卵巢恶性肿瘤患者红细胞CR1密度相关基因多态性与NK细胞活性相关性研究

对 5 1例卵巢癌、 43例良性肿瘤和 40例正常妇女采用PCR PFLP方法测定红细胞CR1(ECR1)密度相关基因多态性 ,采用K5 6 2细胞毒试验测定NK细胞活性。发现卵巢癌患者NK细胞活性明显低于正常人和良性卵巢肿瘤患者 (P <0 0 1)。ECR1密度相关基因多态性高表达型 (HH )的NK细胞活性明显高于ECR1中表达型 (HL )的NK细胞活性 ,而ECR1密度相关基因组HL型的NK细胞活性明显高于ECR1低表达型 (LL )的NK细胞活性。这些结果表明红细胞增强NK细胞活性与红细胞CR1密度相关基因组多态性型别密切相关     

卵巢癌患者红细胞CR1密度相关基因组多态性与血细胞天然免疫活性相关性研究

目的　对卵巢癌患者血细胞天然免疫活性与红细胞CR1密度相关基因组多态性的相关性进行对比研究。方法　对 5 1例卵巢癌、4 3例良性肿瘤患者和 4 0例正常妇女采用PCR RFLP方法测定红细胞CR1(ECR1)密度相关基因多态性 ,采用红细胞或淋巴细胞免疫粘附肿瘤细胞的方法对血细胞天然免疫活性进行了测定。结果　发现卵巢癌患者红细胞和淋巴细胞CR1天然免疫活性明显低于良性卵巢肿瘤患者和正常人。红细胞CR1密度相关基因高表达 (HH)型组的血细胞天然免疫活性明显高于中表达 (HL)型 ,而HL型明显高于低表达 (LL)型。加红细胞组淋巴细胞CR1天然免疫活性明显高于不加红细胞组 (P <0 .0 1)。结论　红细胞增强淋巴细胞CR1天然免疫活性与红细胞CR1密度相关基因型密切相关。     

Ⅱ型糖尿病患者红细胞天然免疫功能变化与CR1密度基因多态性的相关分析

目的　研究Ⅱ型糖尿病 (ⅡDM)患者的红细胞CR1密度基因多态性及红细胞免疫粘附功能 ,探讨ⅡDM患者红细胞免疫粘附功能低下的原因。方法　分ⅡDM组和健康对照组 ,用PCR RELP方法测红细胞CR1密度基因多态性 ,红细胞天然免疫粘附活性用红细胞C3b受体花环率(EC3bRR)及免疫复合物花环率 (ECICR)测定。结果　 (1)ECR1基因构成 ,ⅡDM组HH型为 5 7.14 %、HL型 37.5 0 %、LL型 5 .36 % ;对照组HH型为 6 8.86 %、HL型 2 8.5 7%、LL型 3.5 7% ;ⅡDM组的基因缺陷率为 4 2 .86 % ,对照组为 32 .14 %。两组相比基因构成及缺陷率差异均无显著性 (P >0 .0 5 )。 (2 )与对照组相比 ,ⅡDM组EC3bRR下降 ,ECICR上升 (P <0 .0 1)。 (3)两组组内比较 ,HH型的EC3bRR均明显高于HL型 ,ECICR均低于HL型。结论　ⅡDM患者红细胞CR1密度基因HH型比率下降不显著 ,但红细胞天然免疫功能低下程度与ECR1基因缺陷关系密切相关。不同ECR1基因型的人群红细胞免疫功能有差异 ,HH型的红细胞免疫粘附功能强于HL型。     

肿瘤患者红细胞CR1分子数量及基因多态性的变化

我们建立的红细胞ＣＲ1分子酶联定量测定法 ,具有良好的灵敏性和重复性[1] ,用此种方法测定自身免疫疾病 ,与国外报道的结果完全相同[2 ] 。最近对良、恶性肿瘤患者红细胞ＣＲ1分子的数量表达Ａ4 0 5值进行测定发现 ,恶性肿瘤患者红细胞ＣＲ1分子数量表达较良性肿瘤患者和正常人群都明显下降 ,并且是后天获得性。此点国外尚无报道。本文对良、恶性肿瘤患者红细胞ＣＲ1分子的数量及其基因多态性表达变化进行了研究 ,报告如下。1　材料与方法1.1　病例来源及血标本　 10 2例肝癌患者系第二军医大学附属东方肝胆医院住院确诊病人 ;大肠癌2 6例…     

