不稳定型心绞痛患者CD4+T淋巴细胞miRNA的差异表达

目的 通过检测不稳定型心绞痛患者循环血CD4+T淋巴细胞基因中miRNA的表达谱,筛选与正常对照者差异表达的miRNA,寻找对CD4+T淋巴细胞具有调控作用的miRNA,为进一步阐明miRNA在不稳定型心绞痛发病机制中的作用提供基础.方法 利用密度梯度离心法分离出不稳定型心绞痛患者和对照者外周血中的单个核细胞,免疫磁珠法进一步分离出CD4+T淋巴细胞.采用miRNA基因芯片技术检测CD4+T淋巴细胞miRNA的表达谱,通过分析软件筛选出不稳定型心绞痛患者和对照者CD4+T淋巴细胞差异表达的miRNA.实时荧光定量聚合酶链反应对差异表达的miRNA进行验证.结果 miRNA基因芯片筛选结果显示,相对于对照者,不稳定型心绞痛患者外周血CD4+T淋巴细胞中表达显著上调的miRNA有miR-155、miR-21、miR-424和miR-127-3p,显著下调的有miR-30b和miR-181a.实时荧光定量聚合酶链反应验证结果与芯片筛选结果一致.结论 筛选得到的不稳定型心绞痛患者循环血CD4+T淋巴细胞miRNA差异表达谱,可能参与了不稳定型心绞痛的发生发展.     

基因芯片技术对哮喘病人相关基因的筛选和分析

目的 利用基因芯片技术寻找哮喘病患者与正常人外周血单核细胞之间差异表达基因,拟为哮喘的早期诊断及预防提供分子标记.方法 用淋巴细胞分离液分别提取16例哮喘病患者与16例正常人外周血单核细胞,用QIAGEN Rneasy Kit提取纯化样本总RNA,并合成用荧光标记的cRNA,分别与含有41 000条基因序列的全基因芯片杂交,以基因表达倍数值≥2.0和基因表达倍数值≤-2.0为阈值来确定差异表达基因,然后用Genespring软件利用生物信息学方法对差异表达基因进行功能分类分析.结果 按P＜0.05差异显著性标准,从34 183条表达基因谱中,筛选出哮喘患者与正常对照差异表达2倍以上的基因有4177条,差异表达2倍以上已知与哮喘相关的基因有19条.经代谢途径分析发现这些差异基因主要涉及到炎症反应、免疫反应、防御反应、创伤反应、外部刺激反应等8大功能分类.结论 哮喘的发生涉及众多基因表达的改变,芯片技术可以有效地筛选出哮喘患者与正常对照的差异表达基因,对进一步探索哮喘的发病机制、有效的干预或逆转哮喘具有重要意义.     

基因表达谱芯片在胰腺癌组织差异表达相关基因筛选中的应用

目的：探讨基因表达谱芯片技术筛选胰腺癌组织和癌旁正常组织基因表达谱差异的可行性。方法应用Agilent公司生产的包含27958条DNA的基因芯片检测4例胰腺癌患者胰腺癌组织和癌旁正常组织的基因表达谱,筛选差异表达基因,并用半定量RT-PCR法检测差异基因CD151、S100A4、TIMP-3和NME3表达情况。结果共筛选出46条基因表达谱差异基因,其中26条表达上调、20条表达下调。差异基因CD151、S100A4、TIMP-3和NME3的表达情况与基因表达谱芯片检测结果一致。结论基因表达谱芯片技术可以筛选出胰腺癌组织差异表达相关基因,为胰腺癌分子标志物研究提供了可靠依据。     

