脑梗死患者血浆纤溶酶原激活物抑制物-1活性及其基因多态性研究

目的 :探讨纤溶酶原激活物抑制物 - 1(PAI- 1)活性变化和其基因多态性对脑梗死及其再梗死发病的关系。方法 :采用扩增片段长度多态性及银染技术 ,分析 95例脑梗死患者和 6 0例对照者的白细胞 PAI- 1启动子区域 - 6 75位点 4G/5 G多态性和第四内含子 (CA) n多态性 ,用发色底物测定血浆 PAI- 1活性。结果 :脑梗死组血浆 PAI- 1活性明显高于对照组。再梗死组和初次脑梗死组中 4G纯合子个体占的比例最高 ;并且再梗死组 4G纯合子个体的比例高于初次脑梗死组 (P<0 .0 5 )。脑梗死组和对照组相比在“Z”,“Z+6”,“Z+8”,“Z+10”等位基因频率存在差异 (P<0 .0 5 ) ;在脑梗死组中 ,较短片段的 (CA) n重复和较重复基因型及 4G纯合子个体可能有较高的脑梗死发病倾向及再梗死     

血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与复发脑梗死的关系

目的探讨血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与复发脑梗死之间的关系。方法应用PCR技术和琼脂糖电泳对58例初发脑梗死患者、64例复发脑梗死患者进行了API-1基因启动子4G/5G多态性的检测和分析,并与50例非脑血管疾病对照比较。结果两组脑梗死患者PAI-1基因启动子区4G/5G多态性的基因型频率和等位基因频率与对照组分别比较均有统计学差异(P<0.05),但复发脑梗死组患者PAI-1基因启动子区4G/5G多态性的基因型频率和等位基因频率与初发脑梗死组比较无统计学差异(P>0.05)。结论PAI-1基因启动子区4G/5G多态性是中国人群脑梗死发病的遗传学危险因素,但可能与复发脑梗死无关。     

血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与脑血管疾病的关系

目的 探讨血浆纤溶酶原激活物抑制剂-1基因启动子区4G/5G多态性与脑血管疾病之间的关系.方法 应用PCR技术和琼脂糖电泳对30例脑出血患者、90例脑梗死患者(其中腔隙性脑梗死30例,小面积脑梗死30例,大面积脑梗死30例)进行了API-1基因启动子4G/5G多态性的检测和分析,并与30例非脑血管疾病者对照比较.结果 对照组、脑出血组、脑梗死组基因型频率及等位基因频率分布比较均有统计学差异(P＜0.05).对照组与脑出血组间基因型频率及等位基因频率比较均无统计学差异(P＞0.05).对照组与脑梗死组间基因型频率及等位基因频率比较均有统计学差异(P＜0.05),脑梗死组4G/4G基因型频率(44.4%)较对照组(20%)高;脑梗死组4G等位基因频率(63.3%)较对照组(38.8%)高,比较均有统计学差异(P＜0.05).脑梗死组各亚型基因型频率及等位基因频率比较均无统计学差异(P＞0.05).性别在各组不同基因型中分布:对照组及脑出血组性别在不同基因型分布比较无统计学差异(P＞0.05).脑梗死组性别在不同基因型分布比较有统计学差异(P＜0.05),4G/4G基因型中男性占25%;女性占65%,比较有统计学差异(P＜0.05).腔隙性脑梗死组及小面积脑梗死组性别在不同基因型中分布比较均无统计学差异(P＞0.05).大面积脑梗死组性别在不同基因型中分布比较有统计学差异(P＜0.05),4G/4G基因型男性占21.4%;女性占78.6%,比较有统计学差异(P＜0.05).结论 PAI-1基因启动子区4G/5G多态性在怀化市正常人群中大致分布为:4G/4G占20%;4G/5G占63.3%;5G/5G占16.7%.PAI-1基因启动子区4G/5G多态性与脑出血无关.PAI-1基因启动子区4G/5G多态性与缺血性脑卒中有关,4G/4G基因型可能是缺血性脑卒中的一个独立危险因素,尤其可能与女性大面积脑梗死密切相关.PAI-1基因启动子区4G/5G多态性与缺血性脑卒中的梗死面积无关.     

