实弹射击考核对不同特质焦虑新兵T淋巴细胞亚群及ACTH的影响

目的：研究急性应激对不同特质焦虑新兵的T淋巴细胞亚群及ACTH的影响。方法：状态一特质焦虑问卷（STAI）将新兵分成高、低特质焦虑组各16人。用流式细胞仪及ELISA测定被试基础期（打靶前4d）、应激期（打靶时）、恢复期（打靶后5d）的CD4^＋、CCD8^＋及ACTH浓度。结果：①高特质组3个时期的CD4^＋、CD4^＋／CCD8^＋比值均低于低特质组。CD8＋高于低特质组；高特质组应激期CD4^＋显著下降（P〈0．05）、CD4^＋／CCD8^＋比值与恢复期有显著差异（P〈0．01）．而低特质组仅应激期CD4^＋定量与恢复期有显著差异（P〈0．01）。②实弹射击前、中、后的ACTH浓度，高特质组变化呈极显著差异（P〈0．001），而低特质组应激期与基础期呈显著差异（P〈0．05）。结论：①急性应激影响新兵的CD4^＋、CCD8^＋及其比值，其程度与特质焦虑有关。②应激时高特质组ACTH浓度下降显著大于低特质组，且随应激源消除不易恢复。     

新兵首次实弹射击时心理和生理应激的初步研究

新兵首次实弹射击时心理和生理应激的初步研究＊谭百庆漆兵①刘艳任正洪②北京武警二总队医院应激在神经内分泌研究中早有广泛应用。自７０年代Ｍａｓｏｎ提出心理应激学说［１］，如今已进入到心理生理学的研究领域。在我国，近几年应激的心理学研究有了较大的进展。为了...     

红细胞膜表面分子与红细胞免疫

有关红细胞参与免疫的机能很早就为人们所认识 ,以红细胞膜表面补体受体分子介导的红细胞免疫粘附 (Red Cell Immune AdhesionRCIA)机制是红细胞发挥免疫功能的基本手段。除此以外 ,现代分子生物学研究发现 ,在红细胞膜表面还存在着相当数量的其他免疫相关分子。这些膜表面分子可能同白细胞膜上的免疫分子一样 ,是红细胞发挥包括抗肿瘤免疫在内的多种免疫功能的分子基础。红细胞免疫功能失常与临床上许多种疾病密切相关。了解红细胞膜表面分子情况 ,对于进一步深入开展红细胞免疫研究具有重要意义     

急性军事心理应激障碍的应对与管理

目的探讨有关急性军事心理应激障碍(MASD)的研究进展,重点讨论MASD的应对与管理。方法采用文献回顾法,总结MASD的评估方法、诱发因素及应对措施。结果国内外已发展多个评估MASD的量表,对于诊断MASD具有指导意义;MASD的主要诱因包括战场相关因素、个体认知评价因素、士气和团队凝聚力;MASD的应对措施包括:强化应激耐受训练、加强心理应激障碍管理和实施综合心理减压。结论MASD是军人执行战争或非战争军事任务常面临的心理问题,借鉴已被验证的各种预防措施,有效减少MASD的发生。     

新兵集训应激对肾上腺髓质激素的影响

目的：探讨新兵军事应激条件下肾上腺髓质激素及其代谢产物的变化规律。方法：采用放射免疫分析和微柱法对一个建制连新兵60人训练前后进行血浆肾上腺髓质激素（ADM）及尿液中香草扁桃酸（VMA）的检测,同时与50名老兵进行对照。结果：与老兵组比较,新兵组训练前及训练后血浆ADM及尿液中VMA的水平均显著升高（P〈0.05;P〈0.01;P〈0.05;P〈0.01）,与训练前比较,高强度训练后ADM和VMA水平均明显增高（p〈0.01;P〈0.05）,尤以ADM增高十分显著[训练前（23.72±12.63）pg/ml;训练后（214.97±57.75）pg/ml],其血浆中浓度较训练前增高9倍。结论：①新兵入伍及训练过程中可引起ADM和VMA的应激性增高。②适度的应激反应对人体有利,益于机体快速适应内外环境的变化;而急性强烈或反复的应激反应则是造成应激性损伤的危险因素。     

桂西地区疟疾感染人群红细胞CD59分子表达研究

疟疾曾广泛流行于广西桂西南等中国西南低纬度地区,红细胞不仅为疟原虫提供食物和寄生场所,而且疟疾感染的许多病理特征都跟疟原虫与感染红细胞及其他组织相互作用有关.许多研究显示,疟疾的感染与红细胞免疫功能有关[1],在红细胞膜表面存在着大量的免疫相关分子,它们可能是红细胞发挥抗疟免疫功能的重要分子基础[2],本研究运用流式细胞术测定红细胞表面分子CD59表达,初步探讨了疟疾的感染与红细胞免疫功能关系.     

