对氧磷酯酶-1与动脉粥样硬化性血栓性脑梗死的关系

目的研究中国汉族人对氧磷酯酶-1(PON1)活性及PON1Q/R192基因多态性与动脉粥样硬化性血栓性脑梗死(ATCI)发病的关系.方法采用紫外分光光度法和PCR-RELP方法检测48例ATCI患者和55例相匹配的健康人血清PON1活性及PON1Q/R192基因多态性,同时测定血脂、血糖等指标,并进行统计学分析.结果 ATCI组血清PON1活性为(74.41±18.85)μg/ml,低于对照组[(113.65±26.64)μg/ml,P＜0.05];ATCI组与对照组等位基因频率分别为Q:37%、43%;R:63%、57%,2组间比较差异无显著性,2组间3种基因型的分布差异也无显著性.结论血清PON1活性降低可能是ATCI的独立危险因素,而PON1Q/R192基因多态性与中国汉族人ATCI的发生无关.     

血清对氧磷酯酶-1活性及其基因多态性与动脉粥样硬化性血栓性脑梗死关系的研究

目的研究中国汉族人血清对氧磷酯酶-1(PON1)活性及PON1Q/R192基因多态性与动脉粥样硬化性血栓性脑梗死(ATCI)的关系。方法采用紫外线分光光度法和聚合酶链式反应-限制性片段长度多态性(PCR-RELP)方法,检测48例ATCI患者和55名相匹配的健康人血清PON1活性及PON1Q/R192基因多态性。结果ATCI组血清PON1活性为(74.41±18.85)U/ml,明显低于健康对照组[(113.65±26.64)U/ml](P<0.05)。ATCI组与健康对照组等位基因频率分别为Q:37%及43%;R:63%及57%,两组间等位基因频率及3种基因型分布差异无统计学意义。结论血清PON1活性降低是ATCI的危险因素之一;PON1Q/R192基因多态性与中国汉族人ATCI的发生无相关性。     

脑梗死患者血清对氧磷酶活性与脂质过氧化

目的　探讨对氧磷酶在脑梗死发病机理中的作用 ,其活性改变与脑梗死患者脂质过氧化状态的关系。方法　测定了 39名脑梗死患者与 2 1名年龄相匹配的健康体检者血清对氧磷酶 (PON1)活性、血脂水平、氧化型低密度脂蛋白 (OX LDL)含量、丙二醛 (MDA)水平及超氧化物歧化酶 (SOD)活力。结果　脑梗死组血清PON1活性较对照组明显降低 (95 .94± 4 3.97VS 137.6 9± 5 1.81,P <0 .0 1)、甘油三脂 (TG)、低密度脂蛋白 (LDL)、载脂蛋白B(apoB)较对照组升高 (分别是P <0 .0 1,P <0 .0 1,P <0 .0 5 ) ,OX LDL明显升高 (P <0 .0 1) ,同时SOD活力明显下降 (P <0 .0 1) ,而MDA水平则显著增加 (P <0 .0 1)。结论　在脑梗死发病机理中 ,脂质代谢紊乱、血清PON1活性降低等因素促使脂质过氧化的发生 ,引起动脉粥样硬化。脑缺血、缺氧又进一步促发自由基的链式反应 ,引起脑细胞膜的脂质过氧化损伤 ,导致脑梗死的发生。     

糖尿病并发脑梗死患者脂质的过氧化及对氧磷酯酶活性的变化

目的 探讨2型糖尿病患者及并发脑梗死时体内脂质过氧化物含量及血清对氧磷酯酶-1(PON1)活性的变化及两者之间的关系。方法测定2型糖尿病无并发症组,合并脑梗死组和正常对照组PON1活性,丙二醛(MDA)含量及血脂水平。结果 2型糖尿病组血清PON1活性显著降低,丙二醛含量明显增高,合并脑梗死时PON1活性下降更明显,而丙二醛含量更高,PON1活性与丙二醛含量呈负相关。结论 2型糖尿病患者脂质过氧化物产生增多,血清PON1活性降低促进脑梗死的发生。     

