2型糖尿病患者抵抗素相关因素分析及回归方程的建立

目的探讨抵抗素在2型糖尿病中的变化及其与有关指标的相互关系.方法选择70例2型糖尿病患者以及15名对照者,2型糖尿病患者按体重指数(BMI)分组,应用酶联免疫吸附试验(ELISA)检测外周血中的抵抗素浓度,氧化酶法测定血糖,放射免疫法测定胰岛素.结果糖尿病组抵抗素含量平均为(23.06±9.34) μg/L,显著高于对照组(P<0.01);抵抗素与BMI呈正相关(P<0.01),与葡萄糖曲线下面积(GAUC)呈正相关(P<0.01),与体脂分布呈正相关(P<0.01),与胰岛素抵抗指数呈负相关(P<0.01),与胰岛素曲线下面积无相关关系(P>0.05).并经逐步多元回归得出回归方程抵抗素=-15.869+0.339×GAUC+0.790×BMI.结论糖尿病患者体内有较高浓度的抵抗素,抵抗素与GAUC有密切关系.     

2型糖尿病患者血清抵抗素与血糖、血脂及胰岛素抵抗的关系

目的:探讨2型糖尿病患者血清抵抗素与血糖、血脂及胰岛素抵抗的关系。方法:52例2型糖尿病(T2DM)患者按体质指数(BMI)分为肥胖(BMI≥25kg/m2)(26例)与非肥胖(BMI<25kg/m2)(26例)2组,及17例糖耐量正常的同期健康体检者作为对照组,采用酶联免疫分析法检测空腹血清抵抗素水平;同时行口服葡萄糖耐量(OGTT)和胰岛素释放试验,检测血脂,测量血压、身高、体重、腰围、臀围,计算BMI和腰臀比值(WHR),并以稳态模型(HOMA)计算胰岛素抵抗指数(HOMA-IR)。结果:肥胖T2DM患者血清抵抗素水平(ng/mL)明显高于非肥胖T2DM患者(P<0.01);肥胖T2DM组高于对照组、对照组略高于T2DM非肥胖者,但差异无显著性(P>0.05);女性血清抵抗素水平明显高于男性(P<0.05)。空腹血清抵抗素与BMI、HOMA-IR呈正相关(r=0.403、r=0.337、P<0.001);与FINS及餐后2hINS呈正相关(r=0.652、r=0.428、P<0.001);与甘油三酯呈正相关(r=0.320、P<0.01);与空腹血糖无关而与餐后2h血糖呈负相关(r=-0.303,P<0...     

老年慢性阻塞性肺疾病患者血浆抵抗素水平的研究

目的:分析老年慢性阻塞性肺疾病(COPD)患者血浆抵抗素水平与C反应蛋白(CRP)、血糖(FPG)、胰岛素抵抗及肥胖指标的关系。方法:选择住院的老年COPD患者60例,按病程分为急性加重期和临床稳定期,在不同时期测定血浆抵抗素、CRP、FPG、胰岛素(FINS)、动脉血氧分压(PaO2),测量身高、体重,计算体质指数(BMI)、胰岛素抵抗指数(HOMA-IR)。选择同期健康老年人50例作为对照。结果:COPD急性加重期血浆抵抗素、CRP、FPG、FINS、HOMA-IR均显著高于临床稳定期及对照组(P<0.01)。COPD稳定期FINS和HOMA-IR显著高于对照组(P<0.05),稳定期抵抗素、CRP及FPG与对照组比较差异无统计学意义(P>0.05)。COPD急性加重期抵抗素与CRP呈正相关(r=0.491,P<0.01),与FPG、FINS、HOMA-IR及BMI均不相关。COPD稳定期及对照组抵抗素与CRP、FPG、FINS、HOMA-IR及BMI均不相关。结论:老年COPD急性加重期患者血浆抵抗素、CRP水平升高并伴一定的胰岛素抵抗,抵抗素与CRP存在一定的相关性,与FPG、HOMA-IR及BMI不相关,抵抗素可能参与COPD急性加重期的炎症反应。     