某部新兵集训期心理弹性与应激水平和情绪体验的关系

目的:对某部新兵集训期心理弹性与应激水平和情绪体验的关系研究。方法:某部新兵集训2个月时,采用成人心理弹性量表(RSA)、军人心理应激自评问卷(PSET)和正负性情绪量表(PANAS)对1600名新兵进行调查。结果:1新兵集训期心理弹性总分为(119.55±21.70);2心理弹性与正性情绪呈显著正相关(r=0.642,P0.01),与负性情绪、心理应激水平呈显著负相关(r=-0.107,-0.329;P0.01);3心理弹性高分组在正性情绪得分上显著高于低分组(P0.01),在负性情绪、心理应激水平得分上显著低于低分组(P0.01);4正性情绪、负性情绪和心理应激水平能有效预测心理弹性,总解释率为43.8%。结论:某部新兵集训期心理弹性与正性情绪、负性情绪、心理应激水平密切相关。提升心理弹性训练,有望降低新训时负性情绪体验和心理应激水平,促进心理健康。     

跳伞应激对空降兵新兵神经内分泌的影响

近年来神经内分泌研究成为预防医学和军事医学的优先发展领域和研究前沿。其研究对提高空降兵部队的心理健康水平和紧急状态下的应对能力 ,最大限度减低非战斗减员的发生率具有重要意义。国外跳伞人员 (非伞兵 )神经内分泌学研究偏重于与应激有关的下丘脑—垂体—肾上腺轴系统 (皮质醇、ＡＣＴＨ等 )及内源性阿片肽的研究[1-6] ,对其它系统及神经肽的变化研究甚少。本研究就空降兵新兵群体在跳伞应激状态下精氨酸血管加压素 (ＡＶＰ)、神经肽Ｙ(ＮＰＹ)、降钙素基因相关肽 (ＣＧＲＰ)、神经降压素 (ＮＴ)、血管活性肠肽 (ＶＩＰ)的变化规律…     

补肾复方冲剂对慢性再生障碍性贫血患者红细胞免疫黏附功能和膜分子CD35、CD58表达的影响

目的 探讨补肾复方冲剂对慢性再生障碍性贫血(以下简称慢性再障,CAA)患者红细胞免疫黏附功能和膜分子CD35、CD58表达的影响。方法 以补肾复方冲剂治疗CAA患者6个月,,检测正常对照组与慢性再障组治疗前后红细胞C_(3b)受体花环率(RBC-C_(3b)RR)、红细胞免疫复合物花环率(RBC-ICR)、红细胞膜CD35、CD58分子定量。结果 慢性再障组治疗前RBC-C_(3b)RR、膜CD58分子定量均明显低于正常对照组(P<0.01),RBC-ICR、膜CD35分子定量与正常对照组相比,差异无显著性(P>0.05);治疗后RBC-C_(3B)RR、膜CD58分子定量明显升高,与治疗前比较有显著性差异(P<0.05或P<0.01)。结论 补肾复方冲剂能提高CAA患者红细胞免疫黏附功能和膜分子CD58表达水平。     

小组心理干预对新兵心理健康水平的影响

目的：探讨小组心理干预对新兵心理健康水平的影响。方法：采用症状自评量表（SCL－90）和特质应对方式问卷（TCSQ）对512名新兵进行心理测试，将检测出的64名有心理问题的分为两组，A组（31人）为小组心理干预，B组（33人）为对照组。在集体讲授心理卫生课的基础上，对A组采取小组心理干预。结果：经过4周小组心理干预后，A组有效率为61．29％，B组有效率为33．33％，两组比较有显著性差异（P＜0．01）。SCL－90结果：干预后A组中除恐怖因子分没有变化外，其它各项因子得分明显下降（P＜0．01）。A组的SCL－90总分、阳性项目数、躯体化、强迫、人际关系、忧郁、精神病性因子分与B组相比较有明显低（P＜0．05－0．01）。TCSQ结果：A组中的消极应对得分明显降低（P＜0．01），而B组消极应对得分没有变化。结论：小组心理干预在短期内不仅能有效改善新兵的躯体化、强迫、抑郁、人际关系敏感等常见心理问题，还能促进成功应对方式的形成，掌握自我调节方法，对提高新兵的心身健康水平及我军整体素质提高大有裨益，可推广试用。     