对氧磷酶1基因多态性与缺血性脑卒中的关联研究

目的探讨对氧磷酶1(PON1)基因的rs2299262标签位点(tag SNP)多态性与缺血性脑卒中的相关性。方法本研究共纳入705例缺血性脑卒中患者和406例对照组人群,按TOAST分型标准,分为动脉粥样硬化性脑梗死406例、腔隙性脑梗死299例。以位于PON1基因的rs2299262位点为遗传标记,采用聚合酶链反应(PCR)和限制性片段长度多态性(RFLP)技术检测PON1基因的多态性。结果缺血性脑卒中组、动脉粥样硬化性脑梗死组、腔隙性脑梗死组和对照组的PON1基因型及等位基因频率与对照组的差异无统计学意义(P>0.05)。经性别分层后也未见显著差异。结论PON1基因与缺血性脑卒中的发病可能无关。     

慢性阻塞性肺疾病与缺血性卒中

缺血性卒中和慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）分别位居中 国人口死亡原因的第一位和第三位,近年来两者之间的相关性越来越受到关注。本文总结了近年来 关于缺血性卒中和COPD之间关系的研究进展,就COPD与缺血性卒中的相关性进行探讨,希望能够借 此寻找更加有效的方式共同管理这两种疾病。     

急性脑梗死患者血清可溶性血管黏附分子-1的变化

近几年来，随着对缺血性脑血管病损伤机制研究的深入，脑缺血早期白细胞浸润引起的炎症反应及损伤作用日益受到关注，其中细胞黏附分子与炎症反应密切相关。我们检测了42例脑梗死患者急性期血清中的含量。     

对氧磷酶1基因Gln192Arg多态性与帕金森病的相关性

目的探讨中国汉族人群中对氧磷酶1(PON1)基因Gln192Arg单核苷酸多态性(SNP)与帕金森病(PD)的关系。方法采用等位基因特异性聚合酶链反应(A-S PCR)技术检测186例PD患者和228名健康对照PON1基因Gln192Arg位点SNP的分布,分析各基因型与患者发病年龄和疾病严重程度的关系。结果 PD组和对照组间基因型频率和等位基因频率比较差异均无统计学意义(χ2=0.56,P=0.76;χ2=0.06,P=0.81)。进一步按性别分层分析,两组相同性别间基因型和等位基因频率比较亦未发现有统计学差异存在(P>0.05)。PD患者各基因型与发病年龄和疾病严重程度亦无相关性。结论中国汉族人群中PON1基因Gln192Arg位点SNP与PD无相关性。     

对氧磷酶1基因启动子区-909C/G多态性与脑梗死的相关性

目的探讨中国包头地区人群中对氧磷酶1(PON1)启动子基因-909C/G基因多态性与脑梗死的关系。方法采用聚合酶链式反应-限制性片段长度多态性(PCR-RFLP)方法,对脑梗死患者150例及正常对照组150例PON1启动子基因-909C/G酶切位点的限制性片段长度多态性进行分析。多因素Logistic回归分析脑梗死患者易患因素。结果病例组GG基因型及G等位基因频率均显著高于对照组(P0.05)。多因素Logistic回归分析脑梗死患者易患因素:高血压史、冠心病史、高脂血症、G等位基因增加脑梗死的发生概率,差异有统计学意义(P0.05),高密度脂蛋白(HDL)降低脑梗死的发生概率,差异有统计学意义(P0.05)。结论高血压、高血脂、冠心病、G等位基因是脑梗死发病的危险因素。对氧磷酶1基因-909C/G基因多态性与脑梗死的遗传易感性显著相关,基因型GG可能是脑梗死的危险因子,G等位基因可能是脑梗死的易感等位基因。     

脂蛋白脂酶基因和对氧磷酶1基因联合作用与脑梗死发病的相关性

目的 探讨脂蛋白脂酶(LPL)、对氧磷酶1(PONl)基因联合作用与脑梗死发病的相关性.方法 选取LPL基因2个SNP和PON1基因2个标签SNP,采用聚合酶链反应(PCR)和限制性片段长度多态性(RFLP)技术,对705例脑梗死患者和431例对照组人群进行检测,应用UNPHASED软件、等位基因条件分析的方法,分析基因的联合作用与脑梗死的相关性.结果 LPL基因rs328位点G等位基因分布在动脉粥样硬化性脑梗死组与对照组差异显著(x2=4.83,P=0.034,OR=1.47,95％CI=1.03～2.13);rs326位点G等位基因分布在动脉粥样硬化性脑梗死组与对照组差异显著(x2=3.597,P=0.047,OR=1.64,95％CI =1.12～1.84);PON1基因上的rs2299262位点与LPL基因上的rs328位点联合作用与脑梗死的发病具有相关性(x2=6.26,df =2,P=0.043).结论 LPL基因rs328位点G等位基因携带者患大动脉粥样硬化性脑梗死的风险高于非携带者.LPL基因rs326位点G等位基因携带者患大动脉粥样硬化性脑梗死的风险高于非携带者.PON1基因上的rs2299262位点与LPL基因上的rs328位点联合作用与脑梗死的发病具有相关性.     

