侧脑室中央性神经细胞瘤CT和MRI误诊与鉴别

目的 分析侧脑室中央性神经细胞瘤的ＣＴ和ＭＲＩ表现。方法 回顾性分析经手术病理证实的中央性神经细胞瘤５例,男３例,女２例,年龄２０岁－４４负,平均年龄３0.4岁,ＣＴ检查３例,ＭＲＩ检查４例。结果 肿瘤位于侧脑室内前２／３,边界清楚,ＣＴ平扫呈略高密度,增强扫描肿瘤增强不明显,ＭＲＩ表现为略短Ｔ１,略长Ｔ２信号,本组５例中,３例误诊为室管膜瘤,２例误诊为星形胶质细胞瘤。结论 中央性神经细胞瘤影像学有特征性表现,ＣＴ和ＭＲＩ是该病有效的检查手段,侧脑室前２／３处发生的肿瘤,鉴别诊断应考虑到中央性神经细胞瘤。     

小脑半球肿瘤的ＣＴ诊断

目的：提高小脑半球各肿瘤ＣＴ诊断的正确性。材料与方法：对７０例经手术及病理证实的小脑半球肿瘤ＣＴ表现进行回顾性分析总结。结果：７０例中星形细胞瘤２９例,血管母细胞瘤１６例,转移瘤１５例,脑膜瘤５例,髓母细胞瘤３例,室管膜瘤１例,畸胎瘤１例,本文ＣＴ对小脑半球肿瘤的定位诊断率为１００％,定性诊断率为８６％。结论：根据ＣＴ表现,结合临床表现,绝大多数小脑半球肿瘤可作出正确诊断。     

听神经瘤的低磁场MRI诊断

听神经瘤的低磁场ＭＲＩ诊断万建国听神经瘤是颅神经瘤中最常见的一种，在颅内肿瘤中仅次于胶质瘤，脑膜瘤及垂体瘤。占颅内肿瘤的８％，占桥脑角肿瘤的８０％。本病除了常规影像学检查外，由于ＭＲＩ的高对比度和无创伤以及无骨伪影影响等特点，使其成为诊断听神经瘤最为...     

血管母细胞瘤35例的影像学分析

目的：探讨血管母细胞瘤的影像诊断,材料与方法：回顾性分析３５例经手术病理证实的血管母细胞瘤的ＣＴ和ＭＲＩ表现分析肿瘤的影像特点,结果：多数肿瘤（８０％）,为囊性,表现为脑脊液样密度或信号,囊壁上附有小结节,增强扫描呈明显均一强化,ＭＲ较ＣＴ更易发现小结节,少数（２０％）,表现为实质性肿块,部分合并囊变,结论ＣＴ和ＭＲＩ是诊断血管母细胞瘤的有效方法,对囊性肿瘤可作为定性诊断。     

颈动脉体瘤的综合影像诊断

目的：探讨劲动脉体瘤的超声、ＣＴ、ＭＲＩ、血管造影影像学表现及诊断价值。材料与方法,９例颈本瘤中５例经手术病理证实,４例经血管造影证实,其中２例为双侧。回顾性分析颈动脉体瘤的各种影像学表现,评价其临床价值。结果：各种检查均可显示肿瘤部位及其形态,颈动脉体瘤的Ｂ超超声特点为中等低实质回声,大于３．０ｃｍ的肿瘤可见管道结构,但肿瘤上级观察欠清,２例行彩色多普勒超声显示瘤内网状血管,ＣＴ增强显示为富血管     

髓外硬膜下肿瘤的常规和动态增强MRI研究

目的探讨常规和动态增强ＭＲＩ对髓外硬膜下肿瘤的组织学诊断和肿瘤富血管度的评价。方法使用１０ＴｅｓｌａＭＲＩ系统（ＭａｇｎｅｔｏｍＩｍｐａｃｔ,Ｓｉｅｍｅｎｓ）对１１４例髓外硬膜下肿瘤进行常规扫描,对常见肿瘤（神经鞘瘤、神经纤维瘤、脊膜瘤）的ＭＲＩ征象进行等级相关和回归系数分析,同时对２３例肿瘤进行ＳＥ（２００／１５）序列动态增强扫描,分析ＣＥＲＴ曲线类型。结果得出常见肿瘤的鉴别诊断偏回归方程式,回代结果表明诊断正确率为８１３％。ＣＥＲＴ曲线Ⅰ、Ⅱ、Ⅲ型多见于血管母细胞瘤和脊膜瘤,Ⅳ、Ⅴ型多见于神经类肿瘤。结论常规ＭＲＩ能鉴别大多数髓外硬膜下肿瘤的性质,动态增强ＭＲＩ有助于肿瘤定性诊断和肿瘤富血管度的评价。     

