涎腺混合瘤与Warthin瘤超声造影对比研究

目的 总结涎腺混合瘤与Warthin瘤的超声造影特征,分析二者的差异.方法 回顾性分析我院经手术病理证实的17个涎腺混合瘤和16个Warthin瘤的超声造影特征.结果 混合瘤超声造影表现以同进(76.5％)、向心性(64.7％)、不均匀性(76.5％)、低增强(70.6％)为主,增强后边界多清晰(88.2％),大部分可...     

涎腺混合瘤和Warthin′s瘤的超声造影对比

目的对比分析涎腺混合瘤（PA）和Warthin′s瘤的超声造影（CEUS）特点。 方法回顾性分析2016年6月至2017年11月在南昌大学第一附属医院就诊的65例涎腺肿块患者,对49例涎腺混合瘤患者49个肿块及16例Warthin′s瘤患者的21个肿块进行超声造影检查,获得肿块及周边正常涎腺组织的时间-曲线（TIC）,记录并分析达峰时间（TTP）、曲线下面积（AUC）、峰值强度（PI）和峰值半降时间（TFP）等数据,并进行2组间比较分析。手术病理结果及细针穿刺结果为诊断的金标准。 结果PA组和周边正常涎腺组织的TTP、AUC、PI、TFP分别为（15.23±7.20）s、（366.04±121.59）dB.s、（7.88±2.19）dB、（37.66±11.98）s和（14.76±5.97）s、（319.82±127.46）dB.s、（6.97±2.38）dB、（41.53±15.11）s,两者比较,差异无统计学意义（t=0.352、1.836、1.970、-1.408,P均>0.05）,PA于注射造影剂后呈等进等退、不均匀性等增强;Warthin′s瘤组与周边正常涎腺组织的TTP、AUC、PI、TFP分别为（20.57±5.64）s、（548.42±320.22）dB.s、（8.480±1.94）dB、（61.64±23.64）s和（22.07±6.54）s、（346.98±279.68）dB.s、（6.01±2.51）dB、（47.61±16.40）s,两者比较,除TTP之外,差异均有统计学意义（t=6.299、5.658、4.697,P均<0.05）,Warthin′s瘤为等进慢退、高增强。以慢进和高增强鉴别诊断两者的敏感度、特异度、准确度分别为85.7%（18/21）、69.4%（34/49）、74.2%（52/70）和90.4%（19/21）、42.9%（21/49）、57.1%（30/70）。 结论注射造影剂后,涎腺PA表现为等进等退、不均匀性等增强,而Warthin′s瘤表现为等进慢退、高增强,应用后者的特点对Warthin′s和PA进行鉴别诊断具有较高的敏感度。     

超声造影诊断富血供的涎腺多形性腺瘤与Warthin瘤的价值

目的 研究涎腺高增强的多形性腺瘤(PA)与Warthin瘤的超声造影特征,旨在提高超声造影技术诊断两类肿瘤检测准确度.方法 收集61个病灶的PA与Warthin瘤的高增强超声造影定性特征及时间-强度曲线(TIC),分析并比较其定性特征和参数特征.结果 高增强的PA多呈向心性不均匀高增强,周边呈不规则增强环;Warthi...     

超声造影对涎腺肿块定性诊断的初步研究

目的 探讨超声造影对涎腺肿块定性诊断的价值.方法 采用超声造影剂SonoVue静脉团注观察78个涎腺肿块的超声造影表现,并与手术病理对照.结果 78个涎腺肿块中多形性腺瘤29个(37.2％),Warthin's瘤19个(24.4％),基底细胞腺瘤7个(8.9％),其他良性肿块11个(14.1％),恶性肿瘤12个(15.4％).以肿块呈低增强、增强后边界清楚、周边有完整的增强环、肿块无增大为良性肿块的诊断标准,其准确性为87.2％,敏感性为95.2％,特异性为56.3％,阳性预测值89.4％,阴性预测值75.0％,阳性似然比2.178,阴性似然比0.085.对涎腺发病率最高的三种良性肿瘤即多形性腺瘤、Warthin's瘤、基底细胞腺瘤超声增强表现进行两两比较,多形性腺瘤与Warthin' s瘤、基底细胞腺瘤差异有统计学意义(P＜0.01);而Warthin's瘤与基底细胞腺瘤差异无统计学意义(P＞0.05).结论 涎腺肿块超声造影表现有助于涎腺肿块的鉴别诊断.     

大涎腺腺样囊腺癌的常规超声及超声造影特征

目的探讨大涎腺腺样囊腺癌(ACC)的常规超声、超声造影特征,为临床早期诊断提供依据。方法收集2010年1月至2015年12月因颌面部肿块就诊于浙江省肿瘤医院头颈外科,后经手术及病理证实的17例大涎腺ACC患者的常规超声及超声造影特征。结果 17例大涎腺ACC来源于颌下腺者12例(70.6%),腮腺者5例(29.4%)。病程3~240个月,平均病程为(42.9±62.1)个月。原发14例(82.4%),复发3例(17.6%),复发时间为36~132个月,平均复发时间为(70.7±43.2)个月。9例(52.9%)患者伴面颊部疼痛,1例合并嘴角偏斜,1例合并张口受限,1例合并舌活动障碍。17例均为形态欠规则的低回声结节,3例(17.6%)回声均匀;14例(82.4%)回声不均。11例肿块(64.7%)边界清晰,6例(35.3%)边界不清。4例(23.5%)肿瘤内未见明显血流信号(0级),11例(64.7%)肿瘤内血流信号Ⅰ~Ⅱ级,2例(11.8%)Ⅲ级。大涎腺ACC超声造影均表现为快进、向心性、高增强,增强不均匀,内可见低增强、无增区,增强后边界不清晰。17例ACC均累犯面神经,其中3例(17.6%)合并舌神经侵犯;4例(23.5%)合并脉管瘤栓;4例(23.5%)浸润横纹肌组织;1例合并下颌骨受累;1例(5.9%)合并颈部淋巴结转移。16例(94.1%)组织病理类型为筛孔型,1例(5.9%)为实质型。结论大涎腺ACC更易发生于颌下腺,面神经侵犯率高,常伴有面颊部疼痛及面神经功能障碍。ACC常规超声具有一定的特征性,超声造影具有涎腺恶性肿瘤特征,同时结合其临床特征表现,能显著提高大涎腺的超声诊断率。大涎腺ACC术后远期复发率高,应长期超声随访。     