β-纤维蛋白原-455G/A基因多态性与脑梗死的相关性研究

目的　研究 β 纤维蛋白原基因启动子区域 - 4 5 5G/A基因变异与血浆纤维蛋白原水平及其与脑梗死的相关性。方法　随机抽取住院的高血压脑梗死患者 86例 (脑梗死组 )、高血压非脑梗死患者 85例 (高血压组 )、门诊健康体检者 90名 (对照组 )作为研究对象。β 纤维蛋白原基因启动子区域 - 4 5 5G/A的多态性分析采用多聚酶链反应加HaeⅢ内切酶检测目的基因片段 (PCR RFLP)法 ,血浆纤维蛋白原水平测定采用凝血酶原时间法。结果　血浆纤维蛋白原水平脑梗死组 (4 82± 0 2 6 )显著高于对照组 (4 37± 0 19) (P <0 0 1) ,而高血压组 (4 5 0± 0 2 0 )较脑梗死组及对照组差异均无显著性 (均P >0 0 5 )。脑梗死组A - 4 5 5等位基因的分布频率较高血压组及对照组明显增高 (均P <0 0 1)。脑梗死组及高血压组中 - 4 5 5G/G基因型的血浆纤维蛋白原水平明显低于 - 4 5 5G/A +- 4 5 5A/A的基因型 (均P <0 0 5 ) ,而在对照组不同基因型的血浆纤维蛋白原水平则差异不明显。结论　血浆纤维蛋白原水平受 β 纤维蛋白原基因 - 4 5 5G/A多态性的影响 ,A - 4 5 5等位基因是脑梗死的一个相对独立的危险因素。     

PAI-1基因启动区4G/5G多态性与2型糖尿病并发脑梗死的关系

目的研究PAI-1基因启动区4G/5G多态性在中国北方汉族人2型糖尿病(DM)患者及并发脑梗死(CI)患者中的分布,以及各组中血浆PAI-1抗原水平的变化。方法将280名受试对象分为4组:健康对照组(92例)、非DM脑梗死组(60例)、单纯DM组(88例)及DM并发CI组(40例)。全部受试对象均需应用ELISA法测定血浆PAI-1抗原水平,等位基因特异性引物PCR扩增技术测PAI-1基因启动区4G/5G多态性。结果DM、CI患者血浆PAI-1抗原水平显著升高,中国北方汉族人中,DM组中脑梗死患者5G等位基因频率和5G/5G基因型频率不仅显著高于健康对照组,也显著高于DM无脑梗死组和无DM脑梗死组。在DM组中,5G纯合子携带者发生CI的风险增加3.81倍,有统计学意义。结论PAI-1启动区5G/5G基因型是2型DM患者中CI高发的易感基因型之一。     

脑梗死患者MCP-1启动子区A-2518G基因多态性的研究

目的探讨MCP—1启动子区A-2518G基因多态性与血清中MCP-1水平及哈尔滨地区汉族人脑梗死的关系。方法应用聚合酶链反应-限制性片段长度多态性(PCR—RFLP)方法,检测113例脑梗死患者、98例健康对照者MCP-1启动子区A-2518G基因的多态性。应用ELISA方法,检测39例脑梗死患者、38例健康对照者血清中 MCP-1水平。结果各基因型频率和等位基因频率在正常人群及脑梗死患者中无显著性差异(P>0．05)。GG型 GA型的人群血清中MCP-1表达水平较AA型者高(P<0．05)。结论 MCP-1启动子区A-2518G基因多态性可以影响血清MCP-1水平,但它与哈尔滨地区汉族人脑梗死不相关。     