应用基因芯片检测系统性红斑狼疮患者外周血B淋巴细胞

目的 应用寡聚核苷酸基因表达芯片研究系统性红斑狼疮(SLE)患者与健康志愿者外周血B淋巴细胞基因表达谱的变化.方法 应用包含21522条70 mer长度Oligo DNA的寡聚核苷酸芯片(22K Human Genome Array)分别检测6例SLE患者和6名健康志愿者外周血B淋巴细胞基因表达谱,应用聚类分析法分析差异表达的基因.结果 SLE患者外周血B淋巴细胞和健康志愿者B淋巴细胞之间基因表达谱有显著差异,芯片中聚类表达显著上调的基因15个,主要包括Ⅰ型干扰素(IFN)通路中的相关分子;聚类表达显著下调的基因22个,主要包括神经内分泌相关的精氨酸甲基化转移酶家族等与雌激素代谢相关的基因.进一步对这些差异表达基因进行了初步的功能分类分析,分析结果表明这些基因主要与B淋巴细胞的JAK-STAT信号通路和激素代谢相关.结论 SLE患者外周血B淋巴细胞基因表达谱存在显著差异,芯片显示氨基酸代谢、激素代谢、细胞增殖和凋亡、炎症反应等相关生物学功能的改变可能参与SLE的发病.     

应用基因芯片技术对系统性红斑狼疮患者外周血基因表达谱的初步研究

目的 研究系统性红斑狼疮（SLE）患者与正常对照外周血的基因表达谱的改变，以探讨SLE发病机制，诊断及鉴别诊断，以及基因功能的研究。方法 首先从外周血提取总RNA，反转录合成单链，双链cDNA后，体外转录合成生物素标记的cRNA与基因芯片进行杂交，再通过抗原抗体反应机制标记上荧光染料Cy3后，使用芯片扫描仪进行图像扫描。使用分析软件进行表达差异和聚类分析。结果 在3000多个基因点中，与正常对照相比较，鉴定出94个基因存在表达差异相关基因，其中有33个基因表达上调，61个基因表达下调。这些表达差异基因有细胞因子及受体，转录相关基因，凋亡相关基因，生长分化相关基因，信号转导相关基因，细胞周期相关基因，电子传递和氧化相关基因，转移酶相关, 酶相关基因等。聚类分析结果显示不同的疾病以及不同临床表面的同一疾病其外周血的基因表达谱是有差异的，可以用于疾病的诊断和鉴别诊断。基因聚类发现，根据表达谱聚类在一起的基因存在功能上的相似性，可以用来发现已知基因的免疫相关功能。结论 该基因芯片技术方法有较高的重复性和稳定性，能有效地进行SLE致病基因的筛选，更好地理解SLE发生的分子机制，诊断及鉴别诊断，以及基因功能的研究。     

褪黑素对T淋巴细胞株免疫相关基因表达谱的作用

目的 利用基因表达谱芯片研究T淋巴细胞株(HUT78)在褪黑素作用后免疫相关基因表达的差异性。方法 用Cy5和Cy3两种不同的荧光染料通过逆转录反应将干预组和对照组的HUT78细胞的mRNA分别标记成两种探针，并与载有一组靶基因的基因表达谱芯片进行杂交，通过扫描荧光强度，计算机软件分析，寻找经褪黑素作用后表达有差异的基因。结果 T淋巴细胞株受褪黑素作用24h后，共筛选出42条差异表达基因，其中35条基因上调，7条基因下调。结论 褪黑素激活的人淋巴细胞，是通过对一些基因的调控而发挥免疫调节作用。     

应用基因芯片技术研究原发性胆汁性肝硬化患者外周血单个核细胞基因表达谱特征

目的 应用基因芯片技术分析原发性胆汁性肝硬化患者外周血单个核细胞的基因表达谱特征.方法 选取9例原发性胆汁性肝硬化患者、9名健康对照为研究对象,提取其外周血单个核细胞总RNA,进行人类全基因组寡核苷酸芯片(约22000个基因)检测,筛选出差异表达基因及相关信号通路.结果 原发性胆汁性肝硬化患者外周血单个核细胞中差异表达的基因共有79个,其中21个表达上调,58个表达下调.这些基因对应着27条信号通路,其中有6条通路参与了免疫调控及细胞凋亡过程,分别是自然杀伤细胞介导的细胞毒通路、Toll样受体信号通路、抗原加工提呈通路、细胞因子相互作用通路、T细胞受体信号通路、细胞凋亡通路.结论 原发性胆汁性肝硬化患者外周血单个核细胞中存在特有的差异表达基因,针对这些基因及相关信号通路的进一步研究,将为探索发病机制和寻找生物标志物提供新的方向.     

