血浆D-二聚体水平与急性脑梗死预后的相关性研究

目的探讨D-二聚体与急性脑梗死的预后的相关性。方法应用NycoCard免疫渗滤胶体金显色反应法对住院的首次急性脑梗死患者98例,32例健康对照者血浆D-二聚体进行测定。结果脑梗死组的血浆D-二聚体水平(1.696±0.298mg/L),差异有统计学意义(P<0.01)。血浆D-二聚体水平与梗死灶体积、病情轻重程度呈正相关,尤以梗死灶体积更为明显;且三者之间呈明显正相关。结论急性脑梗死(acutecerebralinfarction,ACI)患者血浆D-二聚体水平可作为判断病情及预后的客观指标。且血浆D-二聚体水平和梗死灶体积、病情轻重程度三者之间具有相关性。     

可溶性细胞间黏附分子与急性期脑梗死体积的关系

目的 检测急性脑梗死(ACI)患者可溶性细胞间黏附分子(sICAM)的水平,评价其与急性期梗死体积的相关性.方法 采用双抗体夹心酶联免疫吸附法测定165例ACI患者血清sICAM～1水平,并与58例脑出血患者和87例健康体检者对照比较.结果 ACI组24h血清slCAM-1水平C(4.73+0.26)mg/L)]明显高于脑出血组((2.81士0.18)mg/L]和健康对照组[(2.64士0.25)mg/L],直至发病后14 d仍高于脑出血组和健康对照组(P均＜0.01).大梗死组(梗死灶＞10 cm3)血清sICAM-1水平[(5.14±0.34)mg/L]明显高于中梗死组[梗死灶4～10 cm3,(4.47±0.20)mg/L)和小梗死组[梗死灶＜4 cm3,(4.12士0.28)mg/L,P均＜0.01].ACI后伴感染组在14 d内血清slCAM-1水平均明显高于不伴感染组(P＜0.05或P＜0.01).结论 血清siCAM水平的变化与ACI梗死灶的大小密切相关.     

再发脑梗死患者血浆D-二聚体与纤维蛋白原变化的临床意义

目的探讨脑再次梗死患者与初次脑梗死患者的血浆D-二聚体、纤维蛋白原的改变。方法分别对68例初次脑梗死患者及68例脑再梗死患者的血浆D-二聚体、纤维蛋白原进行测定并对不同脑再梗死体积患者血浆D-二聚体、纤维蛋白原含量进行对比。结果再次脑梗死组血浆D-二聚体、纤维蛋白原均高于初次脑梗死组（P〈0．05）；在再次脑梗死组大面积梗死灶患者血浆D-二聚体、纤维蛋白原含量明显高于中、小面积梗死灶者（P〈0．05）。结论血浆D-二聚体、纤维蛋白原的变化与脑再梗死的发生及预后有-定的关系，是再发脑梗死事件的重要危险因素。     

血清缺氧诱导因子1α和肿瘤坏死因子α及肝细胞生长因子与脑梗死的关系

目的 探讨缺氧诱导因子1α(HIF-1α)、肿瘤坏死因子α(TNF-α)及肝细胞生长因子(HGF)与脑梗死的关系.方法 入选2013年6-12月我院收治的急性脑梗死患者212例作为观察对象,根据脑梗死类型分为进展性脑梗死(PCI)组105例和稳定性脑梗死(SCI)组107例,选取同期100名健康体检人群作为对照,采用酶联免疫吸附法(ELISA)检测3组研究对象的HIF-1α、TNF-α及HGF;将PCI组患者按照神经功能或梗死病灶大小分组,比较各组间HIF-1α、TNF-α及HGF水平差异.结果 PCI组HIF-1α、TNF-α、HGF分别为(2.3±1.3) ng/L、(4.0±0.5)mg/L、(1.4±0.3)μg/L,显著高于SCI组[(1.1±0.5)ng/L、(3.1±1.3) mg/L、(0.7±0.4) μ#L]和健康对照组[(0.5 ±0.1)ng/L、(1.8±0.4)mg/L、(0.4±0.1)μ昏/L],SCI组显著高于健康对照组,差异均有统计学意义(F值分别为3.14、5.42、1.32,P均＜0.01);PCI轻度组患者HIF-1α、TNF-α、HGF分别为(0.7±0.3) ng/L、(2.9±0.3)mg/L、(0.7±0.5)μg/L,均显著低于中度组[(1.4±0.5)ng/L、(4.9±0.5)mg/L、(1.7±0.4)μg/L]和重度组[(1.4±0.5) ng/L、(4.9±0.5)mg/L、(1.9±0.4) μg/L,中度组显著低于重度组,差异均有统计学意义(F值分别为0.93、4.32、2.31,P均＜0.01);PCI小梗死灶组患者HIF-1α、TNF-α、HGF分别为(0.6 ±0.4)ng/L、(2.7 ±0.4)mg/L、(0.7±0.4)μg/L,均显著低于中梗死灶组[(1.1±0.5)ng/L、(4.4±0.5) mg/L、(1.1±0.2)μg/L]和大梗死灶组[(1.4±0.6)ng/L、(4.8±0.6)mg/L、(1.9±0.5)μg/L];中梗死灶组显著低于大梗死灶组,差异均有统计学意义(F值分别为4.71、2.09、2.45,P均＜0.01).结论 进展性脑梗死患者血清HIF-1仪、TNF-α及HGF水平明显增高,且各指标与进展性脑梗死神经功能缺损程度及梗死灶大小关系密切.     