血小板膜糖蛋白受体基因多态性在缺血性心脑血管病中的作用

心、脑血管病的许多危险因素已被确定,如吸烟、高血压、高血脂、高血糖等,控制这些危险因素可以降低其发病率。在所有心、脑血管病发病因素中只有2/3可以归为可控制的危险因素,其它的遗传变异如血小板和凝血因子的多态性可从几     

Subcortical ischemic vascular dementia

Subcortical ischemic vascular dementia (SIVD) has been proposed as a subtype of vascular cognitive impairment. MRI often discloses "silent" hyperintensities in 20% to 40% of community-dwelling elderly. Efforts to relate MRI-measured lacunes and white matter changes to cognitive impairment have not been straightforward. The possibility that Alzheimer's disease pathology contributes to cognitive impairment increases with age. A rare disorder known as cerebral autosomal dominant arteriopathy with subcortical infarctions and leukoencephalopathy (CADASIL) provides an opportunity to study SIVD in the absence of Alzheimer's disease. Lacunes and deep white matter changes are associated with dysexecutive syndrome. Hypertension, the leading risk factor for sporadic SIVD, is treatable. High priority must be given to reducing vascular risk profiles.     

Subcortical ischemic vascular disease and dementia

Subcortical ischemic vascular disease and dementia (SIVD) incorporate small vessel disease as the chief vascular etiology, lacunar infarct and ischemic white-matter lesions (WMLs) as primary type of brain lesions, subcortical location as the primary location of lesions, and subcortical syndrome as the primary clinical manifestation. It incorporates two clinical entities: Binswanger's syndrome and the lacunar state. Patients with SIVD present with extensive white-matter lesions and multiple lacunae on neuroimaging. SIVD is expected to be a more homogenous subtype of vascular cognitive impairment and dementia. Recently modified NINDS-AIREN research criteria for SIVD have been proposed. Further empirical research is needed to refine the syndrome and stages and validate the brain imaging criteria, as well as to detail the natural history and outcomes of SIVD.     

缺血性脑血管病患者血浆兴奋性氨基酸递质的测定及临床意义

本文应用高效液相色谱法测定了５７例缺血性脑血管病患者和３３例正常对照血浆中兴奋性氨基酸递质和抑制性氨基酸、天冬氨酸明显升高（２６．４８％，２０．２２％）；在缺血发生２４ｈ后开始显著上升，恢复期降至正常水平。血浆抑制性氮基酸，ｒ－氨基丁酸、甘氨酸、丙氨酸在脑缺血急性期也升高，ｒ－氨基丁酸在恢复期下降，而甘氨酸、丙氨酸未见下降。本文结果表明，谷氨酸、天冬氨酸参与人类脑缺血性细胞损伤的病理生理过程；急性缺血性脑血管病患者血浆兴奋性和抑制性氨基酸递质可作为一个敏感指标，早期证实脑缺血的发生，推测缺血的严重程度，具有重要的临床意义。     

Prothrombotic disorders and ischemic stroke in children

Childhood ischemic stroke, including arterial ischemic stroke (AIS) and sinovenous thrombosis (SVT), is relatively rare in children but can result in devastating morbidity and mortality. An understanding of the etiology of childhood stroke is important because strategies for primary and secondary prevention can be devised. Prothrombotic disorders may contribute to the etiology of childhood stroke, and include deficiencies of antithrombin, protein C, protein S, plasminogen, and presence of Factor V Leiden, Prothrombin gene G20210A, dysfibrinogenemia, antiphospholipid antibodies, hyperhomocysteinemia, and elevated lipoprotein (a). The overall incidence of prothrombotic disorders in childhood AIS is estimated to be 20% to 50% in most studies and, in childhood SVT, to be 33% to 99%. In addition, hyperlipidemia, polycythemia, iron deficiency anemia, and platelet disorders may result in a prothrombotic state associated with ischemic stroke. The etiologic contribution of these prothrombotic disorders to initial and recurrent stroke has not been clearly defined; however, additional risk factors are usually present in affected children. Given the prevalence of prothrombotic disorders in childhood stroke, and their likely causative role, children with stroke should be screened for prothrombotic disorders. Future prospective and multicenter studies will elucidate the contribution of specific prothrombotic disorders to initial and recurrent stroke, and optimal therapy.     

