电针结合磁刺激对脑缺血大鼠脑组织含水量和细胞外钙离子浓度的影响

目的 观察电针结合磁刺激对急性脑缺血大鼠脑组织含水量和细胞外钙离子含量的影响。方法 将30只雄性Wistar大鼠随机分成5组：正常组、模型组、电针组、磁刺激组和电针加磁刺激组，每组6只。制作急性大脑中动脉缺血模型，分别施以电针、磁刺激和电针加磁刺激，检测脑组织含水量和局部细胞外钙离子浓度。结果 单纯电针或磁刺激均能降低脑组织含水量和遏止细胞外钙离子浓度降低，而2者合用效果更优。结论 电针结合磁刺激能较好地改善急性脑缺血大鼠脑组织水肿和良性调节细胞外钙离子浓度。     

电针联合经颅磁刺激对急性脑缺血大鼠VEGF及其受体Flk-1表达的影响

目的观察电针联合经颅磁刺激对急性脑缺血大鼠血管内皮生长因子(VEGF)及其受体Flk-1表达的影响.方法将25只雄性Wistar大鼠随机分成5组正常组、模型组、电针组、磁刺激组和电针加磁刺激组.制造大鼠急性大脑中动脉缺血模型后,各治疗组分别施以电针、磁刺激和电针加磁刺激处理,采用免疫组织化学方法观察不同干预方法对VEGF及Flk-1表达的影响.结果免疫组织化学染色结果显示,模型组梗死灶周围VEGF和Flk-1的表达较正常组明显增强(P＜0.05);电针组、磁刺激组和电针加磁刺激组VEGF和Flk-1的表达与模型组比较,均明显增强(P＜0.05),尤以电针加磁刺激组为明显(P＜0.01).结论电针或磁刺激治疗均可增强急性脑缺血大鼠梗死灶周围VEGF和Flk-1的表达,从而减轻缺血后脑损伤,促进脑功能的康复,二者联合应用疗效更佳.     

电针结合经颅磁刺激对脑缺血大鼠VEGF164 mRNA和CD31表达的影响

目的研究电针结合经颅磁刺激对急性脑缺血大鼠血管生成的影响。方法将55只雄性Wistar大鼠随机分成正常组、模型组、电针组、磁刺激组和电针加磁刺激组。复制急性大脑巾动脉缺血模型，分别施以电针、磁刺激和电针加磁刺激方法处理，采用逆转录-聚合酶链反应、免疫组织化学方法，检测VEGF164mRNA及血小板内皮细胞黏附因子（CD31）的表达。结果电针绢、磁刺激组和电针加磁刺激组梗死灶周同VEGF164mRNA和CD31表达增强（P〈0．05或P〈0．01），尤其以电针加磁刺激组明最。结论电针结合磁刺激可以增强急性脑缺血大鼠梗死灶周围VEGF164mRNA和CD31的表达，从而实现非分子水平的治疗性血管生成作用。     

电针对脑缺血大鼠碱性成纤维细胞生长因子和血管生成素及其受体表达的影响

目的观察电针对急性脑缺血大鼠血管新生的影响。方法将30只雄性Wistar大鼠随机分成3组：正常组、模型组、电针组。复制急性大脑中动脉缺血模型,电针“百会”、“水沟”穴,采用免疫组织化学方法,检测碱性成纤维细胞生长因子和血管生成素2及其受体的表达。结果电针组梗死灶周围碱性成纤维细胞生长因子和血管生成素2表达增强,分别为(0．039±0．009)和(0．080±0．023),与正常组和模型组比较差异有统计学意义(P＜0．05)；而血管生成素2受体的表达虽增强,但与其他两组比较差异无统计学意义。结论电针可以增强急性脑缺血大鼠梗死灶周围碱性成纤维细胞生长因子和血管生成素2的表达,促进了梗死灶周围的血管新生。     