原发性肝癌患者红细胞免疫粘附肿瘤细胞能力与红细 …

目的 研究原发性肝癌患者红细胞免疫粘附肿瘤细胞能力与红细胞ＣＲ１基因组密度多态性及活性的相关性。方法 采用ＰＣＲ和ＨｉｎｄⅢ酶切技术测定红细胞ＣＲ１基因组密度多态性变化，同时用ＥＬＩＳＡ和肿瘤红细胞花环试验测定红细胞ＣＲ１活性，并进行比较。结果 原发性肝癌患者红细胞ＣＲ１基因型点突变比率（４３．６％）明显上升，与正常人（２０％）相比，差异有显著性（Ｐ〈０．０５）；原发性肝癌患者３种ＣＲ１基因型的红     

肝硬化患者红细胞CR1粘附活性与肝功能损伤的关系

目的:研究肝硬化患者红细胞CR1粘附活性的变化,探讨其与肝功能损伤程度的相关性。方法:采用红细胞天然免疫功能试验对54例肝硬化患者进行了红细胞CR1粘附活性测定,并与30名正常健康人作比较。结果:肝硬化患者红细胞CR1粘附活性显著地低于正常人组(P<0.01)红细胞CR1粘附活性的变化与ALT密切相关。结论:肝硬化患者红细胞CR1粘附活性与肝功能损伤程度密切相关,对判断病情的严重程度、病情的发展具有重要的临床价值。     

肿瘤患者红细胞CR1基因组密度多态性的变化

目的研究恶性肿瘤患者红细胞ＣＲ１基因组密度多态性变化规律。方法采用ＰＣＲ和ＨｉｎｄⅢ酶切技术对恶性肿瘤红细胞ＣＲ１基因组密度多态性变化进行研究。结果１６４例恶性肿瘤患者红细胞ＣＲ１基因突变率４１．５％，明显高于１８９例正常人群（２１％），特别是年轻恶性肿瘤患者红细胞ＣＲ１基因点突变率可达６６．７％（２１例中），明显高于年轻正常人群（１９．８％，９６例）。在恶性肿瘤患者中红细胞ＣＲ１基因ＨＨ型的红细胞ＣＲ１活性高于红细胞ＣＲ１基因ＬＬ型患者，但低于正常人红细胞ＣＲ１活性。结论这些结果表明，红细胞ＣＲ１基因点突变率升高与免疫发病机理有相关性。     

原发性肝癌患者红细胞免疫粘附肿瘤细胞能力与红细胞CR1基因型及活性相关性分析

目的　研究原发性肝癌患者红细胞免疫粘附肿瘤细胞能力与红细胞ＣＲ１ 基因组密度多态性及活性的相关性。方法　采用ＰＣＲ 和Ｈｉｎｄ Ⅲ酶切技术测定红细胞ＣＲ１ 基因组密度多态性变化,同时用ＥＬＩＳＡ 和肿瘤红细胞花环试验测定红细胞ＣＲ１ 活性,并进行比较。结果　原发性肝癌患者红细胞ＣＲ１ 基因型点突变比率（４３－６ ％ ） 明显上升,与正常人（２０ ％ ） 相比,差异有显著性（ Ｐ＜０－０５） ;原发性肝癌患者３ 种ＣＲ１ 基因型的红细胞ＣＲ１ 活性都明显低于正常人（ Ｐ＜ ０－０１ 或 Ｐ＜０－０５） 。活性变化也不同。结论　原发性肝癌患者红细胞ＣＲ１ 活性及免疫粘附肿瘤细胞能力下降可分为三种不同类型,即原发型、获得型和混合型。     

癌症患者红细胞CR_1基因多态性研究

为了探讨女性癌症患者红细胞补体受体Ⅰ型(ECR_1)密度相关基因多态性的变化,采用血细胞DNA PCR和HindⅢ酶切技术对44例癌症女性患者红细胞CR_1密度相关基因多态性分布进行了测定,发现癌症女性患者红细胞CR_1密度相关基因点突变率高达54.5％,尤其是40岁以下的女性癌症患者红细胞CR_1密度相关基因点突变率(72.73％)比40岁以下女性正常人(20.80％)明显增高。表明年轻女性癌症患者癌变易感性与红细胞CR_1密度相关基因缺陷有一定的关系。     