血红素加氧酶-1基因多态性与脑梗死的相关性

目的探讨血红素加氧酶-1(HO-1)基因启动子基因多态性与ACI患者遗传易感性的关系及碳氧血红蛋白(COHb)在ACI患者中含量的变化。方法采用聚合酶链反应(PCR)和改良双波长分光光度法分析57例急性ACI患者及55例健康对照者血清中HO-1基因启动子(GT)n重复序列不同基因型频率分布特征及碳氧血红蛋白(COHb)含量与ACI的关系。结果ACI组中的Ⅰ类基因型组(携带S等位基因)显著低于2类基因型组(不携带S等位基因)(43.86%比65.45%,P<0.05),提示Ⅰ类基因型与脑梗死的危险性降低相关。ACI组血浆的COHb水平较对照组COHb水平明显升高(t=16.92,P<0.01),提示脑梗死患者血浆COHb含量较高,差异有统计学意义。结论HO-1基因启动子(GT)n重复序列遗传多态性与脑梗死的遗传易感性有关。ACI患者血浆中CO-Hb含量较正常时升高。     

血浆同型半胱氨酸水平及其代谢酶基因多态性与脑梗死的关系

目的　探讨血浆同型半胱氨酸 (Hcy)水平、5 ,10 亚甲基四氢叶酸还原酶 (MTHFR)和胱硫醚 β合成酶 (CBS)基因多态性与脑梗死的关系。 方法　用高效液相色谱仪HPLC FD法和PCR 限制性内切酶片段长度多态性分析及扩增阻滞突变体系法检测 87例动脉粥样硬化性血栓性脑梗死患者和 80例对照者血浆Hcy浓度和MTHFR及CBS基因型。 结果　病例组和对照组平均空腹血浆Hcy浓度分别为 (15 3± 4 3) μmol/L和 (11 3± 3 9) μmol/L ,差异有显著意义 (P <0 0 0 1) ;两组基因型分布、纯合子突变率及等位基因频率差异无显著意义 ;血浆Hcy浓度与MTHFR基因型、CBSG919A基因型、CBST833C基因型、性别和血浆肌酐浓度相关。结论　血浆Hcy浓度升高是脑梗死的独立危险因素 ,单纯的MTHFR和CBS突变并非脑梗死的危险因素。     

新疆哈萨克族内皮细胞蛋白C受体基因多态性与脑梗死的相关性

目的探讨新疆哈萨克族内皮细胞蛋白C受体(EPCR)A6936G基因多态性与脑梗死的相关性。方法运用PCR-限制性片段长度多态性(RFLP)技术检测80例哈萨克族脑梗死患者(脑梗死组)及100名哈萨克族对照者(对照组)EPCR A6936G基因型和等位基因频率。结果脑梗死组出现AA、AG、GG基因型,对照组出现AA、AG基因型;脑梗死组AG+GG基因型及G等位基因频率显著高于对照组(均P<0.05)。结论 EPCR A6936G多态性可能与哈萨克族脑梗死的发生有一定的关系。     

载脂蛋白(a)基因增强子DH Ⅲ多态性与湖南地区汉族人群动脉粥样硬化血栓性脑梗死的相关性

目的研究载脂蛋白(a)基因DHⅢ增强子-1230A/G多态性与湖南地区汉族人群动脉粥样硬化血栓性脑梗死的关系。方法应用聚合酶链式反应-限制性片段长度多态性技术及DNA序列测定法检测湖南地区汉族人群134例动脉粥样硬化血栓性脑梗死患者、110名健康对照者的载脂蛋白(a)基因DHⅢ增强子-1230A/G多态,同时用免疫比浊法检测所有研究对象的血浆脂蛋白(a)水平。结果在动脉粥样硬化血栓性脑梗死组载脂蛋白(a)基因DHⅢ增强子-1230 A/G多态G等位基因频率(0.728)明显高于对照组(0.618;P=0.01);GG型频率(0.500)明显高于对照组(0.400;P0.05)。动脉粥样硬化血栓性脑梗死组各基因型血浆脂蛋白(a)水平均明显高于对照组,差异具有统计学意义(P0.05)。结论载脂蛋白(a)基因DHⅢ增强子-1230 A/G多态性可能与中国湖南地区汉族人群动脉粥样硬化血栓性脑梗死有关;G等位基因可能是动脉粥样硬化血栓性脑梗死的危险因素之一。     

Posterior cerebral artery infarction from middle cerebral artery infarction

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.     