胰腺实性假乳头状瘤的超声及超声造影表现

目的 探讨胰腺实性假乳头状瘤的超声及超声造影表现.方法 分析20例经手术病理证实的胰腺实性假乳头状瘤的超声表现,对其中4例的超声造影表现进行探讨.结果 胰腺实性假乳头状瘤多发生于年轻女性.肿瘤体积较大,边界清晰,多数有包膜.病变呈囊实混合或呈实性肿块.少数病例可见较粗大钙化.肿瘤可发生于胰腺的任何部位,但以胰头多见.4例造影病例于动脉相肿物边缘均可见包膜样环状等增强.其中3例动脉相肿瘤内部呈不均匀低增强伴无增强区,静脉相造影剂消退呈明显低增强;1例动脉相肿瘤内部无明显增强,病理示肿瘤组织绝大部分坏死.结论 胰腺实性假乳头状瘤有其特征性的超声和超声造影表现,超声造影能更准确地反映其组织学特征.     

肌内黏液瘤超声影像特征

目的观察并分析肌内黏液瘤的超声表现特征。方法回顾性分析8例经手术病理证实的肌内黏液瘤的二维及CDFI超声表现特征,并进行文献复习。结果 8例肌内黏液瘤中,5例位于下肢肌肉,2例位于上肢肌肉,1例位于腰大肌;8例均表现为边界清楚,形态规则的肿块,后方回声增强,内部为不均匀弱回声,6例肿块内可见片状无回声区。8例肿块周边均有"亮环征",7例可见"亮帽征"。CDFI显示6例肿块内无血流,2例部分区域内见点线状血流信号。结论肌内黏液瘤好发于四肢骨骼肌,超声表现特征为边界清楚,形态规则,后方回声增强,内部为不均匀弱回声、可见片状无回声区,周边可见"亮环征"及"亮帽征",内部血流多不丰富。     

CEUS鉴别诊断涎腺良恶性病变

目的 探讨CEUS对涎腺良恶性病变的鉴别诊断价值。方法 对87例涎腺病变患者进行CEUS检查,其中良性肿瘤74例,恶性肿瘤13例,观察肿块的增强均匀程度、增强模式、增强边界、增强环和增强后肿块范围,根据肿块及周边腺体组织的时间-强度曲线分析肿块的增强程度、达峰方式和消退方式。比较涎腺良恶性肿瘤间的差异。结果 涎腺良恶性病变间增强程度、增强模式、增强均匀程度、达峰方式及消退方式的差异均无统计学意义（P均 ≥ 0.05）,两者间增强边界、增强环及增强后肿块范围差异均有统计学意义（P均<0.01）。联合应用增强边界、增强环及增强后肿块范围,其鉴别诊断涎腺良恶性病变的敏感度、特异度和准确率为84.62%（11/13）、95.95%（71/74）和94.25%（82/87）。结论 涎腺恶性病变CEUS的主要特征是增强后无完整增强环、增强边界不清、增强后肿块范围增大,三者联合应用对涎腺良恶性病变具有较高的诊断效能。     

胃间质瘤超声表现一例

患者女，33岁。胃部不适5年，偶然发现并触及胃区肿物半个月就诊。超声检查于胃体小弯侧可见不均匀低回声肿块，边界清晰，大小约54mm×50mm，肿块的胃腔侧可见一内凹，宽10mm，深9mm，表面不光滑。超声提示：胃壁实性肿块（胃间质瘤伴溃疡，图1）。     

乳腺导管乳头状瘤的超声图像与超声造影对照分析

目的 观察乳腺导管乳头状瘤的超声图像及超声造影特征,探讨该技术对乳腺导管乳头状瘤的诊断价值.方法 对52例乳头状瘤患者的超声图像特征进行观察,选用SonoVue超声造影剂,对其中13例进行彩色多普勒实时超声造影,对肿块的高频超声图像及造影增强形态、强度及造影时间-强度曲线特征进行了观察,并与病理进行对照.结果 乳头状瘤高频超声图像具有特征性,大体可分为3型,Ⅰ型:导管扩张伴导管内实性肿块及肿块周围有扩张的导管型;Ⅱ型:囊实肿块型;Ⅲ型:实性肿块型,可表现为边界不规则的低回声及边界欠清呈蜂窝状的实质肿块,超声造影多数表现为较均匀及整体性高增强,时间-强度曲线呈快上快下型;结论乳头状瘤超声图像及超声造影具有特征性表现,并与病理学基础有关,两者结合能提高诊断符合率.     

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。