电针对高血压大鼠脑缺血胶质血管网络胶质原纤维酸性蛋白和血管内皮生长因子表达的影响

目的观察电针对易卒中型肾血管性高血压大鼠（RHRSP）脑缺血／再灌注（I／R）后不同时间点脑组织胶质原纤维酸性蛋白（GFAP）、血管内皮生长因子（VEGF）表达及超微结构的影响。方法夹闭SD大鼠双侧肾动脉10周使血压≥180mmHg（1mmHg=0．133kPa）制备RHRSP。将RHRSP随机分为对照组（n=12）、假手术组（n=12）、模型组（n=48）、电针组（n=48）,后两组再用线栓法制备大脑中动脉闭塞（MCAO）模型。采用免疫组化法检测脑缺血2h后再灌注1、7、14、28d脑内缺血区GFAP、VEGF表达,测定脑组织含水量,用电镜观察细胞超微结构变化。结果模型组制模后1d缺血周围半暗区出现GFAP、VEGF阳性细胞表达,均于7d达高峰,14d有所减少,28d明显减少,但仍高于对照组和假手术组（均P〈0．01）;电针组GFAP、VEGF阳性细胞表达在7、14及28d较模型组显著增加（均P〈0．05）。模型组制模后1d脑含水量明显高于对照组和假手术组（均P〈0．01）,随时间延长呈下降趋势;电针组1d、7d时较模型组明显降低（均P〈0．05）。电镜下可见电针组星形胶质细胞和血管壁超微结构较模型组明显减轻。结论电针对RHRSP脑I／R损伤的保护作用可能与增强急性脑缺血梗死灶周围GFAP、VEGF的表达,促进脑缺血区胶质血管单位重建,从而减轻缺血后脑损伤有关。     

电针结合经颅磁刺激对脑缺血大鼠碱性成纤维细胞生长因子和血管生成素及其受体表达的影响

目的:观察电针结合经颅磁刺激对急性脑缺血大鼠血管新生的影响。方法:将25只雄性Wistar大鼠随机分成5组:正常组、模型组、电针组、磁刺激组和电针加磁刺激组。复制急性大脑中动脉缺血模型,分别施以电针、磁刺激和电针加磁刺激方法处理,采用免疫组织化学方法,检测碱性成纤维细胞生长因子(bFGF)和血管生成素2(Ang-2)及其受体(Tie-2)的表达。结果:电针组、磁刺激组和电针加磁刺激组梗死灶周围bFGF、Ang-2表达增强,尤以电针加磁刺激组明显(P<0.01),而Tie-2的表达虽较正常组增高,但各治疗组之间比较差异无显著性意义。结论:电针结合磁刺激可以增强急性脑缺血大鼠梗死灶周围bFGF和Ang-2的表达,促进了急性脑缺血大鼠梗死灶周围的血管新生。     

电针对局灶性脑缺血大鼠神经细胞凋亡及神经生长因子的影响

目的探讨电针督脉经大椎、百会穴对大鼠缺血区脑组织神经细胞凋亡及神经生长因子( nerve growth factor,NGF)的影响,为临床针灸治疗缺血性脑血管疾病奠定理论基础. 方法选用健康雄性 Wistar大鼠 24只.按随机数字表法分为假手术组、缺血组、缺血+电针组,每组 8只.用凝闭一侧大鼠大脑中动脉的脑缺血大鼠为动物模型,采用 TUNEL染色法和免疫组化染色 S0-P法进行观察. 结果缺血组及缺血+电针组中每个脑片 1000个神经细胞中凋亡细胞数目分别为 676± 12及 326± 15,缺血+电针组中,大脑皮质梗死区内 TUNEL染色阳性细胞较缺血组显著减少( P< 0.01);缺血+电针组中 NGF受体免疫阳性表达在细胞数量上及强度上均较缺血组及假手术组明显增强( P< 0.01). 结论电针能抑制脑缺血后脑内神经细胞凋亡,可增强局灶性脑缺血大鼠脑组织的 NGF受体的表达,对缺血性脑损伤具有一定的保护作用.     