肿瘤患者红细胞CD44s与CD58分子的定量测定及意义

目的建立定量测定红细胞CD44s和CD58分子的实验方法,研究其数量变化与肿瘤转移的关系。方法将戊二醛固定的1.2×106红细胞定量“液相包被”于V型板中,依次加入抗CD44s和CD58分子单克隆抗体、碱性磷酸酶标记的第二抗体及可溶性底物,移显色液于比色孔,在405nm比色,计算其A405吸光度值。结果本方法具有良好的敏感性和重复性。非转移性肿瘤患者红细胞CD44s和CD58分子数量表达低于正常人群,但无统计学差异。而转移性卵巢癌和肝癌患者的红细胞CD44s和CD58分子数量明显低于无转移肿瘤患者和正常人群（P＜0.001）。CD44s数量变化与肿瘤患者血清透明质酸(HA)含量变化密切相关。红细胞CD58分子表达变化对红细胞调节淋巴细胞免疫粘附能力有明显影响。结论红细胞CD44s分子数量表达变化与肿瘤转移密切相关;红细胞CD58分子参与机体整体免疫调节。     

肝病患者血浆凝血因子检测的临床研究

血 浆中凝血因子 ,除组织因子 (ＴＦ)、Ⅳ因子(Ｃａ2 +)、Ⅵ因子 (激活的Ⅴ因子 )、因子Ⅷ和因子Ⅷａ链以外的其它凝血因子 ,都是在肝脏中合成。肝病患者常伴有各种凝血因子的异常 ,临床上一般进行凝血酶原时间 (ＰＴ)、活化部分凝血活酶时间 (ＡＰＴＴ)、纤维蛋白原 (Ｆｉｂ)等常规测定 ,而各种凝血因子水平的检测并不多见。本文对 10 8例肝病患者进行ＰＴ、ＡＰＴＴ、Ｆｉｂ检测的同时 ,还进行了凝血因子Ⅱ、Ⅴ、Ⅶ、Ⅷ、Ⅸ、Ⅹ活性测定和分析。1　资料和方法1.1　研究对象正常对照组 ,30名健康人 ,男女各 15人 ,年龄18～ 5 5岁 ,平均 37.…     

白血病患者红细胞CR_1活性及其免疫调节因子测定的临床应用研究

本文采用多种指标检测４２例白血病患者的红细胞、白细胞免疫功能，并与正常人作了比较。肿瘤细胞花环法测定白血病患者红细胞ＣＲ１活性结果比正常人明显降低（Ｐ＜０．０１）；红细胞ＣＲ１活性抑制因子升高、促进因子降低与正常人相比均有显著差别（Ｐ＜０．０１），ＣＩＣ比正常人明显升高（Ｐ＜０．０１）；ＣＤ４、ＣＤ８也比正常人明显降低（Ｐ＜０．０１，Ｐ＜０．０５）。提示：白血病患者红细胞和白细胞免疫功能均发生异常变化。此外，对急性白血病患者部分病例治疗前后的红细胞ＣＲ１活性及其免疫调节因子的变化进行了追踪检测以探讨其临床意义。     

Low expression of erythrocyte complement receptor type 1 in chronic hepatitis C patients

Primate erythrocyte complement receptor type 1 (CR1) plays an essential role in complement-associated immune complex clearance by transporting complexes to macrophages in the liver and/or spleen. Antibody-bound hepatitis C virus, which consists of immune complexes, is observed in patients with chronic hepatitis C. The aim of this study was to clarify the pathophysiological roles of erythrocyte CR1 in hepatitis C virus-infected individuals. We quantified the expression of erythrocyte CR1 with a fluorescence-activated cell sorter system in 57 chronic hepatitis C and 37 chronic hepatitis B cases and 20 normal volunteers. Complement-bound immune complexes were quantified by means of an enzyme-linked immunosorbent assay using anti-C1q and anti-C3d antibodies. Hepatitis C virus-infected patients showed lower erythrocyte CR1 and higher C3d immune complex levels than volunteers (P < 0.01 and P < 0.05, respectively). An inverse correlation was observed between the erythrocyte CR1 and C3d immune complex levels in hepatitis C virus infection (r = - 0.300, P = 0.032). The erythrocyte CR1 levels in hepatitis C virus infection were lower in patients with severe liver inflammation, cirrhosis, or hepato-cellular carcinoma than in those with mild inflammation, whereas the levels did not differ regardless of the disease stage in hepatitis B virus infection. These findings demonstrate that the expression of erythrocyte CR1 is related to immune complex quantity and the severity of liver disease in hepatitis C virus infection. © 1996 Wiley-Liss, Inc.     