基因芯片在同型半胱氨酸诱导动脉粥样硬化基因表达谱变化中的应用

应用基因芯片技术研究同型半胱氨酸诱导动脉粥样硬化的基因表达谱变化。选取3例无冠心病传统危险因素的住院患者，其中1例为血同型半胱氨酸正常的冠状动脉造影正常者，1例为血同型半胱氨酸正常的冠心病患者，1例为高同型半胱氨酸血症的冠心病患者。分离外周血淋巴细胞并抽提总RNA，逆转录制备杂交探针，应用含有1152条基因的人类表达谱芯片进行差异表达谱分析。结果发现，高同型半胱氨酸血症的冠心病患者与血同型半胱氨酸正常的冠状动脉造影正常者比较差异表达的基因177条(组一)，高同型半胱氨酸血症的冠心病患者与血同型半胱氨酸正常的冠心病患者比较差异表达的基因有151条(组三)。组一与组三基因芯片平行比较，二者共同的差异表达基因48条，其中上调基因23条，下调基因25条。结果提示，在差异表达的基因中，有些是凋亡、信号转导、免疫、蛋白质合成及原癌基因等的相关基因，这些基因可能与同型半胱氨酸致动脉粥样硬化发生有关。应用基因芯片技术研究同型半胱氨酸诱导动脉粥样硬化差异表达谱，可能为动脉粥样硬化发病机制研究提供新的思路。     

急性心肌梗死行血栓抽吸患者冠状动脉内微粒与外周血微粒中microRNA基因芯片的差异性表达分析

目的通过基因芯片筛选并分析急性ST段抬高型心肌梗死(STEMI)患者冠状动脉内微粒与外周血微粒中microRNA的表达差异,为进一步研究微粒在急性心肌梗死发病中的作用提供线索。方法收集STEMI行血栓抽吸患者的冠状动脉内抽吸血样及外周血样,运用超速离心法分离STEMI患者冠状动脉内与外周血样中的微粒;通过基因芯片技术对微粒中的microRNA进行测序,构建冠状动脉内血样与外周血样的微粒的microRNA差异表达谱,并对其进行功能学分析与预测。结果 STEMI患者冠状动脉内与外周血中微粒所含有的microRNA有明显差异。通过构建microRNA差异表达谱,找到了307个microRNA具有差异性表达,表达上调221个,下调86个。结论STEMI患者冠状动脉内与外周血微粒所含有的microRNA表达具有显著性差异,其中有49个与心血管疾病密切相关,可以作为进一步研究的靶点。     

应用基因芯片技术筛选胰腺癌相关基因

目的应用基因芯片技术筛选胰腺癌相关基因。方法将14000种人类基因PCR产物按微矩阵排列点样于化学涂层的载玻片上，制成基因芯片。按一步法抽提4例胰腺癌和癌旁正常胰腺组织的总RNA，将等量的RNA分别逆转录合成荧光分子掺人的cDNA一链作探针，混合后杂交上述基因芯片。经严格洗片后用ScanArray 4000扫描仪扫描芯片荧光信号图像，每点上两种荧光信号的强度分别代表Cy5-dCTP和Cy3-dCTP的量，获得的荧光信号图像用计算机分析。结果按差异显著性标准，从14000个基因中筛选出在胰腺癌组织中共同差异表达基因189条，其中已知基因101条，新基因88条。在筛选出的已知基因中，有50条表达上调，51条表达下调。结论基因芯片技术的肿瘤基因表达谱分析能够高通量筛选胰腺癌相关基因。并高效对基因功能进行研究。胰腺癌基因表达谱的分析有助于认识肿瘤发病机制。     

