福辛普利对急性心肌梗死患者早期校正后QT间期离散度的影响

目的：探讨福辛普利对急性心肌梗死（ＡＭＩ）患者早期校正后ＱＴ间期离散度（ＱＴｃｄ）的影响。方法：对３０例ＡＭＩ患者随机单盲分福辛普利治疗组（１５例）和对照组（１５例）,并对治疗前和３ｄ后ＱＴｃｄ、室性心律失常发生率（ＶＡＭ）进行对比分析。结果：ＡＭＩ患者ＱＴｃｄ较正常人明显延长（Ｐ＜０．０１）,伴室性心律失常组较无心律失常组明显延长（Ｐ＜０．０５）;３ｄ后治疗组ＱＴｃｄ、ＶＡＭ较治疗前明显降低（均Ｐ＜０．０１）,对照组ＱＴｃｄ、ＶＡＭ虽亦有下降趋势但较３ｄ前无显著差异（均Ｐ＞０．０５）,治疗组明显低于对照组（Ｐ＜０．０５）。结论：福辛普利可能通过降低ＱＴｃｄ而降低ＶＡＭ,提示血管紧张素转换酶抑制剂降低ＡＭＩ早期病死率可能有该机制参与。     

福辛普利对急性心肌梗死患者早期校正后QT间期离散度的 …

目的 探讨福辛普利对急性心肌梗死（ＡＭＩ）患者早期校正后ＱＴ间散离散度（ＱＴｃｄ）的影响。方法 对３０例ＡＭＩ患者随机单盲分福辛普利治疗组（１５例）和对照组（１５例）,并对治疗前和３ｄ后ＱＴｃｄ、室性心律失常发生率（ＶＡＭ）进行对比分析。结果 ＡＭＩ患者ＱＴｃｄ较正常人明显延长（Ｐ〈０．０１）,伴室性心律失常组较无心律失常组明显延长（Ｐ〈０．０５）;３ｄ后治疗组ＱＴｃｄ、ＶＡＭ较治疗前明显降低（均     

紫外线照射充氧自血回输综合治疗缺血性脑血管病30例

目的：研究紫外线照射充氧自血回输治疗（ＵＢＩＯ）和抗栓酶治疗缺血性脑血管病疗效机制。方法：应用ＵＢＩＯ和抗栓酶治疗缺血性脑血管病３０例，治疗前后观察患者临床表现及血液流变学、血脂、脑血流图变化。结果：治疗后症状、体征明显好转，血液流变学、血脂各项指标明显下降（Ｐ〈０．０５￣０．０１），脑血流图指标改善（Ｐ〈０．０５￣０．０１）。结论：ＵＢＩＯ并抗栓酶疗法具有降低血粘度、血脂、提高血氧孢和度和氧分压     

紫外线照射充氧自血回输治疗血粘血症

采用紫外线照射充氧自血回输法（ＵＢＩ）治疗１２０例高粘血症，同时用常规药物（丹参，低分子右旋糖酐，７０６代血浆）疗法治疗１１８例高粘血症患者对照。结果显示：治疗组治疗前后血液流变学各项指标均有显著性差异（Ｐ〈０．０５）或非常显著性差异（Ｐ〈０．０１）；有效率９１．７５％，与对照组比较有非常显著性差异（Ｐ〈０．０１）。表明ＵＢＩ为治疗高粘血症的有效新途径。     

紫外线照射充氧自血回输疗法治疗慢性活动性乙型肝炎观察

采用紫外线照射充氧自血回输疗法（ＵＢＩＯ）治疗慢性活动性乙型肝炎６０例，治疗４周及８周后治疗组症状、体征改善均优于对照组（Ｐ〈０．０５，Ｐ〈０．０１），总胆红质、谷丙转氨酶及免疫球蛋白下降率差异有非常显著性（Ｐ〈０．０１），总胆红质、谷丙转氨酶在治疗４周或８周恢复正常的例数均高于对照组（Ｐ〈０．０５，Ｐ〈０．０１）。该方法可明显地降低血液粘稠度，改善微循环，增加血氧饱和度，调节免疫功能，并能有效地     