联合检测血清D-二聚体、cTnI及Myo在急性心肌梗死中的诊断价值

目的 联合检测血清D-二聚体、肌钙蛋白I(cTnI)及肌红蛋白(Myo)在急性心肌梗死(AMI)中的诊断意义。方法 将AMI患者130例作为观察组,120例健康人作为对照组,采用日立7602生化仪检测其血清D-二聚体水平,cTnI、Myo水平均采用化学发光法进行检测,采用SPSS17.0统计软件进行数据分析。结果 AMI发病2h后血清D-二聚体、cTnI及Myo浓度分别为(1.71±0.14)mg/L、(1.18±0.28)ng/mL、(90.53±2.36)ng/mL,对照组D-二聚体、cTnI及Myo浓度分别为(0.25±0.12)mg/L、(0.10±0.02)ng/mL、(23.61±4.15)ng/mL,AMI组D-二聚体、cTnI及Myo水平明显均高于对照组,两组比较差异有统计学意义(P<0.05)。联合检测血清D-二聚体、cTnI及Myo水平,对AMI诊断的灵敏度和特异性分别高达94.65%和98.51%。结论 联合检测血清D-二聚体、TnI及Myo对AMI的诊断和治疗具有重要意义。     

D-二聚体检测在静脉血栓栓塞症诊断中的临床意义分析

目的分析D-二聚体检测在静脉血栓栓塞症诊断中的临床意义。方法选取62例本院肿瘤科的化疗患者,患者在2016年1月至2019年1月入院治疗,按照是否发生静脉血栓栓塞分组,观察组(31例)发生静脉血栓栓塞,对照组(31例)未发生静脉血栓栓塞,对比两组患者不同时段的D-二聚体检测结果。结果观察组患者入院时D-二聚体数据为(1.83±2.17)mg/L,与对照组数据差异性不显著,P>0.05;观察组入院后24h D-二聚体数据为(3.12±1.65)mg/L,出院前24h D-二聚体数据为(4.68±1.46)mg/L,其数据较之于对照组差异性显著,P<0.05。结论D-二聚体检测可用于静脉血栓栓塞症的检测诊断,D-二聚体水平越高,患者出现静脉血栓栓塞症的风险就更高,临床中应用加强对高风险患者进行D-二聚体检测。     

血清前白蛋白、胱抑素C和D-二聚体水平对超出NT-proBNP检测上限的心力衰竭患者预后的影响

目的 探讨血清前白蛋白(PA)、胱抑素C和D-二聚体水平对超出N末端B型脑钠肽前体(NT-proBNP)检测上限的心力衰竭患者预后的影响。方法 回顾性选取2018年1月至2020年12月入住衡水市人民医院治疗的超出NT-proBNP检测上限的心力衰竭患者126例。住院期间及出院后30 d随访,以是否发生全因死亡、心衰加重再出院事件将患者分为心血管事件组(n=36)与非事件组(n=90)。观察两组患者血清前白蛋白、胱抑素C及D-二聚体水平。采用二元Logistic回归分析影响心血管事件的危险因素;通过受试者工作特征(ROC)曲线分析前白蛋白、胱抑素C和D-二聚体对发生心血管事件的预测价值。结果 心血管事件组患者的血清前白蛋白水平为(126.72±61.49)mg/L,明显低于非事件组[(209.41±65.02)mg/L],胱抑素C、D-二聚体水平分别为(2.70±0.90)mg/L、(2.74±1.02)mg/L FEU,均明显高于非事件组[(1.72±0.60)mg/L、(1.67±0.81)mg/L FEU],差异均有统计学意义(P<0.05)。二元Logistic显示,前白...     

