心房颤动的电生理重构

心房颤动 (atrial fibrillation,AF)是临床上最常见的一种持续性心律失常 ,其发病率随年龄而增加 ,40岁以下人群发病率约为 0 .2 %～ 0 .3% ,6 0～ 90岁年龄组发病率增至5 %～ 9% [1 ] 。新近 Framingham的研究表明 AF可以成为一种独立的因素使患者病死率增加 [2 ] 。 AF的发病机制尚未完全清楚 ,可能为非单一机制 ,普遍认为持续性 AF是由于心房内的多子波折返 ,每 1个折返环本身都在不停地改变其大小及传导方向。近年来 ,在 AF的基础及临床研究中 ,两个方面的进展具有十分重要的意义 :一是发现部分 AF起源于心房内某些部位如肺静脉口…     

长期运动对十二指肠黏膜一氧化氮合成和铁贮存的调控效应

目的:观察长期运动对十二指肠黏膜一氧化氮合成和铁贮存的影响及一氧化氮对铁贮存的调节作用。方法:实验于2004-04/09在江苏大学医学院铁代谢研究室完成。①健康雌性SD大鼠40只,随机分为静息组、静息并应用一氧化氮抑制剂组、运动组、运动并应用一氧化氮抑制剂组,每组10只。②静息并应用一氧化氮抑制剂组和运动并应用一氧化氮抑制剂组饮用水中含有一氧化氮抑制剂(1g/L),运动组和运动并应用一氧化氮抑制剂组的大鼠游泳3个月。③3个月后分析各组大鼠血浆铁饱和度,一氧化氮浓度以及十二指肠黏膜一氧化氮含量和非血红素铁含量。结果:实验过程中死亡11只,进入结果分析29只(静息组8只、静息并应用一氧化氮抑制剂组5只、运动组8只、运动并应用一氧化氮抑制剂组8只)。①运动及一氧化氮抑制剂对大鼠血浆铁饱和度和一氧化氮浓度的影响:运动组的血浆铁饱和度低于静息组(P<0.01);运动并应用一氧化氮抑制剂组的血浆铁饱和度低于静息并应用一氧化氮抑制剂组(P<0.05),并且高于运动组(P<0.05)。运动组血浆一氧化氮浓度显著高于静息组(P<0.01);运动并应用一氧化氮抑制剂组的血浆一氧化氮浓度低于运动组(P<0.01),与静息并应用一氧化氮抑制剂组差别不显著(P>0.05)。②运动及一氧化氮抑制剂对大鼠十二指肠黏膜一氧化氮和非血红素铁含量的影响:运动组的十二指肠一氧化氮含量高于静息组(P<0.01);静息并应用一氧化氮抑制剂组的一氧化氮含量低于静息组(P<0.01);运动并应用一氧化氮抑制剂组的一氧化氮含量低于运动组(P<0.01),但高于静息并应用一氧化氮抑制剂组(P<0.01),与静息组差别不显著。与静息组比较,运动组和静息并应用一氧化氮抑制剂组的十二指肠黏膜非血红素铁含量均降低(P<0.05)。结论:静息状态下十二指肠黏膜细胞一氧化氮合成具有较高的紧张性,可能参与维持非血红素铁含量。长期运动可刺激十二指肠黏膜一氧化氮合成,降低铁贮存。但其机制是否涉及运动诱导的一氧化氮的直接作用以及是否参与铁吸收的调节有待于进一步研究。     

Bone marrow transplantation for patients with Philadelphia chromosome- positive acute lymphoblastic leukemia

We report the treatment outcome of allogeneic bone marrow transplantation in ten patients with Philadelphia chromosome-positive acute lymphoblastic leukemia. Six patients are alive and well for 6 to 30 months (median 19 months) after transplantation. Four patients died with transplant related complications. In view of the poor prognosis associated with this disease, marrow ablation followed by allogeneic or syngeneic marrow grafting may be the preferred treatment modality if a suitable marrow donor is available.     

Full-length but not truncated CD34 inhibits hematopoietic cell differentiation of M1 cells

CD34 is expressed on human and murine hematopoietic stem and progenitor cells and its clinical usefulness for isolation of stem/progenitor cells has been well established. Although expression of CD34 is regulated in a developmental stage-specific manner, the function of CD34 is not known. Recently we have shown that both a full-length and truncated form of CD34 protein is expressed by hematopoietic cells (Blood 84:691, 1994). To test whether failure to suppress either form of CD34 could affect terminal myeloid differentiation, we constitutively expressed these CD34 proteins in murine M1 myeloid leukemia cells, which can be terminally differentiated to macrophages by treatment with interleukin-6 of leukemia inhibitory factor. Surprisingly our results show that forced expression of the full-length but not the truncated form of CD34 impedes terminal differentiation by these agents. Because the difference between the two forms of CD34 protein resides in the length of their respective cytoplasmic tail domains, our findings strongly suggest that the cytoplasmic domain region of full-length CD34 is responsible for the observed maturation arrest phenotype. These findings suggest a potential negative regulatory role for full-length CD34 in hematopoietic cell differentiation and may explain, at least in part, the block in maturation observed in CD34+ acute myeloid leukemia.     

