COPD病人免疫变化与呼吸机相关肺炎的关系及预防

[目的]研究长期机械通气慢性阻塞性肺部疾病(COPD)病人T细胞亚群、补体及免疫球蛋白的变化规律.[方法]选择2004年3月-2005年2月我院老年病房收治的42例长期机械通气COPD病人为试验组,同时选择34例COPD稳定期的老年病人作为对照组.入选病人均进行免疫球蛋白IgA、IgG、IgM,补体C3、补体C4及CD4、CD8的测定,并计算出CD4/CD8比值.[结果]试验组与对照组比较,IgA、IgG、IgM均增高,补体C3、C4均降低,CD4降低、CD8升高,CD4/CD8降低.经统计学处理,除补体C3无统计学意义(P＞0.05),其余各项指标比较均有统计学意义(P＜0.05).[结论]长期机械通气病人T细胞亚群、补体及免疫球蛋白均异常,呼吸机相关肺炎的发生可能与免疫功能的异常有一定的相关性.     

唐山大地震40年幸存截瘫患者免疫功能分析

目的探讨唐山地震截瘫患者免疫球蛋白及补体水平及其与淋巴细胞亚群的相关性在截瘫患者中的变化及临床意义。方法采集110例截瘫患者静脉血,用比浊法测定血清免疫球蛋白IgG、IgA、IgM、补体C3、C4水平,并与健康对照及2010年测定结果比较。同时与全血淋巴细胞亚群(CD4+Th细胞、CD8+Ts细胞),CD19+B淋巴细胞和CD16+CD56+NK细胞做相关性分析。结果截瘫组血清IgG[(13.15±2.61)g/L]、补体C3[(1.28±0.24)g/L]、C4[(0.30±0.09)g/L]水平显著高于健康对照组,差异有统计学意义(P0.05)。2016年血清中IgG[(13.15±2.61)g/L]、IgA[(2.72±0.99)g/L]、IgM[(1.05±0.46)g/L]水平显著低于2010年,差异有统计学意义(P0.05)。免疫球蛋白中只有IgA与补体C4和NK细胞有相关性(P0.05),补体C4与CD4+和CD8+T细胞和NK细胞均有显著相关性(P0.05)。结论唐山地震截瘫患者免疫球蛋白、补体及淋巴细胞亚群均异于健康人,三者联合检测,对于监测病情和指导治疗有一定参考作用。     

吸毒者免疫功能改变的检测及分析

目的探讨吸毒者细胞免疫[T淋巴细胞亚群（CD3^＋、CD4^＋、CD8^＋、CD4／CD8比值）]、体液免疫[B细胞（CD19^＋）、免疫球蛋白（IgG、IgA、IgM）、补体c3]、非特异性免疫功能指标[自然杀伤（NK）细胞（CD16^＋CD56^＋）及白细胞介素-2（IL-2）]的改变,在临床进行心理干预治疗的同时为吸毒者提供治疗依据。方法收集47例吸毒者及53例健康体检者（正常对照组）外周血,采用流式细胞术（FCM）检测T淋巴细胞亚群（CD3^＋、CD4^＋、CD8^＋、CD4／CD8比值）、B细胞（CD19^＋）、NK细胞（CD16^＋CD56^＋）;采用免疫比浊法检测免疫球蛋白（IgG、IgA、IgM）、补体C3;采用酶联免疫吸附试验（ELISA）检测IL-2。结果吸毒组CD3^＋、CD4^＋、CD19^＋细胞及IgM、补体c3水平明显高于正常对照组（P〈0．05、P〈0．01）;NK细胞（CD16^＋CD56^＋）及IL-2水平明显低于正常对照组（P=0．000）;CD8^＋细胞、CD4／CD8比值及IgG、IgA水平与正常对照组比较差异无统计学意义（P〉0．05）。结论吸毒者免疫功能可能受到了一定的损伤,导致免疫调节功能出现紊乱。     

