CEUS定量分析鉴别诊断乳腺肿瘤的价值及其与微血管密度的相关性分析

目的 采用CEUS时间-强度曲线(TICs)各参数鉴别良恶性肿瘤的价值及其与微血管密度(MVD)间的关系。方法 纳入获得病理诊断的患者79例,其中良性病变56例,恶性病变23 例。手术病理标本切片行免疫组织化学染色检测MVD。采用SonoLiver软件定量分析各参数与MVD关系。结果 乳腺病灶TICs的各参数在良恶性肿瘤之间比较差异无统计学意义(P>0.05);乳腺病灶的IMAX 及QOF明显高于乳腺实质,而且RT、TTP、mTT均较乳腺实质短(P <0.05)。恶性病灶MVD数目为(173.16±64.67)个/mm²,良性病灶MVD数目为(149.01±35.16)个/mm²,差异有统计学意义(P =0.04)。TICs各参数只有IMAX与MVD相关(r=0.229,P=0.048)。结论 乳腺病变CEUS定量参数的IMAX与MVD存在正相关,通过定量分析的峰值强度参数可以初步评估乳腺肿瘤内微血管密度。     

甲状腺单发结节超声造影与微血管密度的相关性

目的 探讨甲状腺单发结节CEUS的特点及其与微血管密度(MVD)间的相关性。方法 对45例甲状腺单发甲状腺结节患者术前行CEUS,分析结节的造影特点;术后以CD34单克隆抗体染色肿瘤组织,于光镜下计数肿瘤的微血管数。结果 结节性甲状腺肿23例,腺瘤8例,甲状腺癌14例,CEUS峰值强度分别为(26.82±4.48)dB,(31.50±4.22)dB,(22.36±6.13)dB,MVD分别为(58.55±7.32)条/高倍视野、(68.67±10.62)条/高倍视野、(35.00±6.16)条/高倍视野,峰值强度与MVD呈正相关(r=0.692,P=0.001)。结论 CEUS对甲状腺结节有一定诊断价值,其峰值强度可反映结节的MVD,可于术前反映结节的血管生成情况。     

胃癌的超声造影参数与微血管密度的相关性

目的 探讨胃癌CEUS参数与微血管密度(MVD)的相关性。方法 对确诊的37例胃癌患者行术前CEUS,分别记录胃癌病变区及正常胃壁TIC曲线的峰值时间(TTP)、增强时间(ET)、曲线上升支斜率(WIR)。计数胃癌病变及其旁正常胃壁的MVD。分析CEUS的TIC参数与MVD的相关性。结果 胃癌病变区TIC的ET、TTP低于其旁正常胃壁(P均<0.05),WIR、MVD高于其旁正常胃壁(P<0.01);胃癌病变区的ET、TTP与MVD呈负相关(r=-0.70、-0.59,P均<0.01),WIR与MVD呈正相关(r=0.70,P<0.01)。结论 对术前经胃镜病理活检确诊的胃癌行CEUS,可以直接显示并评估肿瘤血流灌注状态,从而间接评价新生血管生成程度,可预测肿瘤的发生发展并判断预后。     

pT1期肾透明细胞癌超声造影特点及其与Fuhrman分级的关系

目的 探讨pT1期肾透明细胞癌(CCRCC)的CEUS增强模式、定量参数与Fuhrman分级的关系.方法 回顾性分析经病理证实的83例pT1期CCRCC的CEUS图像及相关参数,观察不同分级肿瘤的CEUS增强模式、程度及增强的均匀性以及肿瘤周边环状高增强(PHR);通过时间-强度曲线软件得到定量数值,包括始增时间(AT)、达峰时间(TTP)和峰值强度(PI),并与病理Fuhrman分级进行比较.结果 不同Fuhrman分级的CCRCC的PHR、△PI值差异均有统计学意义(P均<0.05).FuhrmanⅠ级肿瘤中PHR检出率相对较高,△PI最低;Ⅳ级肿瘤PHR检出率相对较低,△PI最高.各级肿瘤增强均匀性差异无统计学意义(P>0.05).肿瘤CEUS增强模式大多表现为"快进"(61/83,73.49%)、"快出"(34/83,40.96%)和"慢出"(37/83,44.58%),不同分级肿瘤造影模式差异无统计学意义(P>0.05).结论 pT1期CCRCC的CEUS特点与Fuhrman分级有一定相关性;CEUS可为临床提供更多有价值的信息.     

超声造影定量分析鉴别诊断卵巢良恶性肿瘤

目的 探讨CEUS在鉴别诊断卵巢良恶性肿瘤中的应用价值。 方法 纳入因卵巢肿瘤接受手术的患者48例,共51个肿块,于术前1周内行经腹CEUS检查,动态观察肿瘤的造影增强模式,绘制肿瘤ROI时间-强度曲线并获得峰值强度(I_max)、上升时间(RT)、达峰时间(TTP)、平均渡越时间(mTT)及曲线下面积(AUC);比较良恶性肿瘤间各参数差异。 结果 51个肿块中,良性肿瘤24个,恶性肿瘤27个;CEUS中良性肿瘤呈均匀增强,恶性肿瘤呈不均匀增强;恶性肿瘤造影剂I_max、AUC和mTT均大于良性肿瘤(P均<0.05), 而RT和TTP二者间差异无统计学意义(P均>0.05)。 结论 CEUS可准确评价肿瘤内血流灌注特点,在鉴别诊断卵巢良恶性肿瘤中有重要应用价值。     