不同生化指标在脑梗死患者中的表达及对神经功能损伤程度和预后的评估价值

目的探讨D-二聚体、脂蛋白-α(LP-α)、C-反应蛋白(CRP)及同型半胱氨酸(Hcy)在脑梗死(CI)患者中的表达及其价值。方法选择2019年5—12月徐州医科大学附属第三医院收治的100例CI患者作为CI组;另选同期健康体检者100例作为健康对照组。采用胶乳免疫比浊法测定两组血清D-二聚体,采用免疫比浊法测定LP-α,采用干式免疫散射色谱法测定CRP,采用循环酶法测定Hcy水平。再根据美国国立卫生研究院卒中量表(NIHSS)评分将CI组患者分为轻度损伤组(NIHSS评分≤7分)和重度损伤组(NIHSS评分7分),比较不同亚组患者D-二聚体、LP-α、CRP、Hcy水平的差异;对CI组患者随访2个月,根据改良Rankin量表(mRS)评分分为预后良好组(mRS评分≤2分)和预后不良组(mRS评分≥3分),比较不同预后两组患者D-二聚体、LP-α、CRP、Hcy水平的差异。分析D-二聚体、LP-α、CRP、Hcy与NIHSS、mRS评分的相关性。结果 CI组D-二聚体、LP-α、CRP、Hcy水平均明显高于健康对照组〔D-二聚体(mg/L):2.64±0.69比0.76±0.18,LP-α(mg/L):306.15±34.29比122.38±13.84,CRP(mg/L):22.15±6.19比5.04±0.73,Hcy(μmol/L):18.65±3.61比6.07±1.82〕。CI重度损伤组D-二聚体、LP-α、CRP、Hcy水平均明显高于轻度损伤组〔D-二聚体(mg/L):3.49±0.72比2.01±0.56,LP-α(mg/L):417.54±53.51比201.46±27.08,CRP(mg/L):27.48±6.85比16.92±3.71,Hcy(μmol/L):23.15±4.05比15.85±3.29〕。预后不良组D-二聚体、LP-α、CRP、Hcy水平均明显高于预后良好组〔D-二聚体(mg/L):4.18±0.75比1.68±0.31,LP-α(mg/L):476.49±60.51比163.72±23.19,CRP(mg/L):32.57±6.91比11.43±2.64,Hcy(μmol/L):24.96±4.15比13.04±3.17〕,差异均有统计学意义(均P0.01);Pearson相关性分析显示,D-二聚体、LP-α、CRP、Hcy与NIHSS、mRS评分均呈正相关(NIHSS评分:r值为0.635、0.708、0.431、0.454,P值为0.013、0.007、0.029、0.021;mRS评分:r值为0.865、1.054、0.713、0.672,P值为0.000、0.000、0.005、0.009)。结论 D-二聚体、LP-α、CRP、Hcy在CI患者中呈高水平表达,可为CI诊断提供指导,并对神经功能损伤程度及预后有较高评估价值。     

脑梗死患者血清超敏C反应蛋白和血浆D-二聚体水平测定的临床应用

目的观察脑梗死患者血清超敏C反应蛋白(hs-CRP)和血浆D-二聚体水平的变化,并探讨两者水平与脑梗死的关系。方法分别测定90例健康对照者和92例脑梗死患者血清hs-CRP和血浆D-二聚体水平。结果脑梗死患者血清hs-CRP和血浆D-二聚体水平明显高于健康对照者P<0.01)。脑梗死不同临床分型组间hs-CRP和D-二聚体水平两两比较,hs-CRP水平差异有统计学意义(P<0.01),D-二聚体差异无统计学意义。结论 hs-CRP和D-二聚体与脑梗死的发生、发展密切相关;二者联合检测有助于脑梗死的诊断、治疗及预后判断。     

脑梗死患者血清可溶性细胞间粘附分子-1、信号传导及转录激活子-4和肿瘤坏死因子-α水平及临床意义

目的探讨脑梗死患者血清可溶性细胞间粘附分子-1(sICAM-1)、信号传导及转录激活子-4(STAT-4)、肿瘤坏死因子-α(TNF-α)水平及临床意义。方法选取在我院治疗的脑梗死患者105例(病例组),同时选取健康志愿者100例作为对照组,检测各受试者血清sICAM-1、STAT-4、TNF-α水平。结果病例组血清sICAM-1、STAT-4和TNF-α分别为(273. 75±37. 32)μg/L、(218. 25±45. 55) ng/L和(14. 11±2. 01) pg/mL,明显高于对照组(p 0. 05);不同梗死灶体检患者血清sICAM-1、STAT-4和TNF-α差异有统计学意义(P 0. 05),其中大梗死灶患者血清sICAM-1、STAT-4和TNF-α分别为(320. 02±28. 89)μg/L、(260. 83±28. 78) ng/L和(19. 82±3. 11) pg/mL,明显高于小梗死灶和中梗死灶(P 0. 05);不同神经功能缺损患者血清sICAM-1、STAT-4和TNF-α差异有统计学意义(P 0. 05),其中神经功能高度缺损患者血清sICAM-1、STAT-4和TNF-α分别为(317. 50±34. 55)μg/L、(257. 71±29. 50) ng/L和(19. 02±3. 04) pg/mL,明显高于轻度缺损和中度缺损患者(P 0. 05);梗死灶体积与血清sICAM-1、STAT-4和TNF-α呈正相关(r=0. 356、0. 361和0. 334,P 0. 05);NIHSS评分与血清sICAM-1、STAT-4和TNF-α呈正相关(r=0. 487、0. 453和0. 412,P 0. 05)。结论脑梗死患者sICAM-1、STAT-4、TNF-α水平明显升高,与梗死灶体积及神经功能缺损严重程度有关。     

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。