系统性红斑狼疮患者外周血T淋巴细胞亚群、免疫球蛋白及补体变化分析

【摘要】目的探讨T淋巴细胞亚群、免疫球蛋白及补体在系统性红斑狼疮（SLE）患者中的变化及临床意义。方法对55例SLE患者外周血CD3＋、CD4＋、CD8＋T淋巴细胞、免疫球蛋白及补体进行检测分析,另选取50名健康体检者作为对照组。CD3＋、CD4＋、CD8＋T淋巴细胞用流式细胞仪检测,免疫球蛋白及补体采用透射比浊法在全自动生化仪上检测。结果研究组外周血CD3＋、CD4＋、CD8＋T淋巴细胞绝对值及CD4＋／CD8＋比值、C3、C4明显低于对照组,IgG、IgA、IgM明显高于对照组（P〈0．01）。结论SLE患者T淋巴细胞亚群、免疫球蛋白及补体水平变化明显,三者联合检测,有利于病情监测及指导治疗。     

过敏性紫癜患儿的免疫功能变化及临床意义

目的通过检测过敏性紫癜患儿外周血免疫细胞、免疫球蛋白及补体的改变,探讨儿童过敏性紫癜的免疫学发病机制及其意义。方法收集2017年9月至2018年4月收治入院明确诊断为过敏性紫癜的患儿280例,同时随机收集同年龄段健康体检儿童50例(健康对照组),分别采用流式细胞术检测所有儿童外周血T淋巴细胞亚群、B淋巴细胞群及NK细胞群的变化,采用速率散射免疫比浊法检测外周血免疫球蛋白IgA、IgG、IgM、IgE及补体C3、C4水平。结果与健康对照组相比,过敏性紫癜患儿淋巴细胞亚群CD3~+、CD4~+、CD8~+T淋巴细胞及CD16~+CD56~+NK细胞数量明显下降(P0.05),CD19~+B淋巴细胞数量差异无统计学意义(P0.05),但CD19~+B淋巴细胞亚群比例明显增高(P0.05),CD16+CD56+NK细胞比例明显降低(P0.05),其余淋巴细胞比例差异无统计学意义(P0.05);免疫球蛋白IgA、IgG、IgM、IgE及补体C3水平明显增高(P0.05),补体C4差异无统计学意义(P0.05)。结论过敏性紫癜患儿体内免疫功能紊乱,表现为细胞免疫和NK细胞介导的固有免疫功能下调。     

儿童手足口病免疫球蛋白与T淋巴细胞亚群的表达与价值

目的：通过对手足口病患儿的免疫球蛋白与T淋巴细胞亚群检测研究,探讨该疾病细胞及免疫指标在其中的作用与价值。方法采用散射比浊法和流式细胞仪检测50例手足口病患儿及30例健康体检儿童的血清免疫球蛋白IgG、IgA、IgM,以及T淋巴细胞亚群CD3＋、CD4＋、CD8＋水平。结果手足口病组患儿与对照组 IgG、IgA、IgM水平的比较,手足口病组 IgG、IgA水平明显低于对照组,IgM水平明显高于对照组,差异均有统计学意义（P＜0．05）;手足口病组 CD3＋、CD4＋、CD4＋／CD8＋表达水平低于对照组,CD8＋表达水平高于对照组,差异均有统计学意义（P＜0．05）。结论手足口病患儿存在细胞及体液免疫功能紊乱,监测免疫球蛋白与T淋巴细胞亚群可以为临床手足口病患儿的免疫治疗提供理论依据。     

毛细支气管炎患儿免疫功能的变化及临床意义

目的检测毛细支气管炎（简称“毛支”）患儿T细胞亚群和免疫球蛋白、补体等免疫指标，观察其免疫功能的变化以探讨毛细支气管炎的免疫学发病机制。方法对67例毛支组患儿、40例健康对照采用间接免疫荧光法检测T细胞亚群，定时散射比浊法测定免疫球蛋白、补体。结果与健康对照组相比，毛支组CD3^＋（％）与CD8^＋（％）降低，但无统计学意义，CD4^＋（％）与CD4^＋／CD8^＋增高，差异有统计学意义（P〈0．05或〈0．01）；血清IgA降低、IgM升高但无统计学意义，IgG降低（P〈0．05）；血清C3、C4降低（P〈0．01）。结论婴幼儿感染毛细支气管炎后免疫功能发生紊乱和异常，其细胞免疫在感染后可能发挥主要的抗病毒作用，从细胞免疫角度进行研究可能更有利于疾病的严重性判断和更有效的治疗。     

