人睡眠习惯、儿童睡眠姿势异常、母亲管教孩子态度和父亲学历等是影响睡眠时间的主要因素。⑤Logistic回归分析显示,孩子患呼吸系统疾病、父母教育孩子方法、母亲有无睡眠障碍、父母之间关系、儿童体弱多病等是睡眠障碍的主要危险因素。结论:贫困地区儿童睡眠障碍是多因素共同作用的结果;孩子的抚养人应改掉不良的睡眠习惯,为儿童提供良好的生活、睡眠环境;增强儿童身体素质,积极防治呼吸系统疾病,应作为近期降低贫困县小学生睡眠障碍的有效措施。