糖尿病患者骨密度与胰岛素、糖化血红蛋白、体质量指数的相关性分析

目的:探讨糖尿病患者的骨密度改变及相关影响因素。方法:采用双能X线吸收法测定了140例糖尿病患者(1型糖尿病36例,2型糖尿病104例)及60例健康人L2～L4椎体、股骨近端(股骨颈、大转子、Ward's三角区)的骨密度,并同时测定了体质量指数(bodymassindex,BMI)、糖化血红蛋白(HbA1C)及空腹胰岛素水平。结果:1型糖尿病组骨密度(g/cm2)除大转子部位(0.924±0.12)外,其余部位骨密度均明显低于2型糖尿病及健康对照组(t=1.994～2.936,P<0.01～0.05),2型糖尿病组与健康对照组之间各部位骨密度差异无显著性意义(P>0.05)。1型糖尿病组骨质疏松或骨量减少的发生率(83.3%)明显高于2型糖尿病组(38.5%)和健康对照组(20.0%)(χ2=20.226～27.74,P<0.01)。空腹胰岛素水平(mU/L)1型糖尿病组(2.29±0.38)明显低于2型糖尿病组(15.26±3.37)及健康对照组(15.38±2.53)(t=2.912～3.014,P<0.01)。BMI(kg/m2)2型糖尿病组(27.3±4.1)明显高于健康对照组(24.3±2.8)与1型糖尿病组(22.5±3.3)(t=2.317～3.014,P<0.05)。结论:糖尿病患者骨密度与胰岛素水平、HbA1C,BMI显著相关。     

代谢综合征患者与抵抗素的相关性研究

目的探讨代谢综合征(MS)患者血清抵抗素水平与血脂、肥胖和胰岛素抵抗的关系。方法88例MS患者和26例年龄相匹配的正常对照组按体质量指数(BMI)将MS患者分为肥胖组和非肥胖组,采用酶联免疫吸附测定(ELISA)法测定受试者空腹血清抵抗素水平,同时检测其身高、体质量、腰围、臀围、血压、血糖、血脂及胰岛素水平,并计算其BMI、腰臀比和胰岛素抵抗指数。结果MS患者肥胖组与正常对照组相比其血清抵抗素水平明显升高,分别为[(28.08±11.92)μg/L vs(18.96±6.27)μg/L,P<0.01],非肥胖组与对照组比血清抵抗素水平明显升高分别为[(25.96±12.08)μg/L vs(18.96±6.27)μg/L,P<0.01],肥胖组和非肥胖组相比其血清抵抗素水平差异亦有统计学意义(P<0.05),相关分析显示空腹血清抵抗素水平与BMI、腰臀比、胰岛素抵抗指数呈正相关(r值分别为0.31、0.21、0.23,均P<0.05),与血糖、血压、血脂无相关性(P>0.05)。结论MS患者血清抵抗素水平明显升高,且与肥胖及胰岛素抵抗程度有明显的相关性,因而抵抗素可能为肥胖和胰岛素抵抗、MS、2型糖尿病及心血管疾病的主要连接点。     

胰岛素抵抗与2型糖尿病直立性低血压的关系

目的:探讨2型糖尿病及糖尿病合并高血压(diabetesmellituswithhy-pertension,DMH)患者发生直立性低血压(posturalhypotension,PH)与胰岛素抵抗,体重指数(BMI)的关系。方法:糖尿病与DMH患者各62例,其中糖尿病组男38例,女24例,年龄32～72岁。DMH组男36例,女26例,年龄36～78岁。检测两组患者卧、立位血压、BMI、C肽和血糖水平,比较不同患者这些指标的差异。结果:糖尿病发生PH低于DMH(24/62和38/62,χ2=6.323,P<0.01);糖尿病+PH患者与DMH+PH患者卧立位收缩压和舒张压变化幅值(mmHg)高于糖尿病患者(收缩压26.40±1.45和22.60±0.83,F=238.8,P<0.01;舒张压12.60±0.89和12.10±1.42,F=56.3,P<0.01),DMH+PH患者的血C肽(mg/L)显著高于DMH+PH患者(1.25±0.33和1.30±0.22,F=9.9,P<0.01),而胰岛素敏感指数显著低于糖尿病发生PH患者(0.02±0.04和0.03±0.07,F=52.8,P<0.01)。结论:糖尿病合并PH者存在明显胰岛素抵抗,糖尿病合并高血压则更易发生PH。     