急性白血病化疗后输注紫外线照射充氧血液的临床观察

目的：研究紫外线照射充氧血液输注（ＵＢＩＯ）在急性白血病化疗中的作用。方法：３８例急性白血病患者随机分为两组，在化疗后分别输紫外线照射的充氧血液和非照射的血液。结果：ＵＢＩＯ组患者白细胞和血小板在化疗后第二周较对照组有明显升高（Ｐ〈０．０１），化疗后的不充反应症状明显改善，出血感染发生率减少，３０天化疗间歇期的输血量由非照射时的２．８次×４０ｍｌ降为２．１次×４００ｍｌ（Ｐ〈０．０５）。治疗后１个     

紫外线照射充氧自血回输治疗慢性肺心病血液高凝状态的研究

应用紫外线照射充氧自血回输（ＵＢＩＯ）治疗慢性肺心病血液高凝状态５６例，另以５６例作对照。结果表明，总有效率ＵＢＩＯ组为９３％，对照组为７１％，两组差异有显著性（Ｘ２＝４．３８，Ｐ＜０．０５）．ＵＢＩＯ组凝血时间、红细胞压积、纤维蛋白原定量、纤维蛋白降解产物、抗凝血酶ＩＩＩ异常变化的改善比对照组明显（Ｐ＜０．０５），全血粘度、血浆粘度、红细胞变形和球结膜微循环的血管形态、周围状态及总积分改善非常显著（Ｐ＜０．０１），ＰａＣＯ２下降，ＰａＯ２，ＳａＯ２上升非常显著（Ｐ＜０．０１～０．００１），对照组改善不明显（Ｐ＞０．０５）．     

紫外线照射充氧自血回输并的治疗白塞综合征

目的 探讨紫外线照射充氧自血回输（ＵＢＩＯ）治疗白塞综合征（ＢＳ）的作用机制。方法动态观察２２例ＢＳ患者ＵＢＩＯ治疗前后血流变学、超氧化物歧化酶（ＳＯＤ）、谷胱甘肽过氧化物酶、脂质过氧化物（ＬＰＯ）、丙二醛（ＭＤＡ）、过氧化氢酶（ＣＡＴ）、肿瘤坏死历子（ＴＮＦ）、白细胞亚结构的变化,以药物治疗的１１例ＢＳ患者为对照组作疗效比较。结果 ＵＢＩＯ后ＢＡＳ患者血中ＳＯＤ、ＧＳＨｐｘ、ＣＡＴ含量较治疗前明     

紫外线照射充氧自血回输疗法对急性脑血管病病灶的影响

目的：观察紫外线照射充氧自血回输疗法（ＵＢＩＯ）治疗急性脑血管病对患者颅内病灶的影响。方法：对经ＵＢＩＯ治疗的患者５８例和对照组５２例，进行治疗前后头颅ＣＴ病灶体积缩小差值比较。结果：脑梗塞ＵＢＩＯ组２６例，对照组２２例，治疗前后颅内病灶体积缩小差值，两组间差异有非常显著性（Ｐ＜０．０１）。脑出血ＵＢＩＯ组３２例，对照组３０例，治疗前后颅内病灶体积缩小差值，两组间差异有显著性（Ｐ＜０．０５）；颅内血肿体积缩小差值，两组差异有显著性（Ｐ＜０．０５）。结论：ＵＢＩＯ有助于急性脑血管病患者颅内病灶的吸收与缩小。     

急性心肌梗塞患者QT离散度的测定及其临床意义

为了观察急性心肌梗塞（ＡＭＩ）病人ＱＴ离散度（ＱＴｄ）的变化,我们测定了２５例ＡＭＩ患者的ＱＴｄ、心率校正ＱＴ离散（ＱＴｃｄ）和改良心率校正ＱＴ离散度（ＱＴＬｃｄ）,并与２５例正常对照比较,发现ＡＭＩ组上述三个指标均明显高于对照组（Ｐ＜０．００１）,且ＡＭＩ随病情好转,上述三个指标也明显下降（Ｐ＜０．００１）,同时发现ＡＭＩ有室性心律失常组较无室性心律失常组上述三个指标明显增高（Ｐ＜０．０１）。提示ＱＴ离散度可作为ＡＭＩ疾病转归及预测室性心律失常的指标。     

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。