乙型肝炎病毒对载脂蛋白B表达的影响及其机制探讨

目的 探讨乙型肝炎病毒(HBV)对载脂蛋白B(ApoB)表达的影响,并探讨其调节机制.方法 采用RT-PCR和Western blot法检测HepG2和HepG2.2.15中ApoB mRNA和蛋白的表达,全自动生化分析仪Olympus 5400检测HBV患者和健康对照者ApoB血清学水平,分析健康对照者、慢性乙型肝炎、肝纤维化和肝癌患者中ApoB表达水平的差异,将HBV感染性克隆pHBV1.3转染HepG2细胞,RT-PCR和Western blot法检测ApoB和微粒体甘油三酯转移蛋白(MTP)表达水平的变化.结果 HepG2.2.15细胞中ApoB mRNA和蛋白的表达水平较HepG2低;ApoB在慢性乙型肝炎患者和肝纤维化患者的血清学水平明显低于健康对照者(P＜0.05);HBV能够在mRNA和蛋白水平抑制ApoB和MTP的表达.结论 HBV可能通过抑制MTP的表达抑制ApoB的合成和分泌.

Abstract：

Objective To explore the effect of hepatitis B virus(HBV) on the expression of apolipoprotein B(ApoB) and its regulatory mechanism. Methods mRNA and protein expression of ApoB in HepG2 and HepG2.2.15 cells was measured by RT-PCR and Western blot, serum ApoB levels in patients with HBV infection and in healthy individuals were measured by biochemical analyzer Olympus 5400, the expression of ApoB difference among healthy individuals, patients with chronic hepatitis B, liver cirrhosis, and hepatocellular carcinoma were analyzed, HBV infectious clone pHBV1.3 was tranfected into HepG2 cells,and expression of ApoB and microsomal triglyceride transfer protein(MTP) was measured by RT-PCR and Western blot. Results Expression of ApoB mRNA and protein was lower in HepG2.2.15 cells than in HepG2 cells, serum apoB levels was much lower in patients with chronic hepatitis B and liver cirrhosis as compared to healthy individuals( P ＜0.05 ), HBV could inhibit the expression of ApoB and MTP at mRNA and protein levels. Conclusion HBV may downregulate the synthesis and secretion of ApoB via inhibits the expression of MTP.     

Effect of plasmapheresis on ligand binding capacity and expression of erythrocyte complement receptor type 1 (CR1) of patients with systemic lupus erythematosus (SLE)

The functional activity and the expression of CR1 on the erythrocytes (E) of patients with SLE were, respectively, determined by measuring the binding to E of either complement-opsonized bovine serum albumin (BSA)-anti-BSA immune complexes (ICC) or specific anti-ECR1 MoAbs. We found that both the functional activity and levels of ECR1 in SLE patients homozygous for ECR1 high density allele were significantly lowered compared with healthy controls having the same allele. Soon after plasmapheresis there was a significant increase in E ICC binding activity, and this increased functional activity was stable. Moreover, plasmapheresis reduced the level of immune complexes demonstrable in the circulation of the patients. The expression of ECR1 determined with several different anti-CR1 MoAbs was also elevated as a consequence of plasmapheresis. This elevation was observed for both MoAb 1B4, which competes for the ICC binding site of ECR1, and for MoAb HB8592, which does not, but the time course for the increase in binding of the two MoAbs was different, in that the epitope recognized by MoAb 1B4 increased more rapidly. The present results, considered in the context of previous findings, suggest that more than one mechanism may be operative with respect to the effects of the plasmapheresis in increasing ECR1 levels defined by different epitopes on the molecule.     

