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1.
目的观察急性脑梗死患者血浆同型半胱氨酸(Hcy)水平,探讨该指标与患者神经功能缺损的相关性。方法将2017年1月~2018年1月我院收治的急性脑梗死患者180例设为观察组,并根据美国国立卫生研究院卒中量表(NIHSS)评分分为轻度组82例、中度组60例、重度组38例;另将同期我院行健康体检者120例设为对照组。所有受试者均测定血浆Hcy水平,比较两组血浆Hcy水平及观察组中不同神经功能缺损程度组的治疗前后NIHSS评分和血浆Hcy水平。结果观察组血浆Hcy水平明显高于对照组,差异有统计学意义(P0.05),重度组治疗前、后NIHSS评分和血浆Hcy水平均明显高于轻度组和中度组,差异均有统计学意义(P0.05),中度组治疗前、后NIHSS评分和血浆Hcy水平均明显高于轻度组,差异均有统计学意义(P0.05),即血浆Hcy水平与血清NIHSS评分呈正相关;相较于治疗前,观察组中3组患者NIHSS评分和血浆Hcy水平均明显下降,差异均有统计学意义(P0.05)。结论急性脑梗死患者的血浆Hcy水平明显升高,且与神经功能缺损程度呈正相关,可作为患者病情严重程度及预后的判断指标。  相似文献   

2.
目的探讨缺血性脑卒中患者N端脑钠肽前体(NT-proBNP)和血清同型半胱氨酸(Hcy)水平在评估患者预后效果中的应用价值。方法 152例缺血性脑卒中患者(脑卒中组)和同期120例健康志愿者(健康组),检测两组血清NT-proBNP和Hcy水平,同时分析缺血性脑卒中患者脑卒中梗死体积、美国国立卫生研究院卒中量表(NIHSS)评分与NT-proBNP和Hcy表达水平的关系。结果脑卒中组NT-proBNP和Hcy表达水平均高于健康组(P0.05);不同神经功能损伤程度和脑梗死体积患者,NT-proBNP和Hcy表达水平比较,差异有统计学意义,且轻度损伤(小梗死)中度损伤(中梗死)重度损伤(大梗死)(P0.05);NIHSS评分和脑梗死面积与NT-proBNP、Hcy表达水平呈正相关(P0.05)。结论缺血性脑卒中患者血清NT-proBNP、Hcy表达水平为高表达,且患者脑梗死面积、NHISS评分与NT-proBNP、Hcy表达水平存在明显相关性,故NTproBNP、Hcy可用于评估缺血性脑卒中病情程度。  相似文献   

3.
目的探讨脑梗死急性期(ACI)患者血浆纤维蛋白原(Fib)水平的改变及其与病情和预后的关系。方法检测250例脑梗死患者(ACI组)和226名健康成人(健康对照组)的血浆Fib含量。在ACI患者入院当天和4周时进行临床神经功能缺损程度评分(NDS)。结果 ACI组血浆Fib水平异常率明显高于健康对照组(44.8%vs.9.3%,P<0.01);NDS重型患者血浆Fib含量[(5.82±1.51)mg/L]明显高于中型[(4.17±1.09)mg/L]、轻型[(4.26±1.15)mg/L]患者(均P<0.01)。血浆Fib含量升高组患者住院4周时显著进步和进步者明显低于Fib正常组(均P<0.01),而无变化和恶化者明显高于Fib正常组(均P<0.01)。结论 ACI患者血浆Fib水平均明显升高,病情重的患者升高更明显,血浆Fib含量升高的患者预后较差。  相似文献   