衰老和脑梗死的发病与细胞免疫的相关性研究

目的：探讨急性脑梗死患者和不同年龄正常人周围血T淋巴细胞亚群和免疫球蛋白水平的关系。方法：采用APAAP法及SIRD法，测定不同年龄组周围血T淋巴细胞亚群CD3、CD4、CD8和免疫球蛋白IgG、IgA、IgM水平。结果：正常老年前期及老年组CD4明显低于青壮年组，脑梗死组CD3、CD4、CD4／CD8又明显低于正常组；各组中CD3、CD4、CD4／CD8有随增龄而有明显降低或降低趋势，CD8有随增龄而增高趋势；IgG、IgA、IgM各组无明显差异。结论：衰老和脑梗死的发病与细胞免疫有关，与体液免疫无关。     

机采血小板对无偿献血者免疫功能的影响

目的探讨机采血小板对无偿献血者免疫功能的影响。方法采用整群随机抽样选择2004年1月-2007年6月来本站的无偿献血者、无偿单采血小板者作为研究对象,分别测量其体内免疫球蛋白IgG、IgM、IgA水平及T淋巴细胞亚群CD3、CD4、CD8含量和CD4/CD8比值,并进行比较。结果无偿单采血小板者和无偿献血者的IgG、IgM、IgA水平,以及T淋巴细胞亚群CD3、CD4、CD8含量和CD4/CD8比值,其差异均无统计学意义（P〉0.05）。结论严格遵守操作规程并按规定单采血小板,对人体血小板计数及免疫功能均无影响。     

衰老和脑梗死的发病与细胞免疫的相关性研究

目的探讨急性脑梗死患者和不同年龄正常人周围血T淋巴细胞亚群和免疫球蛋白水平的关系。方法采用APAAP法及SIRD法,测定不同年龄组周围血T淋巴细胞亚群CD3、CD4、CD8和免疫球蛋白IgG、IgA、IgM水平。结果正常老年前期及老年组CD4明显低于青壮年组,脑梗死组CD3、CD4、CD4/CD8又明显低于正常组;各组中CD3、CD4、CD4/CD8有随增龄而有明显降低或降低趋势,CD8有随增龄而增高趋势;IgG、IgA、IgM各组无明显差异。结论衰老和脑梗死的发病与细胞免疫有关,与体液免疫无关。     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.     

创伤高血糖与感染和MODS早期诊断和干预

本文详细介绍了创伤后血糖应激适度理论,以及高血糖与感染和多器官功能不全综合征的关系;提出涉及胰岛B细胞功能不全的MODS实验诊断新方案和极化液个体化干预新措施,可早期发现创伤MODS、降低感染率及MODS发生率和病死率。     

腹膜后纤维化与肾积水发生关系的临床研究

目的：探讨腹膜后纤维化（RPF）导致肾积水的原因及诊治经验。方法：回顾分析2004年1月—2010年12月24例腹膜后纤维化致肾积水患者的诊治资料。结果：（1）RPF患者常见首发症状为腰背痛或腹痛（69.2%）;（2）红细胞沉降率（ESR）增快和血清IgG4升高最常见。超声检查仅提示上尿路积水。RPF的静脉肾盂造影（IVP）和CT尿路成像（CTU）表现具有特征性。IVP肾盂输尿管显影不良时,CTU能较清晰的显示上尿路影像。CT扫描发现腹膜后软组织肿块9例（37.5%）,优于超声检查;（3）输尿管松解和腹腔化手术治疗22例;行肾切除术1例;行输尿管置双J管术1例。最终确诊为继发性RPF8例,其中4例为术前诊断,3例为术中腹膜后软组织肿块冷冻活检证实,1例为术后病理证实;（4）特发性RPF手术后肾积水均获长期缓解,而继发性RPF的预后取决于原发疾病及其治疗方案。结论：影像学检查是诊断RPF的重要手段,CTU优于超声检查和IVP。输尿管松解和腹腔化手术可以使特发性RPF输尿管梗阻得到长期的缓解,术中对肿块进行冷冻活检有助于鉴别特发性和继发性RPF,及时调整治疗方案。     

