Early circulating erythroid progenitors (BFU-E) in sickle cell anemia

Sickle cell anemia (SS) patients can be divided into two sub-populations according to peripheral HbF levels. Patients with low (<9%) HbF levels (LFSS) are characterized by an increased number of circulating BFU-E in active DNA synthesis, and release of burst promoting activity (BPA) by unstimulated low density (LD) adherent cells. In contrast, circulating BFU-E from SS patients with high (>9%) HbF levels (HFSS) are normal in number, largely in resting phase, and their LD cells do not release BPA-like activity.More recently further heterogeneity has been found among these two groups. In LFSS patients GM-CSF is constitutively produced by unstimulated monocytes. In contrast, HFSS patients' adherent cell depletion increases cycling of BFU-E in culture. CM from HFSS patients inhibits BFU-E expression in culture. Hence, LD adherent cells from HFSS patients may release an inhibitory factor(s). The nature of this factor has to be determined.In addition, there are distinct subpopulations of BFU-E responsiveness to growth factor (GM-CSF, IL-3): a) LFSS patients have a homogeneous BFU-E population, equally responsive to GM-CSF and IL-3; b) HFSS patients, in addition to this subpopulation, have a subset of BFU-E dependent exclusively on IL-3 which is 20 to 40% of the total number of circulating BFU-E. This is similar to BFU-E from normal individuals. Hence, LFSS BFU-E represent an actively proliferating population, equally responsive to GM-CSF and IL-3, controlled by at least constitutively produced GM-CSF and possibly other factors.These observations suggest a significant modification in BFU-E behavior in the subset of SS patients with low HbF levels and high hemopoietic stress. The heterogenous regulation of BFU-E in SS disease seems to be an epiphenomenon of HbF levels, and not vice-versa.     

Functional and physical communication between oncoproteins and tumor suppressors

The discovery of oncogenes (c-onc’s) and tumor suppressors (TS’s) has led to the concept that cancer arises from defects in each of these classes of genes or their products. More recently, it has been appreciated that c-onc and TS proteins often affect one another’s functions. Within this context, I review the two classical TS’s, p53 and the retinoblastoma protein, and the consequences of their inactivation. The various forms of genomic instability (GI) that underly the high mutation rates of transformed cells are then discussed. Particular emphasis is placed upon the concept that GI is not only an integral part of the transformed state but is a prerequisite. Increased oxidative DNA damage, and/or an inabiliy to repair it, can lead to GI. The review then discusses recent observations showing that loss of the TS protein peroxiredoxin 1 (prdx1) and increased expression of the c-onc protein c-Myc, each leads to increased oxidative DNA damage. The critical nature of the c-onc-TS interaction is underscored by that occurring between prdx1 and c-Myc, with the former protein regulating the production of DNA-damaging reactive oxygen species by the latter. The intimate association between these proteins and others serves as a paradigm for the exquisite balancing act that c-onc’s and TS’s must maintain in order to properly control normal DNA replication and cellular proliferation while simultaneously minimizing the acquisition of potentially neoplastic mutations. Received 10 May 2005; received after revision 3 July 2005; accepted 19 July 2005     

再生障碍性贫血中VEGF和MVD的相关性研究

目的：研究再生障碍性贫血患者血管内皮生长因子（VEGF）的表达,微血管的生成与疾病病理临床改变的关系。方法：用免疫组织化学染色方法检测35g4再生障碍性贫血患者和35例正常人的骨髓蜡块的VEGF表达情况,并用CD34标记血管内皮细胞,对VEGF和微血管密度（MVD）的表达进行平均光密度测定。结果：再生障碍性贫血骨髓的VEGF表达低下,MVD也降低,与正常对照组比较有显著差异（P〈0．05）。VEGF和MVD的表达呈显著正相关（r=0．988,P〈0．01）。结论：VEGF在再生障碍性贫血中的下调可能和MVD的改变有着密切的关系,针对血管生成的治疗可成为再生障碍性贫血治疗的另一新途径。     

中医方法冶疗再生障碍性贫血的体会

本文主要介绍作者1975—1985年应用中医方法,诊治再生障碍性贫血病12例,收效较佳,从诊治中体会到治疗上应注意:一、病证有机结合,识病则全面掌握疾病的本质,以病概全貌。辨证分型则能立法选药定方;二、建立综合性、系统性和持久性治疗方法,是治疗再障成败关键;三、补虚要注意人体脏腑间相互资助的作用和药疗要与食疗相结合;四、新感驱邪,药忌猛峻,妇女经来要防崩;五、中医辨证重要,但掌握血象变化不可缺。     

再生障碍性贫血病人红细胞膜骨架蛋白的研究

十二烷基磺酸钠—聚丙烯酰胺凝胶电泳(简称为SDS-PAGE)方法分离12例再生障碍性贫血(简称再障)病人红细胞膜蛋白,发现其中有6例红细胞骨架蛋白带1、带2和带4有不同程度减少或缺损。同时用扫描电子显微镜观察其红细胞形态,发现亦有不同程度异常,表现为棘状、刺状及波浪状。提示红细胞骨架蛋白的含量与红细胞的形态有密切关系。     