4.
目的:分析血浆同型半胱氨酸(Hcy)、脂联素(APN)水平与阿尔茨海默病(AD)患者认知功能障碍程度之间的关系。方法:回顾性分析96例AD患者临床资料,根据临床痴呆评定量表(CDR)将其分为轻度AD亚组38例、中度AD亚组39例及重度AD亚组19例;将同期健康志愿者30例纳入对照组。比较AD不同亚组和对照组血浆Hcy、APN、β-淀粉样蛋白(Aβ)40、Aβ42水平及简易精神状态检查量表(MMSE)评分的差异,分析血浆Hcy、APN水平与AD患者MMSE评分、血浆Aβ水平的相关性。结果:血浆Hcy水平重度AD亚组高于轻、中度AD亚组和对照组,中度AD亚组高于轻度AD亚组和对照组,轻度AD亚组高于对照组(P0.05);血浆APN、Aβ42水平及MMSE评分重度AD亚组低于轻、中度AD亚组和对照组,中度AD亚组低于轻度AD亚组和对照组,轻度AD亚组低于对照组(P0.05)。AD患者血浆Hcy水平与其MMSE评分和血浆Aβ42水平呈显著负相关性(P0.05);血浆APN水平与其MMSE评分和血浆Aβ42水平呈显著正相关性(P0.05)。结论:AD患者随病情加重血浆Hcy水平显著升高,血浆APN水平显著降低,其与AD患者认知障碍程度密切相关,检测该指标对评估患者病情、指导临床治疗有一定价值。  相似文献   

5.
目的 探究血浆同型半胱氨酸(Hcy)水平与急性脑梗死(ACI)的相关性。方法 选取陕西省森工医院2018年1月至2020年1月收治的ACI患者及进行常规体检的健康者各100例,分别纳入观察组与对照组,比较两组血浆Hcy水平;比较不同美国国立卫生研究院卒中量表(NIHSS)评分、梗死灶面积患者血浆Hcy水平;同时根据Hcy水平分为高Hcy组(≥15μmol/L)与低Hcy组(<15μmol/L),比较两组预后;采用Pearson相关分析血浆Hcy水平与NIHSS评分、改良Rankin量表(mRS)评分的关系。结果 观察组血浆Hcy水平为(16.74±2.90)μmol/L,明显高于对照组的(9.52±1.68)μmol/L,差异有统计学意义(P<0.05);血浆Hcy水平在神经缺损轻度、中度、重度患者中依次升高,差异有统计学意义(P<0.05);大梗死灶患者血浆Hcy水平明显高于中梗死灶患者、小梗死灶患者,差异有统计学意义(P<0.05);高Hcy组患者预后良好率为48.7%,明显低于低Hcy组的75.0%,差异有统计学意义(P<0.05);Pearson相...  相似文献   

6.
目的观察脑梗死患者血清同型半胱氨酸(Hcy)和血浆D-二聚体水平的变化,并探讨二者的相关性。方法测定90例脑梗死患者和89例健康对照者的血清Hcy及血浆D-二聚体水平,并分析患者组两指标间的相关性。结果脑梗死患者血清Hcy、血浆D-二聚体水平显著高于健康对照组(P0.05)。脑梗死患者Hcy轻度及中度增高组Hcy水平与D-二聚体水平呈正相关(r分别为0.504、0.633,P值均小于0.05)。结论血清Hcy、血浆D-二聚体水平升高与脑梗死的发生有密切关系;在一定范围内,D-二聚体随Hcy的增高而增高。  相似文献   

7.
目的探讨同型半胱氨酸(Hcy)、平均血小板体积(MPV)、高敏C反应蛋白(hs-CRP)以及纤维蛋白原(FIB)检测在急性脑梗死中的诊断价值。方法选择急性脑梗死患者130例,按照神经缺损程度将患者分为轻度损伤组37例、中度损伤组62例以及重度损伤组31例,再选择70名健康受试者作为正常对照组,比较急性脑梗死各损伤程度组与正常对照组各指标水平变化情况以及各指标水平之间的相关性。结果急性脑梗死患者Hcy、MPV、hs-CRP及FIB水平均显著高于正常对照组(P0.05);轻度损伤组、中度损伤组与重度损伤组患者Hcy、MPV、hs-CRP及FIB水平比较,差异均具有统计学意义(P0.05),且损伤程度越重,其Hcy、MPV、hs-CRP及FIB水平越高;在Hcy、MPV、hs-CRP及FIB 4个指标间两两均呈显著正相关关系(P0.05)。结论Hcy、MPV、hs-CRP及FIB水平在急性脑梗死患者明显增高,且与病情程度密切相关,对了解患者病情的进展以及评估预后有着重要的价值。  相似文献   