微血管密度不同的乳腺肿瘤实时灰阶超声造影表现

目的 应用实时灰阶超声造影技术评价乳腺肿瘤新生血管,探讨不同微血管密度(MVD)乳腺肿瘤的超声造影表现。方法 收集在我院接受乳腺肿瘤切除术的患者57例,良性肿瘤30例,恶性肿瘤27例。采用实时灰阶超声造影技术观察肿瘤增强模式及造影参数:峰值强度(PI)和达峰时间(TTP)。对肿瘤进行免疫组化染色,计算MVD。按照MVD均值将患者分为高MVD和低MVD组,比较两组超声造影参数的差异。结果 57例乳腺肿瘤患者MVD均值为(44.51±10.11)个/高倍视野(×200)。高MVD组肿瘤区PI值高于低MVD组(P＜0.05);高MVD组和低MVD组肿瘤造影剂分布差异有统计学意义(P＜0.05),其余参数差异均无统计学意义(P均>0.05)。结论 超声造影后PI值较高、呈不均匀增强的肿瘤,其恶性可能较大,MVD亦较高。     

卵巢癌超声造影与血管生成拟态和MVD的相关性分析

目的 分析不同时期裸鼠卵巢癌移植瘤血管生成拟态(VM)密度、微血管密度(MVD)及其CEUS参数的相关性。方法 分别建立生长21天组、28天组裸鼠移植瘤模型,每组10只,对两组移植瘤模型行CEUS检查,分析各组时间强度曲线(TIC)及相关参数。应用CD31及PAS双重染色检测卵巢癌中VM表达及MVD。对两个时期移植瘤造影的峰值强度(PI)与相应的VM密度及MVD进行相关性分析。结果 成功制备移植瘤模型。CEUS显示,21天组、28天组的峰值强度(PI)、达峰时间(TTP)、持续时间(TTD)差异有统计学意义(P<0.05)。染色检测显示,21天组、28天组VM密度、MVD差异均有统计学意义(P均<0.05)。21天组PI与VM密度、MVD均呈正相关(r=0.657、0.652,P均<0.05);28天组PI与VM密度无相关性(P>0.05),PI与MVD呈正相关(r=0.687,P=0.03)。结论 不同时期卵巢癌CEUS与VM密度或MVD密切相关,对卵巢癌早期诊断有一定价值。     

超声造影定量评价动脉粥样硬化斑块新生血管及其与组织病理学的相关性

目的 应用CEUS技术定量评价动脉粥样硬化斑块增强强度及其与病理染色所示的新生血管密度的相关性。方法 选取新西兰白兔25只,高脂饲养4周后,以球囊扩张腹主动脉,再高脂饲养16周,建立动脉粥样硬化模型;行常规超声及CEUS检查,观察不同类型斑块的增强情况,应用时间-强度曲线定量分析动脉粥样硬化斑块的增强强度,以CD31染色观察斑块内新生血管的密度。应用非配对t检验比较软斑与硬斑造影强度及新生血管密度的差异;Pearson相关分析动脉粥样硬化斑块CEUS增强强度与斑块新生血管密度的相关性。结果 二维超声诊断为软斑的斑块在CEUS中的增强强度明显高于硬斑(P<0.05);软斑的新生血管密度明显高于硬斑(P<0.05);斑块内新生血管密度与斑块造影增强强度存在明显相关性(r=0.75,P<0.001),与斑块增强强度/管腔增强强度亦存在明显相关性(r=0.68,P<0.001)。结论 CEUS可定量评价兔动脉粥样硬化斑块的增强情况;斑块增强强度与斑块内新生血管密度具有良好的相关性。     

乳腺肿瘤CEUS特点及时间-强度曲线参数与微血管密度的关系

目的探讨CEUS鉴别乳腺良、恶性肿瘤的价值,观察CEUS时间-强度曲线各参数与微血管密度(MVD)的相关性。方法对88例乳腺肿瘤患者(恶性52例,良性36例)行实时CEUS,分析肿瘤特点,记录时间-强度曲线各参数值,计算MVD。结果良、恶性肿瘤在CEUS增强强度、增强形态、增强边界及有无穿支血管方面差异均有统计学意义(P均<0.05)。恶性肿瘤峰值减半差值时间(ΔHT)、峰值强度(PI)、MVD均高于良性肿瘤,差异有统计学意义(P均<0.05)。PI与MVD呈显著正相关(r=0.85,P<0.05)。结论 CEUS有助于判断乳腺肿瘤的良、恶性,且肿瘤增强强度与MVD有关。     

肾透明细胞癌超声造影增强模式与Fuhrman核分级的关系

目的 探讨肾透明细胞癌(ccRCC)的CEUS超声造影增强模式与Fuhrman核分级的关系。方法 对62例ccRCC患者行CEUS检查,观察超声造影表现,分析时间-强度曲线指标,评价ccRCC增强模式与Fuhrman核分级的关系。结果 不同Fuhrman核分级ccRCC间,病灶直径差异均有统计学意义(P均<0.05),假包膜显示率差异均无统计学意义(P均>0.05),时间-强度曲线峰值时间差异均有统计学意义(P均<0.05)。Fuhrman核分级Ⅰ级ccRCC的CEUS增强模式以"慢进慢退"为主(14/35,40.00%),Fuhrman核分级Ⅱ级和Ⅲ级ccRCC曲线尖度均高于Ⅰ级(P均<0.05)。结论 ccRCC的CEUS增强模式、时间-强度曲线峰值时间及曲线尖度均与Fuhrman核分级有关。     

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。