血管母细胞瘤和血管母细胞性脑膜瘤的病理研究

对９例血管母细胞瘤和６例血管母细胞性脑膜瘤作比较研究。９例血管母细胞瘤均为发生于小脑的良性肿瘤，内皮细胞和间质细胞ＦⅧＲＡ阳性，间质细胞ｖｉｍｅｎｔｉｎ强阳性。６例血管母细胞性脑膜瘤，３例位于大脑，１例位于小脑，２例位于脊椎；其中５例肿瘤有不同程度的间变，３例肿瘤呈浸润性生长；瘤细胞ｖｉｍｅｎｔｉｎ强阳性，其中２例瘤细胞ｋｅｒａｔｉｎ阳性。大多数血管母细胞性脑膜瘤组织病理学改变和生物学特性与软组织血管外皮瘤相似，提示其可能为来自脑脊膜血管的血管外皮细胞瘤。     

肾上腺偶发瘤的CT和MRI评价

肾上腺偶发瘤的ＣＴ和ＭＲＩ评价王东①王振祥②徐家兴①肾上腺偶发瘤是指无症状和体征而偶然发现的肾上腺占位性病变，肿瘤的检出和组织特性的确定主要依靠影像学检查。作者收集了３１例肾上腺偶发瘤，对其ＣＴ和ＭＲＩ征象进行分析，旨在探讨ＣＴ和ＭＲＩ的诊断价值。１...     

晚期嗅神经母细胞瘤的影像学诊断

嗅神经母细胞瘤是鼻腔内罕见的神经源性肿瘤。本文回顾性分析５例经病理证实的嗅神经母细胞瘤的ＣＴ和ＭＲＩ影像资料,并结合文献评价了ＣＴ和ＭＲＩ的诊断价值。１材料与方法 本组５例中,男２例,女３例,年龄３９～６３岁,平均５５．３岁。 ２例用岛津 ＳＣＴ ５０００Ｔ全身 ＣＴ机扫描, １例用岛津ＳＣＴ １００头部ＣＴ扫描,层厚、层距均为１０ｍｍ,ＣＴ增强扫描时,静脉注射６０％泛影葡胺６０ｍｌ。另外２例使用Ｐｈｉｌｉｐｓ Ｇｙｒｏｓｃａｎ ＮＴ ０．５Ｔ超导磁共振成像系统 ＳＥ序列扫描, Ｔ１ＷＩ ＴＲ＝４５６～４８…     

颅内混合瘤的CT表现与病理、超微结构和免疫组化研究

胶质母细胞瘤和纤维肉瘤、血管内皮瘤的混合瘤少见。本文 10例颅内混合瘤系经ＣＴ检查 ,并经手术、病理确诊 ,现在报告如下。1　资料与方法　　 10例中 ,男 6例 ,女 4例。年龄 8～ 6 4岁 ,平均 37.2岁。 10例均经ＣＴ检查 ,先平扫 ,后行增强检查。增强剂使用 6 0 %泛影葡胺、优维显 2 0 0 370型。扫描层厚 10ｍｍ ,间隔 5～ 10ｍｍ。ＣＴ机为日立颅脑ＨＦ型、日立Ｗ 4型、岛津 5 0 0 0ＴＸ型。 10例肿瘤均经手术病理证实。其中 1例两次肿瘤手术。肿瘤切片用ＨＥ染色 ,光镜观察。取 7例肿瘤组织按常规电镜制样 ,用ＪＥＭ 10 0Ｂ透射电镜观察…     

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.     

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。     

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.     

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。