8.
目的观察老年脑梗死患者血清同型半胱氨酸(Hcy)、凝集素样氧化型低密度脂蛋白受体-1(sLOX-1)及高迁移率族蛋白1(HMGB1)水平的变化情况,分析其与神经功能缺损程度及预后的关系。方法选取2014年5月至2016年5月在该院就诊的脑梗死患者120例作为研究组,另选取50例健康体检者作为对照组,按照美国国立卫生研究所脑卒中量表(NIHSS)和预后情况分别对患者进行分组,测定各组研究对象血清Hcy、sLOX-1及HMGB1的表达水平,分析其与NIHSS及预后的关系。结果脑梗死组患者血清中Hcy、sLOX-1和HMGB1水平均高于对照组,重度神经功能缺损患者Hcy、sLOX-1和HMGB1水平均高于中度组和轻度组,中度组患者血清各项指标表达水平亦高于轻度组,差异均有统计学意义(P0.05);预后不良组患者血清Hcy、sLOX-1和HMGB1水平均高于预后良好组,差异均有统计学意义(P0.05)。结论脑梗死患者血清Hcy、sLOX-1及HMGB1水平与NIHSS及预后均有良好的相关性,在脑梗死病情诊断及预后改善中有重要临床价值。  相似文献   

9.
目的:探讨血清同型半胱氨酸(Hcy)与血浆纤维蛋白原(FIB)在脑梗死诊断中的价值。方法:选取急性脑梗死患者168例作为病例组,同时选取健康体检者80例作为对照组。检测2组血清Hcy和血浆FIB水平。病例组采用美国国立卫生研究院神经功能缺损量表(NIHSS)评定神经功能。结果:病例组血清Hcy和血浆FIB水平明显高于对照组(P0.05);病例组血清Hcy、血浆FIB水平与NIHSS评分呈正相关(r=0.880、0.854,P0.05);Hcy+FIB诊断急性脑梗死的检测效能高于血清Hcy和血浆FIB。结论:血清Hcy与血浆FIB联合检测可作为急性脑梗死辅助诊断的指标,并且在病情评估中有一定价值。  相似文献   

10.
目的研究治疗前同型半胱氨酸(Hcy)、纤维蛋白原(FIB)联合N末端脑钠肽前体(NT-proBNP)检测在老年脑梗死远期预后预测中的效能。方法选取2017年5月—2019年8月收治的109例老年脑梗死作为研究组,根据美国国立卫生研究院卒中量表(NIHSS)评分分为轻度组42例、中度组35例和重度组32例。同时选取128例健康体检者作为对照组。比较不同研究对象Hcy、FIB、NT-proBNP水平差异。统计研究组远期预后情况,多因素Logistic回归分析影响远期预后的相关因素;受试者工作特征(ROC)曲线分析Hcy、FIB、NT-proBNP对患者远期预后的预测价值。结果研究组Hcy、FIB、NT-proBNP水平高于对照组(P0.01)。中度组和重度组Hcy、FIB、NT-proBNP水平高于轻度组,且重度组高于中度组(P0.05)。NIHSS评分、Hcy、FIB、NT-proBNP异常升高均为影响老年脑梗死患者远期预后的独立危险因素(P0.01)。Hcy、FIB、NT-proBNP及三者联合预测老年脑梗死患者远期预后的曲线下面积分别为0.801、0.812、0.844及0.917,以三者联合最大。结论治疗前Hcy、FIB、NT-proBNP水平在老年脑梗死患者中随神经功能缺损严重程度增加而升高,且是影响患者远期预后的独立危险因素,并有一定预测价值。  相似文献   

11.
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.  相似文献   

12.
Fibrinogen and fibrin structure and functions   总被引:12,自引:0,他引:12  
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.  相似文献   

13.
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.  相似文献   

14.
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。  相似文献   

15.
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。  相似文献   

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17.
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。  相似文献   

18.
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.  相似文献   

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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。  相似文献   

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