乳糜尿患者非增强MR淋巴成像研究：与直接淋巴管造影术后CT对照

目的 探讨乳糜尿患者非增强MR淋巴成像（3D Unenhanced MR lymphography，MRL）淋巴管-泌尿系瘘道定位与胸导管异常，与直接淋巴管造影（Direct lymphangiography，DLG）术后CT对照。 方法 回顾性分析24例乳糜尿患者MRL及DLG术后CT资料，由两位医师盲法阅片，评价淋巴管-泌尿系瘘道位置和胸导管梗阻相关征象。MRL评价指标包括：肾淋巴管及其他腹膜后淋巴管扩张，胸导管扩张和胸导管周围迂曲淋巴管。DLG术后CT评价指标：肾淋巴管和泌尿系对比剂返流，髂干和胸导管出口区淋巴管对比剂返流。 结果 MRL显示19例(79.2%)患者淋巴管-泌尿系瘘道：2例位于双肾，6例位于左肾，10例位于右肾，1例位于膀胱。DLG术后CT显示26患者淋巴管-泌尿系瘘道：6例位于双肾，7例位于左肾，10例位于右肾，1例位于膀胱。MRL与DLG术后CT结果一致性一般(kappa=0.601, p<0.001)。两种检查方法对单侧肾脏水平淋巴管-泌尿系瘘判断差异有统计学意义（χ2=22.463，P<0.001），MRL灵敏度Sen=69.0%，特异度Spe=100%。2例患者DLG及术后CT对比剂未达胸导管颈段，MRL可显示其中1例颈段胸导管。MRL发现2例合并单侧双肾盂输尿管畸形患者。 结论 MRL能作为乳糜尿患者无创显示淋巴管-泌尿系瘘道的初步检查方法，可显示胸导管梗阻情况，与DLG术后CT有较好互补性。     

原发性乳糜性心包积液淋巴回流障碍的直接淋巴管造影和MSCT表现

目的 探讨直接淋巴管造影(DLG)和MSCT诊断乳糜性心包积液淋巴回流障碍的价值.方法 回顾性分析9例乳糜性心包积液的DLG及造影后MSCT资料;7例伴乳糜胸,其中1例伴乳糜痰;8例接受胸导管梗阻解除术.结果 9例DLG和MSCT均表现为胸导管出口梗阻;5例合并心包区反流,其中4例通过扩张的支气管纵隔干反流.8例接受胸导管出口梗阻解除术,术后病情好转.结论 DLG和MSCT可显示原发性乳糜性心包积液胸导管及属支异常,并能显示心包腔与淋巴系统的异常交通,后者可能是治疗的关键.     

直接淋巴管造影及造影后CT成像在合并乳糜性胸、腹腔积液的淋巴管肌瘤病诊治中的初步应用

目的 探讨直接淋巴管造影及造影后CT成像在合并乳糜性胸、腹腔积液的淋巴管肌瘤病(LAM)诊治中的作用。 方法 收集我院经病理或影像学典型表现证实的12例LAM患者的直接淋巴管造影及造影后CT资料,并与手术相对照。 结果 CT示12例LAM均伴有乳糜性胸腔积液,5例伴有腹腔积液,2例伴有盆腔积液。12例LAM直接淋巴管造影及造影后CT均不同程度出现腹膜后和(或)髂淋巴管扩张,5例于直接淋巴管造影时出现胸导管扩张,1例胸导管回流不畅,5例胸导管未显影,1例部分显影。12例LAM中11例接受手术治疗均取得良好疗效。 结论 直接淋巴管造影和造影后CT成像可为合并乳糜性胸、腹腔积液的LAM的诊断和治疗提供重要依据。     