CD59锚定蛋白对CD55介导的T细胞信号转导的增强效应

目的:研究糖基磷脂酰肌醇(GPI)锚定蛋白CD59对CD55介导T细胞信号转导的增强效应。方法:实验分为未转染的Jurkat细胞组(Ⅰ组)、转染空质粒的Jurkat细胞组(Ⅱ组)及转染CD59干扰质粒的Jurkat细胞组(Ⅲ组)。用RT-PCR检测3组细胞中的CD59基因表达水平。用噻唑蓝(MTT)比色法、免疫印迹技术和激光共聚焦扫描显微镜分别检测CD55与CD59联合作用对3组Jurkat细胞的增殖效应,Src家族酪氨酸激酶(SrcPTK)磷酸化的水平及细胞内钙离子的变化。结果:稳定转染后,Ⅲ组细胞CD59分子的表达被成功抑制。Ⅰ组和Ⅱ组细胞CD55与CD59联合作用后增殖能力,SrcPTK磷酸化水平及钙离子浓度均明显高于Ⅲ组(P<0.05);但Ⅰ组和Ⅱ组之间无差异。结论:CD59可增强CD55对T细胞信号转导的效应。     

Levels of expression of complement regulatory proteins CD46, CD55 and CD59 on resting and activated human peripheral blood leucocytes

The cell surface complement regulatory (CReg) proteins CD46, CD55 and CD59 are widely expressed on human lymphoid and non-lymphoid cells. This study aimed to compare systematically levels of CReg expression by different leucocyte subsets and to determine whether levels were increased following activation in vitro. Levels of each CReg protein were similar on freshly isolated monocytes and all major lymphocyte subsets, except that CD4(+) cells expressed significantly less CD46 than CD8(+) cells (P < 0.05) while the reverse was observed for CD55 (P < 0.02). CD56(+) cells, predominantly natural killer cells, expressed significantly lower levels of CD59 than T cells (P < 0.02). CD45RO(+) cells had higher levels of surface CD46 and CD59, but lower levels of CD55, than CD45RO(-) cells (P < 0.02); CD25(+) cells also expressed significantly less CD55 than CD25(-) cells (P < 0.002). Neutrophils expressed higher levels of CD59, but lower levels of CD55, than monocytes. Following activation with phytohaemagglutinin, CD46 was up-regulated on all leucocyte subsets with the exception of CD56(+) cells. Both CD55 and CD59 were also markedly up-regulated on monocytes, and CD55 expression was greater on CD8(+) than CD4(+) cells following activation (P < 0.02). Lipopolysaccharide treatment did not significantly alter B-cell expression of CReg proteins whereas CD55 and CD59, but not CD46, were significantly up-regulated on monocytes (P < 0.02). These observations that CReg proteins are up-regulated on certain activated leucocyte subsets indicate that levels would be increased following immune responses in vivo. This could enhance both protection against local complement activation at inflammatory sites and also the immunoregulatory properties of these leucocytes.     

CD55、CD59、CD34对AA-PNH早期诊断研究应用

目的：探讨CD55、CD59、CD34抗原在再障．阵发性血红蛋白尿综合征(AA-PNH)的早期诊断中的价值，寻找AA-PNH早期诊断敏感指标，进而达到早期发现、早期诊断、早期治疗的目的。方法：应用流式细胞仪测定AA-PNH综合征患者的CD55、CD59、CD34抗原变化关系，并与PNH、AA等疾病组以及正常对照组CD55、CD59、CD34抗原相互变化关系，经过统计学处理，找出相关性。结果：结果表明AA—PNH、PNH CD55、CD59、CD34抗原较AA及其他疾病组及正常对照组明显减低，并与溶血试验中溶血程度呈正相关，且早于其他溶血指标。结论：CD55、CD59、CD34抗原表达率可作为PNH、AA-PNH综合征早期诊断最敏感指标，并与预后转归密切相关。     

可溶性嵌合补体抑制分子的构建及表达

目的：制备能抑制补体活化的2个关键环节（C3/C5转化酶和MAC的形成）的一种新型、高效补体抑制剂。方法：先设计引物，然后通过PCR技术扩增重组可溶性CD46/CD55/CD59嵌合分子cDNA片段，重组于pSecTagA真核表达载体上，分别利用COS-7细胞和中国仓鼠卵巢（Chinese hamster ovary，CHO）细胞进行表达，并用抗人CD46多克隆抗体及抗人CD55、CD59单克隆抗体对表达产物进行western bolting鉴定。结果：DNA测序证实，前端带有小鼠IgGκ链前导序列，后端融合有编码6个组氨酸碱基的CD46/CD55/CD59嵌合分子cDNA片段的阅读框完整。免疫印迹结果显示，表达的重组蛋白分别能与抗人CD46多克隆抗体和抗人CD55、CD59单克隆抗体结合。结论：成功构建并在真核细胞内表达了重组可溶性CD46/CD55/CD59嵌合分子，为进一步研制和开发新一代多功能、多靶点补体抑制剂奠定了基础。     