电针对局灶性脑缺血大鼠神经细胞凋亡及神经生长因子的影响

目的：探讨电针督脉经大椎、百会穴对大鼠缺血区脑组织神经细胞凋亡及神经生长因子(nerve growth factor，NGF)的影响，为临床针灸治疗缺血性脑血管疾病奠定理论基础。方法：选用健康雄性Wistar大鼠24只。按随机数字表法分为假手术组、缺血组、缺血+电针组，每组8只。用凝闭-侧大鼠大脑中动脉的脑缺血大鼠为动物模型，采用TUNEL染色法和免疫组化染色SO-P法进行观察。结果：缺血组及缺血+电针组中每个脑片1000个神经细胞中凋亡细胞数目分别为676&;#177;12及326&;#177;15，缺血+电针组中，大脑皮质梗死区内TUNEL染色阳性细胞较缺血组显著减少(P&;lt;0．01)；缺血+电针组中NGF、受体免疫阳性表达在细胞数量上及强度上均较缺血组及假手术组明显增强(P&;lt;0.01)。结论：电针能抑制脑缺血后脑内神经细胞凋亡，可增强局灶性脑缺血大鼠脑组织的NGF受体的表达，对缺血性脑损伤具有一定的保护作用。     

电针对脑缺血再灌注大鼠海马区胰岛素样生长因子-1表达的影响

目的 观察电针对大脑中动脉缺血再灌注大鼠缺血脑组织海马区神经细胞凋亡及胰岛素样生长因子-1（IGF—1）的影响。方法 采用大脑中动脉线栓法制备大脑中动脉闭塞（MCAO）再灌注模型，分别应用TUNEL染色法、免疫组化法观察脑缺血再灌注及电针对大鼠缺血脑组织海马区神经细胞凋亡及IGF-1的影响。结果 脑缺血再灌注后大鼠缺血侧海马CA1区凋亡细胞数显著增多（模型组与正常组、假手术组比较，P〈0．01），IGF-1阳性表达数目少量增加，胞浆染色呈轻-中度阳性（模型组与正常组、假手术组比较，P〈0．05），电针组大鼠缺血侧海马CA1区的凋亡细胞数减少，IGF-1的阳性表达数目增加，胞浆染色呈中-强阳性（电针组与模型组比较，P〈0．01）。结论 电针可降低大鼠缺血侧海马CA1区的凋亡细胞数，增强IGF-1的阳性表达；早期电针治疗对脑缺血损害的有效防治作用，可能是通过上调IGF-1表达、抑制神经元凋亡的机制实现的。     

电针治疗大鼠急性缺血性脑损伤的作用机制

目的观察急性脑缺血后及电针治疗后大鼠脑组织中电压门控型钠通道亚型Nav1.6表达,探讨电针治疗急性缺血性脑损伤的作用机制。 方法选取144只健康SD大鼠用线栓法制作大鼠脑缺血模型,按随机数字表法分为脑缺血组、电针治疗组和药物治疗组,每组48只大鼠,另取24只健康SD大鼠作为假手术组,分别于脑缺血后6h、1d、2d、3d四个不同观察时间点取材后,应用实时定量荧光聚合酶链反应（PCR）检测Nav1.6表达,荧光法检测钙离子浓度,氯化三苯四唑染色检测脑梗死体积。 结果假手术组大鼠神经功能缺损Joshua评分均为0分,余3组缺血后6h、1d和2d时的Joshua评分均呈逐渐增高趋势,但在缺血3d时的Joshua评分与组内缺血2d时比较均有所降低,且各组组内差异均有统计学意义(P<0.05)。在大鼠脑缺血后不同时间点,电针治疗组Nav1.6表达先上调然后逐渐下调,组内比较,差异有统计学意义(P<0.05);钙离子浓度亦是早期升高,后期降低,且差异均有统计学意义(P<0.05);脑梗死体积百分比增大明显,组内差异有统计学意义(P<0.05)。以大鼠脑缺血3d时为例,在大鼠脑缺血后相同时间点与假手术组、脑缺血组和药物治疗组相比,电针治疗组的Joshua评分［（2.55±0.42）分］最低,Nav1.6表达［光密度值（0.387±0.023）］下调最明显,钙离子浓度［（448.4±12.4）nmol/L］最低,脑梗死体积百分比［（22.27±1.34）%］最小,且组间差异均有统计学意义(P<0.05)。 结论电针治疗脑缺血后大鼠可抑制缺血脑组织Nav1.6的表达,减少细胞Na+内流,减少细胞内Ca2+浓度,减轻缺血脑损伤;电针治疗对急性缺血性脑损伤的保护作用可能是通过抑制Nav1.6的表达来实现。     

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。