影像学检查在胸导管末端探查术治疗淋巴管肌瘤病合并乳糜胸术式选择中的价值

目的 探讨影像学检查在胸导管末端探查术治疗淋巴管肌瘤病（LAM）合并乳糜胸术式选择中的诊断价值。方法 回顾性分析经临床和/或病理证实的34例LAM合并乳糜胸患者的临床和影像学资料。所有患者均接受放射性核素⁹⁹Tc^m-右旋糖酐（DX）淋巴显像和CT淋巴管造影（CTL）检查。根据⁹⁹Tc^m-DX淋巴显像对胸导管分型：Ⅰ型为异常浓聚型;Ⅱ型为异位引流型;Ⅲ型为未显影或一过性显影型,Ⅰ型和Ⅱ型为胸导管异常。根据CTL对胸导管分型：Ⅰ型为扩张型;Ⅱ型为末端梗阻型;Ⅲ型为主干缩窄型;Ⅳ型为异位引流型;Ⅴ型为未显示型。以Ⅰ~Ⅳ型为胸导管异常。评价2种方法显示胸导管病变的一致性。结果 ⁹⁹Tc^m-DX淋巴显像显示Ⅰ型17例,Ⅱ型3例,Ⅲ型14例。58.82%（20/34）的LAM合并乳糜胸病例存在胸导管病变。CTL显示Ⅰ型15例,Ⅱ型3例,Ⅲ型5例,Ⅳ型2例,Ⅴ型9例,73.53%（25/34）的LAM合并乳糜胸病例存在胸导管病变。2种方法显示胸导管是否存在病变的一致性较好（Kappa=0.679）。CTL胸导管分型中,Ⅰ型和Ⅱ型多采用胸导管—静脉吻合术或胸导管末端松解术解除梗阻,Ⅲ型多采用胸导管末端压迫带/粘连松解术解除梗阻,Ⅳ型根据胸导管异常回流路径来选择手术入路和手术方式,Ⅴ型多采取保守治疗。结论 CTL优于⁹⁹Tc^m-DX淋巴显像,能准确显示胸导管的病变情况,为胸导管末端探查术治疗LAM合并乳糜胸的术式选择提供影像学依据。     

CT淋巴管成像及胸部平扫CT诊断乳糜痰

目的 观察直接淋巴管造影(DLG)后CT淋巴管成像(CTL)及平扫CT诊断乳糜痰的价值。方法 回顾性分析17例乳糜痰患者CTL及胸部平扫CT资料,观察淋巴管异常及胸部其他异常表现。结果 17例CTL均见碘化油异常沉积,分布于颈根部、纵隔区、胸腔和胸壁,以颈静脉角区最为常见,部分可见肺部碘化油反流及多处淋巴管扩张;胸部平扫CT显示肺、胸膜、纵隔及心包等多处异常,以支气管血管束增粗最为常见。结论 CTL对诊断乳糜痰有一定价值;胸部平扫CT可显示乳糜痰患者肺及胸部其他结构异常改变。     

CT淋巴管成像诊断原发性乳糜尿

目的 观察CT淋巴管成像(CTL)诊断原发性乳糜尿的价值。方法 分析37例原发性乳糜尿,比较CTL与直接淋巴管造影(DLG)所见淋巴管形态、淋巴回流,泌尿系统、胸腹盆部淋巴管异常及腹盆腔、腹膜后、肺、纵隔及骨骼等其他异常;以Kappa检验评价二者诊断原发性乳糜尿的一致性。结果 CTL显示对侧髂淋巴反流、对侧腰干反流及支气管纵隔干反流优于DLG(P均<0.05),诊断一致性中等(Kappa均>0.40);二者显示同侧及对侧肾脏淋巴反流几乎完全一致(Kappa均>0.80),而CTL能进一步显示肾脏及肾周异常淋巴管分布;DLG显示颈干及锁骨下干反流优于CTL(P<0.05),二者显示同侧髂、腰干及腹膜后淋巴管纡曲扩张差异均无统计学意义(P均>0.05),诊断一致性中等及以下(Kappa均<0.50)。CTL显示对比剂异常反流至胸部14例、腹盆部36例,5例复杂性淋巴管畸形及8例淋巴管瘤等;DLG仅显示7例胸部及5例腹盆部对比剂异常反流。结论 CTL显示肾脏反流、肾周异常淋巴管分布及对侧髂、腰干反流具有重要价值,而DLG显示胸导管末端反流更具优势;联合应用...     