探讨儿童慢性顽固性咳嗽与支原体感染的关系及临床治疗观察

目的探讨儿童慢性顽固性咳嗽与肺炎支原体（MP）感染的关系及临床疗效观察。方法采用回顾性研究方法对于现将2005年3月至2008年3月在我院的55例确诊慢性顽固性咳嗽患儿,主要表现为肺炎支原体感染为临床特点进行分析,并进一步临床治疗研究。结果①临床特点：在55例确诊慢性咳嗽的患儿中,以慢性顽固性咳嗽为主要症状。58％（32／55）的病例无肺部体征;②外周血：85％（47／55）的病例外周血变化不大,WBC（4—10）×10 9／L之间,嗜酸性粒细胞增多;③特别检查：47．27％（26／55）肺炎支原体IgM（MP—IgM）抗体阳性,83．64％（46／55）PeR技术检测肺炎支原体特异性DNA;④X光报告为多种形式。结论肺炎支原体（MP）感染是引起儿童慢性顽固性咳嗽的病因之一,对儿童慢性咳嗽,特别是顽固性咳嗽的诊治中应更加重视。     

Acetaminophen and acetylcysteine dose and duration: Past,present and future

Abstract

Acetylcysteine has been utilized successfully in the treatment of acetaminophen overdose since the 1970s. Although prospective trials as to efficacy and safety of acetylcysteine were conducted, there were no randomized controlled trials. This commentary addresses the reasons for this, and the background to choice of dose of acetylcysteine utilized in the oral and IV dosing regimens. Nomograms to predict possible hepatotoxicity based upon time of ingestion of acetaminophen were developed from a relatively arbitrary definition of toxicity as an aspartate aminotransferase/alanine aminotransferase (ALT/AST) greater than 1000 IU/L. While these have proved generally useful, patients still continue to develop hepatic damage after acetaminophen overdose, particularly if they present late after ingestion. The optimum management of these patients remains unclear, and one area of uncertainty is the dose and duration of acetylcysteine in various circumstances. This article discusses the issues that need to be elucidated to better target changes in acetylcysteine dose. The potential for measurements of other markers to improve treatment selection is the subject of further research.     

VEGF和NSE在良恶性嗜铬细胞瘤中的表达及意义

目的探讨肿瘤标志物血管内皮生长因子（VEGF）和神经元特异性烯醇化酶（NSE）在良、恶性嗜铬细胞瘤组织中的表达,分析其可能的临床价值及病理学意义,为临床鉴别良、恶性嗜铬细胞瘤提供辅助依据。方法应用免疫组化（SP法）检测16例恶性嗜铬细胞瘤、18例良性嗜铬细胞瘤及17例正常肾上腺髓质组织中细胞因子VEGF和NSE表达情况,显微镜下判断组织切片的染色结果。结果①恶性嗜铬细胞瘤VEGF表达明显强于正常肾上腺髓质和良性嗜铬细胞瘤（P〈0.01）。良性肿瘤和正常肾上腺髓质的VEGF表达差异无统计学意义（P〉0.05）。恶性嗜铬细胞瘤强阳性率明显高于良性嗜铬细胞瘤（P〈0.01）。②良、恶性嗜铬细胞瘤NSE表达差异有统计学意义（P〈0.05）,良性嗜铬细胞瘤NSE的表达高于正常肾上腺髓质的NSE表达（P〈0.05）。恶性嗜铬细胞瘤强阳性率高于良性嗜铬细胞瘤（P〈0.05）。③VEGF和NSE共同阳性表达在良、恶性嗜铬细胞瘤之间差异有统计学意义（P=〈0.01）。结论临床上检测VEGF和NSE可能为鉴别良、恶性嗜铬细胞瘤提供辅助依据,共同检测VEGF和NSE可能提高良、恶性嗜铬细胞瘤鉴别的敏感性。