ABO基因检测在预测胎儿血型中的应用

目的：探讨利用ABO基因分型方法来预测胎儿血型的可行性。方法：收集O型孕妇25例,提取孕妇外周血血浆中胎儿游离DNA,PCR-SSP法检测SRY基因,利用聚合酶链反应-限制性片段长度多态性分型（PCR-RFLP）检测胎儿ABO血型基因型。结果：在25例样本中,23例实验成功,2份样本扩增失败,22例与胎儿出生后的血型一致,1例不一致。结论：应用基因检测方法来预测胎儿ABO血型,准确性高,安全性好,值得临床推广应用。     

COPD患者营养不良与T淋巴细胞凋亡及其表面Fas、FasL、Bcl-2表达的关系

目的探讨COPD患者营养不良对T淋巴细胞亚群CD4＋、CD8＋T细胞凋亡及其细胞表面Fas、FasL、Bcl-2抗原表达的影响。方法选取COPD稳定期患者30例,正常对照组20例,流式细胞仪测定T淋巴细胞亚群细胞凋亡率、及其表面Fas、FasL、Bcl-2抗原表达水平,测定体质指数、三头肌皮皱厚度等指标评估营养状况。用单因素方差分析进行统计。结果 ：1.COPD患者外周血中CD4＋的凋亡及其表面Fas、FasL抗原表达均较对照组增加,营养不良组又高于营养正常组,而其表面Bcl-2的抗原表达降低。COPD稳定期患者血清CD4＋凋亡及其表面CD4＋Fas、CD4＋FasL的表达均与体质指数负相关,而CD4＋Bcl-2与体质指数则呈正相关。结论营养不良促进COPD患者CD4＋T淋巴细胞的凋亡,可能是通过Fas/FasL,Bcl-2发挥作用。     

中国北方汉族人基质金属蛋白酶12基因多态性与慢性阻塞性肺疾病易感性的关系

目的 :研究中国北方汉族正常人、吸烟慢性阻塞性肺疾病 (COPD)患者、吸烟非COPD患者基质金属蛋白酶 12 82位点等位基因和基因型分布频率 ,初步探讨此基因多态性对COPD发病的影响。方法 :应用聚合酶链反应限制性片段长度多态性法 ,检测 10 0例北方汉族正常人 ,14 8例吸烟COPD患者 ,97例健康吸烟者基质金属蛋白酶 12 82位点等位基因和基因型。结果 :14 8例吸烟COPD患者基质金属蛋白酶 12 82位点基因型AA、AG及GG频率分别为 95 0 4 %、4 96 %及 0 ,等位基因A、G频率分别为97 6 4 %、2 36 % ,与 10 0例正常人、97例健康吸烟者的分布比较差异无显著性。结论 :在中国北方汉族人中 ,MMP12基因A 82G等位基因多态性与我国北方汉族吸烟COPD发病无关。     

Differential Expression of Vitamin E and Selenium-Responsive Genes by Disease Severity in Chronic Obstructive Pulmonary Disease

Abstract

Antioxidant nutritional status is hypothesized to influence chronic obstructive pulmonary disease (COPD) susceptibility and progression. Although past studies relate antioxidants to gene expression, there are no data in patients with COPD. This study investigated the hypothesis that antioxidant status is compromised in patients with COPD, and antioxidant-responsive genes differentially express in a similar pattern. Lung tissue samples from patients with COPD were assayed for vitamin E and gene expression. Selenium and vitamin E were assayed in corresponding plasma samples. Discovery based genome-wide expression analysis compared moderate, severe, and very severe COPD (GOLD II-IV) patients to mild and at-risk/normal (GOLD 0-I). Hypotheses-driven analyses assessed differential gene expression by disease severity for vitamin E-responsive and selenium-responsive genes. GOLD II-IV COPD patients had 30% lower lung tissue vitamin E levels compared to GOLD 0-I participants (p = 0.0082). No statistically significant genome-wide differences in expression by disease severity were identified. Hypothesis-driven analyses of 109 genes found 16 genes differentially expressed (p_adjusted < 0.05) by disease severity including 6 selenium-responsive genes (range in fold-change -1.39 to 2.25), 6 vitamin E-responsive genes (fold-change -2.30 to 1.51), and 4 COPD-associated genes. Lung tissue vitamin E in patients with COPD was associated with disease severity and vitamin E-responsive genes were differentially expressed by disease severity. Although nutritional status is hypothesized to contribute to COPD risk, and is of therapeutic interest, evidence to date is mainly observational. The findings reported herein are novel, and support a role of vitamin E in COPD progression.     