Role of p21 RAS in p210 bcr-abl transformation of murine myeloid cells

The p21 RAS product has been implicated as part of the downstream signaling of certain nonreceptor tyrosine kinase oncogenes and several growth factor receptor-ligand interactions. We have reported that the chronic myelogenous leukemia oncogene p210 bcr-abl transforms a growth- factor-dependent myeloid cell line NFS/N1.H7 to interleukin-3 (IL-3) independence. In these p210 bcr-abl-transformed cells (H7 bcr-abl.A54) and in two other murine myeloid cell lines transformed to IL-3 independence by p210 bcr-abl, endogenous p21 RAS is activated as determined by an elevated ratio of associated guanosine triphosphate (GTP)/guanosine diphosphate (GDP), assayed by thin-layer chromatography of the nucleotides eluted from p21 RAS after immunoprecipitation with the Y13-259 antibody. Treatment of p210 bcr-abl-transformed cells with a specific tyrosine kinase inhibitor herbimycin A resulted in diminished tyrosine phosphorylation of p210 bcr-abl and associated proteins, without major reduction in expression of the p210 bcr-abl protein itself. Inhibition of p210 bcr-abl-dependent tyrosine phosphorylation resulted in a reduction of active p21RAS-GTP complexes in the transformed cells, in diminished expression of the nuclear early response genes c-jun and c-fos, and in lower cellular proliferation rate. To further implicate p21 RAS in these functional events downstream of p210 bcr-abl tyrosine phosphorylation, we targeted G- protein function directly by limiting the availability of GTP with the inosine monophosphate dehydrogenase inhibitor, tiazofurin (TR). In p210 bcr-abl-transformed cells treated for 4 hours with TR, in which the levels of GTP were reduced by 50%, but GDP, guanosine monophosphate, and adenosine triphosphate (ATP) were unaffected, p210 bcr-abl tyrosine phosphorylation was at control levels. However, expression of c-fos and c-jun nuclear proto-oncogenes were strongly inhibited and p21 RAS activity was downregulated. These findings show that p210 bcr-abl transduces proliferative signals, in part, through downstream activation of p21 RAS. Furthermore, p21 RAS activity is linked to pathways that regulate c-jun and c-fos expression.     

Haemophilus aphrophilus bleb infection after a mitomycin trabeculectomy

Background: Haemophilus aphrophilus is a rare cause of ocular infection. It has been reported once as a cause of late-onset endophthalmitis in a patient with an inadvertent bleb after cataract surgery. We present a case of Haemophilus aphrophilus bleb infection after a mitomycin trabeculectomy.
Methods: A 56-year-old woman presented with a bleb infection 10 weeks after a mitomycin C augmented trabeculectomy at a University tertiary referral practice of one of the authors (GET). The causative organism was Haemophilus aphrophilus , identified by the Toronto Public Health Laboratory, Ontario, Canada.
Results: The bleb infection resolved following topical, subconjunctival and intravenous antibiotic therapy. A formal bleb revision was required to repair a persistent bleb leak.
Conclusion: Patients who have had trabeculectomies augmented with mitomycin C may be predisposed to bleb infection with unusual organisms. Prompt diagnosis and treatment is necessary to control the infection. Increased awareness and communication with laboratory personnel may increase the isolation of this fastidious organism.     

运动对铁吸收的影响及其作用途径

目的:综合分析运动对铁吸收的影响及其作用途径。资料来源:检索Pubmed1950-01/2006-04有关运动对铁吸收的影响及其作用途径的文献,检索词为“iron absorption,iron metabolism,exercise”。同时检索万方数据库1994-01/2006-03有关运动对铁吸收的影响及其作用途径的文献,检索词为“铁吸收,铁代谢,运动”。资料选择:初选后,有关铁吸收、运动对铁吸收影响及其调节机制的文献被选中。发表于2002年后的文献被优先选择,排除重复实验和Meta分析。资料提炼:检索到9000篇文献,大部分是关于铁吸收调节机制的文献,其中40篇有关运动和铁吸收及其调节机制,30篇作为代表性研究文献被引用。资料综合:运动可导致低铁状态,影响运动能力,这种低铁状态的形成及其调节与铁吸收相关。但是,对于运动如何影响铁吸收存在两种截然相反的观点,一种观点认为运动促进铁吸收;另一种观点认为运动降低铁吸收。最近的研究已经显示运动可能通过机体铁水平、一氧化氮、Hepcidin、促红细胞生成素、低氧以及基因突变(如HFE突变)调节铁吸收。结论:有关运动影响铁吸收的研究仍是初步的,在运动情况下如何调节铁吸收尚有待研究,这对于进一步分析运动诱导的低铁状态的本质以及运动员和运动健身人群是否需要以及如何补充铁具有重要意义。     

X型胶原蛋白与骨骼生长发育关系的研究进展

X型胶原是近年来发现的一种新型胶原,它只存在于生长发育期的即将骨化的软骨内,以液态均相的形式分布于细胞外基质,并启动软骨骨化。它具有特异性合成、局限性分布、一过性存在的特征。许多骨骼系统疾病与X型胶原的异常有着密切的关系。     

Apoptosis in peripheral lymphocytes in systemic lupus erythematosus: a review

There is increasing evidence to suggest that abnormalities in apoptosis may play a part in the pathogenesis of systemic lupus erythematosus (SLE). For example, there is now considerable evidence that bel-2 expression is enhanced in a proportion of peripheral T cells, but not in B cells, in SLE patients and correlates with overall disease activity regardless of the activity index employed. Further work is required to establish whether enhanced bel-2 expression by some T cells in SLE patients is related to their activation or intrinsically enhanced by genetic predisposition. Mutations in Fas result in a lymphoproliferative syndrome and may play a role in accelerating autoimmune disease. A report of three children with mutations in Fas has once again focused attention on this regulator of apoptosis. The relationships between inducers and inhibitors of apoptosis may differ in different cell types, and must be elucidated before the implications of observations made in lymphocytes from SLE patients can be fully understood.