实验兔皮内、皮下注射钆双胺行间质MR淋巴管成像对脊柱旁淋巴干显像的对比分析

目的 探讨经兔足背皮内、皮下注射钆双胺行脊柱旁淋巴干MR成像的可行性。方法 选取新西兰大白兔8只,首先经足背皮内注射钆双铵（皮内组）,间隔3天后再经皮下注射（皮下组）,采集冠状位三维扰相梯度回波序列（fl3d-cor）图像,分别评价腰淋巴干及胸导管的显示情况。结果 皮内组显示所有兔两侧腘窝淋巴结、髂淋巴结及主动脉下淋巴结明显强化,强化持续时间大于30 min,最长达90 min;6例腰淋巴干全程及乳糜池明显强化;5例可见部分胸导管强化。皮下组显示所有兔两侧腘窝淋巴结均明显强化,但腰淋巴结、腰淋巴干及胸导管未见强化。腰淋巴干及胸导管强化程度总评分皮内组与皮下组差异有统计学意义（t=100.00,P=0.0002）。结论 足背皮内注射钆双胺淋巴管成像能较皮下注射更好地显示腰干淋巴管。     

CT淋巴管造影对乳糜尿的诊断价值

目的 探讨CT淋巴管造影对直接淋巴管造影术后乳糜尿的诊断价值.方法 回顾性分析11例乳糜尿患者的核素淋巴显像、直接淋巴管造影、CT淋巴管造影并经手术证实的所有资料.结果 11例乳糜尿患者中,核素淋巴显像发现胸导管扩张8例,腰干增宽5例,肾盂显影7例;直接淋巴管造影发现胸导管扩张10例,腰干淋巴管纡曲、扩张11例,对侧腰干、腹膜后淋巴管反流4例,向肾盂反流10例;CT淋巴管造影发现胸导管扩张9例,右淋巴管扩张1例,腰干、腹膜后、髂、盆腔淋巴管纡曲、扩张11例,对侧腰干、腹膜后淋巴管反流10例,肾盂、肾窦反流11例.结论 CT淋巴管造影可以发现更多病变淋巴管,并清晰显示其周围解剖关系,对核素淋巴显像和直接淋巴管造影的低空间分辨力起到补充作用.     

直接淋巴管造影后MSCT诊断乳糜胸

目的探讨直接淋巴管造影(DLG)后MSCT诊断乳糜胸的价值。方法回顾性分析30例乳糜胸患者的DLG及DLG后MSCT成像资料,将MSCT与DLG影像相对照。结果 DLG后MSCT显示造影侧髂及腹膜后淋巴管扩张、纡曲30例(100%),与DLG相吻合;出现对侧髂腰部反流和腹膜后淋巴管扩张13例(43.33%),DLG显示9例(30.00%,P=0.13);出现腹腔反流4例(13.33%),DLG显示3例(10.00%,P=1.00);胸导管出口受阻20例(66.67%),DLG显示22例(73.33%,P=0.50);胸导管部分未显影9例(30.00%),DLG显示8例(26.67%,P=1.00);对比剂入血10例(33.33%),DLG显示4例(13.33%,P=0.07);对比剂漏出至胸腔8例(26.67%),DLG显示1例(3.33%,P=0.02)。两种检查均显示1例(3.33%)肺内淋巴管扩张(P=1.00)。结论 DLG后MSCT成像与DLG互为补充,可为乳糜胸的诊断及治疗提供重要依据。     

骨淋巴管瘤CT淋巴管造影及常规CT表现

目的 探讨骨淋巴管瘤CT淋巴管造影（CTL）及常规CT表现。方法 回顾性分析79例病理证实或临床综合诊断为骨淋巴管瘤患者的临床及影像学资料。79例均接受直接淋巴管造影及造影后CT平扫,16例接受CT平扫及增强检查,分析其CTL和常规CT表现。结果 骨淋巴管瘤CT表现为骨内单发或多发低密度影,多位于脊柱（n=71）及骨盆（n=73）。79例中,囊状病变37例,筛网状病变18例,24例二者均存在;28例患者所有骨病变均可见硬化边,47例患者部分骨病变可见硬化边,4例患者所有骨病变均未见硬化边。骨内病变增强CT扫描均未见强化。CTL检查中,24例病变内可见碘化油沉积。结论 骨淋巴管瘤CTL及常规CT表现较具特征性,且常伴淋巴系统其他异常改变,有助于诊断。     

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。