Systemic CD4+ T-cell activation is correlated with FEV1 in smokers

The inflammation of the lungs in chronic obstructive pulmonary disease (COPD) is characterised by increased numbers of macrophages, neutrophils and T-cells. Decline in lung function in these patients has been correlated to the number of CD8+ T-cells present in the lung as well as to a decline in the ratio of CD4+/CD8+ T-cells. Although systemic components are likely to be present, circulating lymphocyte populations in COPD patients have not been well characterised. This study aimed at correlating lung function to expression of five different T-cell activation markers on peripheral blood CD4+ and CD8+ T-cells in COPD patients and matched smokers. Furthermore, proportions of lymphocyte populations and degree of systemic T-cell activation in COPD patients were compared to that in smokers and never-smokers. Peripheral blood lymphocytes from six never-smokers, eight smokers and 17 smokers with COPD were analysed using flowcytometry. The number of lymphocytes per millilitre was higher in smokers than in never-smokers. No differences were found between the three groups in regard to proportions of lymphocyte populations, but the number of CD4+ T-cells in smokers was higher than in both never-smokers and COPD patients. The degree of T-cell activation was similar in all patient groups; however, a clear correlation between CD69 expression on CD4+ T-cells and lung function (FEV(1)% of predicted) was found when examining current smokers, with or without COPD. Elevated numbers of CD69+ CD4+ T-cells in blood thus seem to be protective against airway obstruction in smokers while still exposed to cigarette smoke, the main inducer of COPD.     

桂北地区HIV-1感染者HIV-1病毒亚型分布观察

目的观察桂北地区HIV感染者HIV-1病毒亚型分布。方法采集桂北地区80例HIV-1感染者的静脉血,提取其中单个核细胞的DNA,用巢氏PCR扩增病毒膜蛋白env基因的C2-V3区,对PCR纯化产物进行测序,并应用GCG软件等对序列进行分析。结果通过PCR扩增得到env基因序列55份,分属4个亚型,分别为B型1份,CRF07-BC型19份,CRF08-BC型23份,CRF01-AE型8份,C型4份。感染途径为静脉吸毒者16例,性34例,非法献血2例,不详3例。16例吸毒感染者中CRF08-BC型12例,CRF07-BC型4例。34例性行为感染者中CRF07-BC型19例,CRF08-BC型11例,CRF01-AE型4例。结论桂北地区HIV感染者存在HIV-1亚型多样。静脉吸毒感染者以CRF08-BC型为主。性行为感染者以CRF07-BC型和CRF08-BC型为主。     

中国大陆人散发性先天性巨结肠症患者内皮素受体B基因的研究

目的 探讨中国大陆人散发性先天性巨结肠症（sHD）易患基因内皮素受体B（EDNRB）的突变与多态性特征。方法 以92例sHD及其中32例患儿双亲为研究对象，并以60例正常儿为对照。提取受检者外周静脉血DNA，采用聚合酶链反应-单链构象多态性技术（PCR-SSCP）对EDNRB基因外显子-2（exon-2）进行分析，并通过DNA测序检测阳性标本的核苷酸改变方式，与文献报道的其他种族sHD同一基因特征做比较。结果 全部标本EDNRB基因exon-2均未发现突变与多态性位点的存在。结论 中国大陆人sHD患者EDNRB基因的exon-2不存在突变与多态性位点。     

