肝棘球蚴病的CT诊断(附138例报告)

本文报告了138例经手术病理证实的肝包虫病的CT表现,包括103例肝细粒棘球蚴病和35例肝泡状棘球蚴病。两型包虫病的CT表现各有其特征:前者表现为边缘光滑、密度均匀的囊肿,CT值近于水。而囊壁的显示及钙化、子囊出现和囊膜剥离征象则具有特征性;后者的CT特点为不规则的低密度灶内常伴钙化、病灶中心液化坏死,周边部见到小囊泡,邻近肝边缘收缩内陷,健叶代偿性肥大,其中以小囊泡征象和钙化最为重要,文章着重讨论了本病CT表现的病理基础。     

肝包虫病的CT和MR诊断

目的 探讨肝包虫病的CT和MRI表现.方法 临床手术、病理证实的肝包虫病42例,就其CT和MRI表现回顾性分析并就相关文献进行复习.结果 本组肝细粒棘球蚴病占85.71%,蛋壳样或条带状钙化、"囊内囊"、"飘带征"等为其主要表现;肝泡球蚴病占14.29%,钙化、"小泡征"、"半岛征"及囊腔或液化、坏死等为其主要表现;MR T2WI显示囊壁及纤维间隔、飘带征等优于CT,但钙化显示逊于CT.结论 CT和MR均可诊断肝包虫病,CT在综合诊断方面优于MR.     

肝脏泡状棘球蚴病的CT诊断探讨

目的通过对肝脏泡状棘球蚴病患者CT检查、随访，探讨CT对肝脏泡状棘球蚴病的诊断价值。方法回顾性分析14例经生化检查、手术及病理检查结果证实的肝脏泡状棘球蚴病的CT表现。结果14例肝脏泡状棘球蚴病患者CT检查①平扫肝实质内均见低密度实性占位，边缘模糊。②病灶内均见散在颗粒状钙化，分布呈地图状、放射状，部分钙化灶可相互融合。散在颗粒状钙化征象在CT诊断泡状棘球蚴病中具有特异性。③CT增强检查病灶均无强化改变。具有②、③特征可对肝脏泡状棘球蚴病做出定性诊断。结论CT对肝脏泡状棘球蚴病的诊断有较大价值。     

CT诊断肝脏包虫病的价值及误诊分析

目的：探讨CT检查在肝脏包虫病诊断中的价值,并进行误诊分析。方法：收集经病理证实的18例肝脏包虫病病例,并以术后病理结果为金标准,回顾分析患者的CT影像特点,并评估CT检查诊断肝脏包虫病的价值。结果：18例肝脏包虫病患者中,经CT检查准确诊断者为14例,CT诊断准确率为77.8%,另4例患者分别被误诊为肝囊肿2例,血管瘤1例,肝癌1例。肝细粒棘球蚴病患者为17例,其中单纯囊肿型9例,CT图像上表现为肝内囊性低密度灶,单发或多发,呈圆形或类圆形,其中2例可见囊壁弧形或蛋壳样钙化,长短、厚薄不一;1例囊内钙化,CT图像上表现为类圆形或球形钙化灶;1例为多发钙化,既可见囊壁钙化型,也可见球形钙化灶型;含子囊型6例,表现为囊中囊、轮状或蜂窝状改变;混合型1例,可见钙化型病灶及含子囊型病灶。合并感染后,患者的CT表现为囊内密度增高,囊壁增厚。肝泡状棘球蚴病患者1例,CT平扫表现为密度不均匀,边界模糊的斑片低密度影,并伴肺播散,该例CT表现为肝内病灶范围广泛、两肺多发类似病灶,被误诊为原发性肝癌伴两肺转移。另有2例患者的CT表现为病灶单发囊性病灶,无囊壁,增强CT图像上未见强化,被误诊为肝囊肿;1例患者的CT表现可见球形钙化,被误诊为硬化性血管瘤。结论：CT检查能准确显示肝包虫病的类型、发生部位、范围和程度,但表现为单纯囊肿型时,需要与肝囊肿鉴别;肝泡状棘球蚴病的影像学表现复杂,需与原发性肝癌鉴别。     

超声显像诊断40例包虫病和介入治疗

人体包虫病常见的有细粒棘球蚴病和泡状棘球蚴病,前者远多于后者,包虫病为畜牧区危害人民健康的常见寄生虫病之一,内蒙古地区也有流行.本文对40例包虫病患者进行分析和治疗,现报告如下.     