Hereditary vestibulo-cochlear dysfunction and vascular disorders

A family is described with a progressive autosomal dominant vestibulocochlear dysfunction resulting in a Dandy syndrome, head movement dependent oscillopsia and hearing loss. The history was negative for other neurological or otological diseases (including infectious diseases) or use of neuro-ototoxic drugs, except for a high incidence of vascular disorders (hypertension, stroke, and heart infarction).     

Hematologic disorders associated with ischemic stroke

Hematological disorders underlie a small proportion of all ischemic strokes. The association of these coagulation abnormalities with ischemic stroke is not always clear. The etiology of stroke still remains uncertain in a large number of cases and proper screening for coagulation abnormalities and the discovery of new coagulation disorders will probably increase the rate of strokes attributable to these causes. Since large case-control studies with unselected and consecutive stroke patients from different ethnic origins have not yet been performed to determine the role of coagulation abnormalities in ischemic stroke, our knowledge is dependent on case reports and small series of mostly younger patients. Extensive hematologic evaluation of unselected stroke patients will likely yield little useful information and be too expensive. Every stroke patient needs a careful evaluation, and in selected cases, this should include coagulation parameters. Patients with unexplained strokes after a careful evaluation, previous thrombotic episodes, or a positive family history for thrombosis, are good candidates for further coagulation studies. As long as the hypercoagulable state persists, both arterial and venous thromboembolic recurrences can be expected. Many of these patients may benefit from anticoagulants. In patients with hereditary coagulation disorders, studies should be extended to close relatives. Since some coagulation tests are fairly expensive, provide only equivocal data, and are not widely available, we advise a step-by-step approach starting with the patient and family history.     

Neuropathologic substrates of ischemic vascular dementia

Ischemic vascular dementia (IVD) is a relatively uncommon entity, in the course of which multiple ischemic brain lesions result in progressive cognitive and memory impairment. Ischemic brain lesions may also aggravate the neuropsychologic deficit of Alzheimer disease (AD). In this review we summarize our experience based upon autopsy examination of the central nervous system in 20 patients (age range 68-92 years) enrolled in a longitudinal investigation of structural, neurochemical, functional neuroimaging, and neuropsychologic components of IVD, especially dementia associated with cerebral microvascular disease. While cystic infarcts were present in the CNS of 5 patients, the most commonly observed neuropathologic abnormalities were lacunar infarcts and microinfarcts--both types of lesion were encountered in over half of patients' brains. Evidence of (remote) hippocampal injury was found in 11/20 patients. Severe atherosclerosis and arterio/ arteriolosclerosis were both associated with the occurrence of multiple lacunar infarcts. Pronounced cerebral amyloid angiopathy (CAA) was noted in a single patient, who also showed other microscopic changes of severe AD. While fairly unusual as a nosologic entity, IVD appears to correlate with widespread small ischemic lesions distributed throughout the CNS. We furthermore propose an approach to quantifying the burden of ischemic vascular and parenchymal disease that may be associated with a dementia syndrome. A brief review of neuropathologic features of vascular dementia (both familial and sporadic) is presented.     

缺血性脑卒中的超早期血管再通方法

随着缺血性脑卒中的日益高发和发病年龄的日趋年轻化,对超早期患者给予积极有效的血管再通治疗以恢复血流供应,对于脑卒中的治疗及后期功能康复均具有至关重要的意义。目前应用于临床的血管再通方法主要包括静脉溶栓、动脉溶栓、机械性再通和桥接治疗等。本文介绍了国际公认的缺血性脑卒中超早期临床血管再通方法,并针对缺血性脑卒中超早期血管再通方法应用中存在的一些争议热点进行讨论。