Antigen-presenting cell exosomes are protected from complement-mediated lysis by expression of CD55 and CD59

Exosomes are secreted nanometer-sized vesicles derived from antigen-presenting cells, which have attracted recent interest as they likely play important roles in immune regulation, and their use as cell-free tools for immunotherapy has been proposed. Liposomes used clinically as transport vehicles can activate the complement system, leading to their rapid degradation and significant inflammatory toxicity. The use of isolated exosomes in therapy, therefore, may also elicit complement activation, reducing their potential efficacy. We have examined the expression and functional roles of the membrane regulators of complement (CD46, CD55 and CD59) on antigen-presenting cell-derived exosomes. Exosomes express the glycosylphosphatidylinositol (GPI)-anchored regulators CD55 and CD59, but not the transmembrane protein CD46. Antibody blocking of CD55 in the presence of sensitizing antibody (w6/32) and human serum resulted in increased C3b deposition and significantly increased exosome lysis. Blockade of CD59 also resulted in significant lysis, while blocking both CD55 and CD59 increased lysis still further. We conclude that exosomes express GPI-anchored complement regulators in order to permit their survival in the extracellular environment.     

The complement regulatory proteins CD55 (decay accelerating factor) and CD59 are expressed on the inner acrosomal membrane of human spermatozoa as well as CD46 (membrane cofactor protein)

The complement regulatory proteins CD55 and CD59 are expressed on the plasma membrane of human spermatozoa, whereas CD46 is only on the inner acrosomal membrane (IAM) which becomes surfaced exposed after the acrosome reaction when sperm assume fertilisation-competence. CD55 & CD59, two glycosylphosphatidylinositol (GPI)-anchored proteins, have been detected previously in some studies also in the acrosomal region of chemically fixed spermatozoa but never demonstrated at this site on unfixed spermatozoa. Dual labelling immunofluorescence and confocal microscopy on fresh unfixed spermatozoa, with minimal subsequent time to fixation, has shown CD55 to be markedly expressed on the IAM, more than on the plasma membrane. However, unlike for CD46, CD55 displayed patchy staining over the acrosome, with some variation between individual spermatozoa. All IAM-associated CD55 was localised within GM1-containing lipid rafts. CD59 was expressed also on the IAM, but in a pronounced granular pattern with more variation observed from one spermatozoa to another. Both CD55 & CD59 were released from the IAM by PI-PLC, demonstrating them to be GPI-anchored. Analysis of acrosome-reacted spermatozoal CD55 by Western blotting revealed a novel single 55 kDa protein lacking significant oligosaccharides susceptible to glycosidases. Antibody-induced membrane rafting and release of CD55 & CD59 in vitro may have influenced previous results. Significant coexpression of CD55 & CD46 on the IAM suggests some functional cooperation at this site.     

Use of complement regulators,CD35, CD46, CD55, and CD59, on leukocytes as markers for diagnosis of viral and bacterial infections

Several complement regulatory proteins exist on self-cells to prevent damage by the serum complement system. In the present study, we aimed to perform quantitative analysis of membrane-bound complement regulators, CR1 (CD35), MCP (CD46), DAF (CD55), and MIRL (CD59), on peripheral blood neutrophils, monocytes, and lymphocytes from healthy controls (n = 36) and febrile patients diagnosed with either bacterial (n = 21) or viral (n = 26) infections. Our results show that: (a) increased CD35 and CD55 levels on neutrophils and monocytes present potent markers of bacterial infection, (b) increased expression of CD46 on monocytes is an indicator of viral infection, and (c) increased CD59 expression on neutrophils and monocytes is a general infection marker. Additionally, CD19-positive B-lymphocytes represent practically the only lymphocyte population capable of expressing CD35. We further developed two novel clinical flow cytometric markers (indices), specifically, clinical mononucleosis (CM)-INDEX (incorporating CD35, CD55, and CD59 expression on lymphocytes) and clinical bacterial infection (CBI)-INDEX (incorporating CD35 and CD55 expression on neutrophils and lymphocytes), for the effective detection of viral mononucleosis and bacterial infection, respectively. In summary, bacterial and viral infections induce different expression patterns of membrane-bound complement regulators in human leukocytes, which may be effectively exploited in clinical differential diagnosis.