B超在腹部包虫病鉴别诊断中的应用

包虫病是一种人畜共患的寄生虫病，根据其流行病学、形态学、形态病理、临床过程及转归等，国内将此分为两种类型：一种由细粒棘球绦虫的囊性包虫病和由多房(泡状)棘球绦虫所致的泡状棘球蚴病(泡型包虫病)。根据国内外献报道及我院统计，以囊型包虫病居多。本组均为囊性病，报道如下。     

超声在筛检大鼠肝泡状棘球蚴病模型中的应用价值

目的 评价超声在筛检大鼠肝泡状棘球蚴病模型中的应用价值.方法 采用经皮肝脏穿刺注射泡状棘球蚴组织混悬液的方法,制备原发性HAE模型,40只Wistar大鼠接种6个月后行B超检查及开腹探查.结果 B超检查示21只大鼠感染泡状棘球蚴,19只未感染,感染率52.50%.开腹探查证实B超检查21只阳性中1只未感染,19只未感染中1只为阳性.B超检查的灵敏度为95.24%,特异性为94.74%,假阳性率为4.27%,假阴性率5.27%.结论 B超检查诊断大鼠肝泡状棘球蚴感染的灵敏度及特异度均较高,可做为一种无创性筛选大鼠肝泡状棘球蚴感染的方法.     

泡型包虫病脑转移的MRI特征

目的 探讨泡型包虫病脑转移的MRI特征,提高对该病的认识。方法 20例脑转移性泡型包虫病均行MRI、CT、B超和实验室检查,经临床手术病理证实,资料完整。结果 20例脑转移性泡型包虫病,均有原发肝泡型包虫病史,其中12例曾行手术治疗,8例行B超引导下肝穿刺治疗或活检;20例中,单发病灶4例（20%）,多发病灶16例（80%）;合并肺转移6例,肾和肾上腺转移3例。MRI表现为类圆形或不规则形多发聚集的小囊泡样改变,断面呈＂蜂窝状＂,T1WI和T2WI均以低信号为主。病灶周围伴有明显水肿。4例于肝静脉和门静脉内显示＂泡球蚴＂栓子。结论 颅脑是泡型包虫病最好发生转移的部位之一。MRI＂蜂窝状＂小囊泡样改变,T1WI和T2WI均为低信号是其特征性表现。     

高强度聚焦超声波杀伤小鼠体内细粒棘球绦虫棘球蚴的声像变化

目的探索高强度聚焦超声波（high intensity focused ultrasound,HIFU）对动物体内细粒棘球绦虫棘球蚴的杀伤作用。方法用采自感染包虫病羊肝内的原头节接种小鼠腹腔,建立小鼠棘球蚴病模型。用一定剂量的HIFU照射小鼠腹腔棘球蚴后,B超观察HIFU杀伤棘球蚴的破坏作用并测量照射区域灰度值。结果HIFU对棘球蚴有明显的急性杀伤作用,随着HIFU照射时间延长,HIFU治疗时B超图像改变,囊腔边界渐模糊,囊内逐渐模糊,回声增强。在一定的照射强度下,随着照射时间的延长,灰度值逐渐减少。结论高强度聚焦超声破坏小鼠体内棘球蚴,B超声像图及灰度值证明其改变。     

左肺泡状棘球蚴病1例报告

棘球蚴病分二种类型,一是多见的由细粒棘球绦虫所引起的棘球蚴病;二是较少见的由多房性棘球绦虫所致的泡状棘球蚴病。泡状棘球蚴病以发生在肝脏多见,但少数原发性病变也可发生在脑、肺、脾、肾等处。我院于去年曾收住1例肺泡状棘球蚴病,现报     

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。