Th17和Treg细胞以及其相关细胞因子在慢性丙型肝炎以及丙型肝炎肝硬化病人外周血中的变化及意义

目的：〖HTSS〗研究Th17和Treg细胞以及其相关细胞因子在慢性丙型肝炎以及丙型肝炎肝硬化病人外周血中的变化及意义,以探讨其在慢性丙型肝炎及丙型肝炎肝硬化发病中的作用。 〖HTH〗方法：〖HTSS〗用流式细胞和ELSIA技术检测慢性丙型肝炎及丙型肝炎肝硬化病人外周血Th17和Treg细胞表达率以及IL 6、IL 10、TGF β、IL 17血清学水平,分析上述指标在健康对照组和慢性丙型肝炎组以及肝硬化组之间的差异。 〖HTH〗结果：〖HTSS〗慢性丙型肝炎病人的Th17细胞表达率(133%±030%)以及IL 6［(810±242）ng/L］、IL 17［(1670±473）ng/L］血清水平明显高于健康对照组Th17 细胞表达率(114%±019%)以及IL 6［(670±172）ng/L］、IL 17［(1229±188）ng/L］血清水平,P＜005;丙型肝炎肝硬化组和慢性丙型肝炎组病人外周血的Treg细胞表达率(621%±076%,589%±085%)明显高于健康对照组的Treg细胞表达率（551%±059%）,P<005;丙型肝炎肝硬化组病人Th17/Treg的比值（019±002）明显低于慢性丙型肝炎组（022±003）和健康对照组（021±003）,P<005;丙型肝炎肝硬化组外周血IL 10水平［（1621±376）ng/L］和TGF β水平［（515±083）ng/L］显著高于慢性丙型肝炎组［（1436±278）ng/L;（447±087）ng/L］和健康对照组［（1401±301）ng/L;（443±098）ng/L］,P<005。 〖HTH〗结论：〖HTSS〗Th17和Treg细胞以及其相关细胞因子参与了丙型肝炎慢性化和肝硬化的进程,Th17和Treg细胞以及其相关细胞因子在丙型肝炎慢性化和肝硬化的治疗和预防方面可能具有重要的意义。     

慢性乙型肝炎,肝硬化患者外周血LAK细胞活性和sIL—2R测定的意义

采用＾３Ｈ－ＴｄＲ释放法测定５１例慢性肝病患者（ＣＰＨ１０例、ＣＡＨ２３例、ＬＣ１８例）外周血ＬＡＫ细胞活性，并用酶联法测定患者血清中ｓＩＬ－２Ｒ含量；与２９例正常对照组比较，发现肝病患者ＬＡＫ活性降低，ＨＢＶＤＮＡ阳性组ＬＡＫ活性较阴性组低（Ｐ〈０．０５），ｓＩＬ－２Ｒ增高，且慢性肝病组ＬＡＫ活性与ｓＩＬ－２Ｒ水平呈负相关，说明ＬＡＫ活性与机体免疫功能状态有关，ＨＢＶ的复制和高浓度的ｓＩＬ－２Ｒ     

Expression of vascular adhesion protein-1 in atopic eczema

BACKGROUND: Vascular adhesion protein-1 (VAP-1) is an adhesion molecule with an enzymatic activity which partakes in the migration process of lymphocytes. The aim of this study was to investigate VAP-1 expression in atopic eczema (AE) in comparison with healthy controls and psoriatic individuals. MATERIAL AND METHODS: Forty adult patients suffering from AE aged between 18 and 56 years were included in the study. The control group consisted of 35 healthy volunteers aged between 19 and 49 years and of 71 psoriatic patients aged between 23 and 89 years. The serum concentration of soluble VAP-1 (sVAP-1) was evaluated by ELISA and VAP-1 expression in the skin by immunohistochemistry. RESULTS: Serum level of sVAP-1 in AE patients before treatment was significantly higher compared with healthy volunteers. Similarly, a higher mean number of VAP-1-positive vessels was found in both lesional and nonlesional atopic skin compared with healthy skin. Treatment of AE resulted in a significant reduction in the serum level of sVAP-1. On the other hand, both the serum level of sVAP-1 and the number of dermal vessels with expression of VAP-1 were significantly lower in AE patients compared with psoriatic individuals. CONCLUSION: This study indicates the important role of VAP-1 in the pathogenesis of chronic inflammatory cutaneous disorders, including AE.