超氧化物歧化酶基因多态性及其活力与慢性阻塞性肺疾病的易感性研究

目的 探讨锰超氧化物歧化酶(Mn-SOD)及细胞外超氧化物歧化酶(EC-SOD)基因多态性与血浆中SOD活力及COPD易感性的相关性.方法 收集114例COPD患者(COPD组)和80名健康者(对照组)外周血,提取全血细胞DNA,采用基因测序及限制性片段长度多态性分析检测两组Mn-SOD(G5774A)和EC-SOD G(-4466)T基因多态性;提取外周血血浆,检测2组血浆中SOD活力.结果 COPD组Mn-SOD 的GG、AG和AA基因型频率分别为27.2%(31/114)、53.5%(61/114)和19.3%(22/114),与对照组[46.3%(37/80)、37.5%(30/80)和16.2%(13/80)]比较,差异有统计学意义(χ2=7.681,P<0.05);COPD组A等位基因频率(46.1%,105/228)显著高于对照组(35.0%,56/160),Mn-SOD 5774A等位基因是COPD的易感基因(OR=1.585,95%CI为1.045～2.404,P<0.05);AG和AA基因型与极重度COPD有相关性(χ2=12.345,P<0.01).COPD组EC-SOD的GG、GT和TT基因型频率分别为76.3%(87/114)、22.8%(26/114)和0.9%(1/114),G、T等位基因频率分别为87.7%(200/228)和12.3%(28/228);对照组GG、GT基因型频率分别为71.3%(57/80)和28.7%(23/80),G、T等位基因频率分别为85.6%(137/160)和14.4%(23/160),未检测到TT基因型,2组间基因型及等位基因频率分布比较,差异均无统计学意义(χ2值分别为0.631和0.361,均P>0.05).COPD组SOD活力[(84±17) kU/L]明显低于对照组[(109±15) kU/L].结论 Mn-SOD(G5774A)位点基因多态性可能与COPD的易感性相关,Mn-SOD的5774A等位基因可能是COPD的易感基因,AG和AA基因型与极重度COPD有相关性;COPD患者存在SOD活力下降,提示COPD患者存在氧化/抗氧化失衡.

Abstract：

Objective To explore the association of genetic polymorphism of superoxide dismutase (SOD) and superoxide dismutase activity in chronic obstructive pulmonary disease. Methods A total of 114 patients with COPD (the COPD group) and 80 healthy volunteers (the control group) were enrolled in this study. Peripheral blood was taken and whole blood cell genomic DNA was extracted. The genetic polymorphisms of Mn-SOD (G5774A) and EC-SOD G (-4466)T genes were determined by DNA sequencing and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Peripheral blood plasma was collected and the functional activity of SOD was determined by a SOD kit. Results The distribution of the Mn-SOD genotype frequencies (GG, AG, AA) between the patients [27.2% (31/114), 53.5% (61/114) and 19.3% (22/114)] and the controls [46.3% (37/80), 37.5% (30/80) and 16.2% (13/80)] were significantly different (χ2=7.681, P<0.05). The A allele gene frequencies of the patients (46.1%, 105/228) were significant higher than those of the controls (35.0%, 56/160), and subjects with the A allele gene of Mn-SOD were more likely to have COPD [OR=1.585, 95%CI (1.045-2.404), P<0.05]. The AA and AG genotypes of Mn-SOD were correlated with the most severe COPD (χ2=12.345, P<0.01). The distribution of the EC-SOD genotype frequencies (GG, GT, TT) was 76.3%(87/114), 22.8%(26/114), 0.9% (1/114) in the patients and 71.3% (57/80), 28.7% (23/80), 0% (0/80) in the controls. The allele gene frequencies of the EC-SOD (G, T) were 87.7% (200/228), 12.3% (28/228) in the patients and 85.6% (137/160), 14.4% (23/160) in the controls. There were no significant differences in the distribution of the different genotypes or allele gene frequencies between the patients and the controls in the EC-SOD genes (χ2=0.631, P>0.05; χ2=0.36, P>0.05). The SOD activity of COPD patients [(84±17) kU/L] was significant lower than that of the healthy controls [(109±15) kU/L]. Conclusions Mn-SOD(G5774A) genetic polymorphism is related to the development of COPD. The Mn-SOD 5774A allele gene may be one of the predisposing genes for COPD. The AA and AG genotypes of Mn-SOD were correlated with the most severy COPD. The decrease of blood plasma SOD activity in COPD patients indicates a dysfunction of the oxidant/antioxidant defense system in the disease.     