影响2型糖尿病合并高血压患者血清瘦素水平的因素分析

目的:研究2型糖尿病合并高血压患者血清瘦素水平的变化。方法:随机选取2型糖尿病患者60例,肥胖者30例与非肥胖者30例,2型糖尿病患者合并高血压60例,肥胖者33例与非肥胖者27例,正常对照组30例。分别检测以上3组患者的空腹瘦素、空腹和餐后2h血糖、胰岛素和C肽、糖化血红蛋白(glucosylatedhemoglobin,HbA1c)、体质量指数(bodymassindexBMI)、血压、总胆固醇、三酰甘油、高密度脂蛋白、低密度脂蛋白,并计算胰岛素敏感指数(insulinsensitivityindex,ISI)。结果:2型糖尿病患者血清瘦素水平与BMI、空腹胰岛素、C肽和餐后2h胰岛素、C肽水平、性别呈正相关(r=0.548,0353,0.391,0.332,0.362,0.373,P<0.01),高血压组高于其他两组(P<0.05或0.01),肥胖者犤高血压与非高血压组FINS分别为(24.62±0.83),(18.32±0.90)mIU/L犦高于非肥胖者犤(17.21±0.71),(15.24±0.62)mIU/L犦(P<0.05或0.01),与ISI呈负相关(r=0.33,P<0.01),血糖控制的差异对瘦素没有产生影响。结论:2型糖尿病合并高血压患者血清瘦素水平受到高胰岛素血症、胰岛素抵抗、肥胖和血脂等多因素的影响,但与血糖水平无关。     

肥胖人群脂联素、抵抗素和胰岛素抵抗水平的研究

目的探讨肥胖患者血清脂联素、抵抗素和胰岛素抵抗水平的变化及意义。方法分别测定106例肥胖者和107名健康对照者的体重指数(BMI)、腰围、臀围、空腹胰岛素、空腹血糖、血脂、脂联素和抵抗素水平,计算胰岛素抵抗指数(HOMA-IRI)。结果肥胖者的体重指数(BMI)、体脂分布百分比(BF)、HOMA-IRI、抵抗素、脂联素、总胆固醇(TC)、载脂蛋白B(apo B)与健康对照组比较,差异均有统计学意义(P<0.01、P<0.05)。脂联素和抵抗素均与BMI、BF和HOMA-IRI呈正相关([脂联素:相关系数(r)分别为0.439、0.236、0.398,P均<0.01;抵抗素:r分别为0.296(P<0.01)、0.175(P<0.05)、0.827(P<0.01)],抵抗素与腰臀比(WHR)呈正相关(r=0.169,P<0.05)。结论脂联素能较好地预测BMI和HOMA-IRI,抵抗素能较好地预测BMI。脂联素与抵抗素水平的变化可能导致肥胖和胰岛素抵抗,在向糖尿病的发生发展过程中起了一定作用。     

血浆抵抗素水平与2型糖尿病及肥胖的相关性分析

目的测定初次确诊为糖尿病患者的血浆抵抗素水平,分析抵抗素与性别、体重指数、空腹胰岛素、血糖、胰岛素抵抗指数、甘油三脂、胆固醇的相关性。方法受试者精确测量身高、体重、计算体重指数(BMI),同步检测空腹血糖(FPG)、胰岛素(FINS)、计算胰岛素抵抗指数(IR)、胆固醇(CH)、甘油三脂(TG),酶联免疫吸附试验(ELISA)测定血浆抵抗素(Resistin)水平。结果糖尿病组血浆抵抗素水平与对照组相比较,差异无统计学意义(P>0.05);无论是糖尿病组还是对照组,肥胖者的抵抗素水平与非肥胖者的抵抗素水平相比校,差异无统计学意义(P>0.05);男性与女性的抵抗素水平相比较,差异亦无统计学意义(P>0.05)。同时,相关分析显示,抵抗素与BMI(r=-0.1110,P>0.05)、FINS(r=-0.2291,P>0.05)、FPG(r=0.1128,P>0.05)、IR(r=-0.2700,P>0.05)、TG(r=-0.0078,P>0.05)、CH(r=-0.1450,P>0.05)均无相关性。结论血浆抵抗素水平在2型糖尿病组与对照组间无统计学差异,提示血浆抵抗素可能不是肥胖和2型糖尿病之间联系的主要因素。     

2型糖尿病患者血清抵抗素水平的变化研究

目的探讨人血清抵抗素水平与2型糖尿病的关系.方法 2型糖尿病患者48例和正常对照组47例,采用酶联免疫分析法检测空腹血清抵抗素、胰岛素水平;同时测血糖、血压、血脂、身高、体重,计算腰围、臀围、体重指数、腰臀比值和胰岛素敏感指数、胰岛素抵抗性、胰岛B细胞功能.结果 2型糖尿病组的体重指数、甘油三酯、血清抵抗素水平显著高于正常对照组（P＜0.05）;相关分析显示血清抵抗素水平与体重指数、腰围、空腹胰岛素、血压呈正相关.在正常对照组,血清抵抗素水平与胰岛素敏感指数、胰岛素抵抗性、胰岛B细胞功能相关.而且血清抵抗素水平在糖尿病肥胖组显著高于糖尿病非肥胖组和正常对照组（P＜0.05）.结论 2型糖尿病患者血清抵抗素水平升高,与肥胖相关,血清抵抗素可能是联系肥胖和2型糖尿病的重要因素.     

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。