失血性贫血小鼠恢复过程中骨髓基质金属蛋白酶变化

目的:观察失血性贫血小鼠恢复过程中骨髓基质金属蛋白酶-2和-9(MMP-2,MMP-9)的变化,并探讨其在造血调控中的作用.方法:采用全自动血细胞分析仪、免疫组化和酶谱电泳法分别检测失血性贫血小鼠恢复过程中外周血RBC和Hb数量、骨髓细胞MMP-2和MMP-9表达以及骨髓造血微环境MMP-2和MMP-9的活性变化.结果:(1)与正常对照组相比外周血RBC和Hb数量失血后第1d急剧下降.随着恢复时间的延长,二者数目逐渐上升,到第9d已接近正常对照组水平.(2)在正常对照组检测到了较弱的MMP-2和MMP-9的表达.与正常对照组相比,失血后1d组、3d、5d和7d组小鼠骨髓细胞中MMP-2和MMP-9表达明显增加,MMP-2和MMP-9表达分别于失血后5d和3d达到峰值.与1d组相比,3d组小鼠骨髓细胞中MMP-2和MMP-9表达以及5d组小鼠骨髓细胞中MMP-2表达明显增加.(3)正常对照组中检测到proMMP-2,proMMP-9和MMP-9 3条酶带,MMP-9的活性最强.失血后1d,proMMP-2,proMMP-9和MMP-9的活性均急剧升高.随着恢复时间的延长,3者的活性逐渐降低,到第9d时恢复到接近正常对照组水平.结论:失血性贫血小鼠可能通过骨髓细胞中MMPs表达增加以及骨髓造血微环境中MMPs活性升高来促进骨髓造血功能增强,使外周血RBC和Hb的数量恢复到正常水平.     

肿瘤相关性贫血的中西医研究进展

贫血是肿瘤患者常见的并发症,其发生率及严重程度与性别、年龄、肿瘤类型、分期、化放疗等有关.贫血可引起组织缺氧,使患者生活质量降低,是影响肿瘤患者生活质量的重要因素.贫血程度与化疗疗效、化疗药物的敏感性及耐药性密切相关.贫血患者常规化疗预后较差.低血红蛋白可使肿瘤组织放疗敏感性降低,是放疗患者预后差的独立预后因素.肿瘤相关性贫血的病因是多样的,包括肿瘤自身因素、治疗因素及营养因素等.促红细胞生成素(EPO)的使用是治疗肿瘤相关性贫血的主要方法,可以有效提高患者的血红蛋白水平,改善肿瘤患者的生活质量,提高肿瘤化放疗的疗效.随着中医对肿瘤相关性贫血认识的不断深入,中医药在肿瘤相关性贫血的治疗中取得了良好的疗效.     

鸡传染性贫血病的研究进展

对鸡传梁性贫血病的病源，流行病学及发病机理，临床病理变化，诊断及防制措施做了系统概述。     

T细胞亚群及负调节因子对再障发病的影响

综述T淋巴细胞亚群的分布与活化异常、Th1/Th2细胞分布平衡及负调节因子IFN-γ、TNF-ɑ活化水平的改变与再生障碍性贫血发病的关系.     

2005年与2010年武汉市中小学学生贫血情况分析

目的:了解武汉市中小学学生缺铁性贫血的现状及发展趋势,为教育及卫生部门制订有针对性的防治措施提供科学依据。研究对象为2010年和2005年武汉市城乡7岁、9岁、12岁、14岁和17岁男女学生。方法:利用WHO1972年标准筛查贫血,将贫血程度分为"边缘性"、"轻度"、"中度以上"3度,对城乡各年龄组男女学生两次调研的贫血率及贫血程度构成比进行对比分析。结果:2005-2010年的5年中,武汉市乡村学生的贫血率有大幅度下降,城区学生的贫血率有较大幅度上升,城乡贫血学生大多数为边缘性贫血。城乡男生多数年龄组边缘性贫血的比率增加、轻度贫血的比率下降,男生的贫血程度总体有所减轻。而城乡女生则相反,贫血程度总体有所加重。城区男女学生和乡村女生在学龄初期(7岁、9岁)和青春期的中后期(14岁、17岁)更容易出现贫血率的上升和贫血程度的加重。乡村男生的贫血率和贫血程度均向好的方向发展,变化趋势较为乐观。城区女生是突出的薄弱群体,不仅贫血率上升,贫血程度较重的比率也较高。结论:有关部门应高度重视城区学生贫血情况较大幅度恶化的趋势,应将防治重点放在城区学生(尤其是女生)群体,特别是学龄初期和青春期这两个阶段。