Highly sensitive polymerase chain reaction methods show the frequent survival of residual recipient multipotent progenitors after non-T-cell- depleted bone marrow transplantation

Twenty-four male patients grafted for various pathologies with the marrow of a female donor and presenting a complete donor-type hematopoiesis when analyzed by polymerase chain reaction (PCR) amplification of minisatellite sequences 33.6.3 and MS51 (0.1% to 1% sensitivity) were studied by the highly sensitive technique of PCR amplification of the Y-chromosome-specific DYZ1 sequence (0.01% sensitivity). Residual recipient male cells were detected in all peripheral blood samples collected within 1 year posttransplantation. These residual cells were present in both the lymphocyte and polymorphonuclear cell fractions when such a separation was performed by Ficoll gradient centrifugation and, for samples of 13 of 15 patients, at comparable levels in both fractions. In 3 samples collected from 3 patients 4 months or more posttransplantation, residual recipient cells were detected in the polymorphonuclear cell fraction but were present at a lower level or were undetectable in the lymphocyte fraction. These cells are of hematopoietic origin because they were detected at equivalent levels in whole blood and in B and T lymphocytes sorted with antibody-coated magnetic beads. They were not detected in samples collected more than 15 months posttransplantation for 6 of 7 patients. The persistence of residual recipient cells within 1 year posttransplantation is not restricted to male patients receiving a transplant from a female donor because they were also detected in 2 female patients using an allele-specific amplification method for the thyroid peroxydase gene that also has a high sensitivity (0.01%). Our results indicate that at least residual recipient myeloid progenitors and possibly totipotent hematopoietic stem cells may survive intensive pretransplant conditioning regimen and support a transient residual hematopoiesis of the host posttransplantation.     

Circulating adhesion molecules in patients with chronic obstructive pulmonary disease

The place of adhesion molecules that have a role in the immigration of intravascular leukocytes to the tissue with inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD) is controversial. Our purpose in this study was to examine the levels of soluble intracellular adhesion molecule-1 (sICAM-1) and Mac-1 (CD11b/CD18), lymphocyte function associated antigen-1 (LFA-1) in both neutrophils and lymphocytes in stable patients with COPD and in the healthy control groups consisting of non-smokers, and in smokers without COPD and also to evaluate the relationship between the parameters related to the severity of the disease. Peripheral venous blood samples of all the individuals were collected, and levels of sICAM-1 was measured quantitatively with ELISA method. Flow cytometry was used for Mac-1 and LFA-1 levels. Twenty-four stable patients with COPD (group I), 13 smokers (group II) and 14 healthy non-smokers (group III) were included in this study. In the COPD group, 12 smokers patients were considered as group IA, and 12 patients with non-smokers and biomass exposure were considered as group IB. No statistically significant differences were seen in LFA-1 examined in peripheric blood (PB) neutrophils and lymphocytes and sICAM in groups I, II, and III. Mac-1 examined in PB neutrophils was found to be significantly lower in group I when compared to groups II and III, however no difference could be seen in smokers' group of II and the control group III. Mac-1 examined in PB lymphocytes were found to be higher in group I according to group II, however no statistically significant difference was seen between group I and control group. No statistically significant differences were seen in all adhesion molecules levels in group IA and group IB. As a result; it was found that Mac-1 levels in PB neutrophils were decreased with the developing of COPD and Mac-1 levels in PB lymphocytes were decreased in smokers, however increased following the development of COPD. No differences existed in sICAM and LFA-1 levels dependent on smoking and/or COPD.