Postprandial cerebral infarction

Some neurological diseases are accompanied by autonomic dysfunction. Postprandial hypotension (PPH) is one disorder accompanied by autonomic dysfunction. Although the major symptoms of PPH are fall and syncope, PPH is sometimes overlooked because of its non-specific symptoms, such as dizziness, nausea, and light-headedness. Because PPH could result in decreased cerebral perfusion pressure accompanied by a decrease in blood pressure, PPH may be linked to the risk of hemodynamic stroke or transient ischemic events, especially in patients with chronic cerebral large vessel occlusion/stenosis. Whether chronic cerebral large vessel occlusion or stenosis causes symptomatic ischemic events depends on the patient’s compensatory collateral circulation and cerebral vasoreactivity. Therefore, we hypothesized that cerebral blood flow assessment could be essential for stratifying patients at high risk of postprandial cerebral infarction. However, there have been few reports on the association between cerebral blood flow and the occurrence of postprandial cerebral infarction. In a literature review, we identified seven cases of postprandial cerebral infarction. Postprandial cerebral infarction occurs in patients with chronic cerebral large vessel occlusion/stenosis accompanied by cerebral blood flow reduction. Non-pharmacotherapeutic and pharmacotherapeutic approaches could improve postprandial cerebral infarction; however, one patient with poor compensatory collateral circulation and reduced cerebral vasoreactivity experienced recurrent symptomatic episodes even with sufficient medical treatment and needed extracranial-intracranial bypass surgery. Physicians should be aware of PPH as it can complicate neurological disorders. Long-term blood pressure monitoring for the detection of PPH and cerebral blood flow assessment is needed in patients with cerebral large vessel occlusion/stenosis to prevent postprandial cerebral infarction.     

Perinatal cerebral infarction

The diagnosis of perinatal cerebral infarction, although frequently suggested clinically, has been made most commonly at postmortem examination; few infants surviving stroke are reported in the literature. We evaluated 18 infants with perinatal cerebral infarction in a recent twelve-month interval. Seven were preterm neonates, 6 of whom had experienced neonatal intraventricular hemorrhage. Three full-term infants were thought to have experienced cerebral infarction in utero and had evidence of well-defined strokes on computed tomographic scans performed shortly after birth. Eight infants developed stroke at term. The most common cause of cerebral infarction in our series was perinatal asphyxia. Fourteen of the infants were seen with neonatal seizures. Fourteen of the 18 have died or are faring poorly at 4 to 12 months of age (corrected).     

外伤性脑梗塞

外伤性脑梗塞(post-traumatic cerebral infarction,PTCI)是颅脑损伤的并发症,多种原因导致这并发症,包括脑血管痉挛,直接占位效应压迫脑血管,血管损伤和血栓形成.本研究的目的是根据CT、MRI和脑血管造影来研究外伤性脑梗塞的影像学特征和机制.     

Neonatal cerebral infarction

Neonatal cerebral infarction in term infants has many possible causes, including bacterial meningitis, inherited or acquired coagulopathies, trauma, and hypoxia-ischemia. However, a specific cause often cannot be identified. Neurologic symptoms in the neonatal period are often subtle and nonspecific, even in infants with large infarctions involving an entire cerebral artery distribution. The most common presenting symptom is focal motor seizures of the contralateral limbs. Cranial magnetic resonance imaging, especially with diffusion-weighting, is the most sensitive imaging modality, although ultrasonography with Doppler imaging of cerebral blood flow is useful in the neonate who is too ill to transport. Neurodevelopmental outcome is often surprisingly good, with many infants making a complete recovery of motor function. The effect of neonatal stroke on cognitive function, especially language acquisition and emotional and social development, has not been fully established.     

Diffuse cerebral symptoms in convalescents from cerebral infarction and myocardial infarction

In order to evaluate occurrence and cause of a number of diffuse cerebral symptoms (DCS), such as impaired memory, inability to concentrate, emotional instability, irritability, etc., 44 survivors of cerebral infarction (CI) and 40 survivors of myocardial infarction (MI) were seen 6-26 months after onset for psychometric testing and an interview about DCS. Although surprisingly common in both groups, DCS were significantly more frequent in CI patients than in MI patients. 1/2 of the former and 1/3 of the latter complained of 5 or more symptoms. In contrast, a significant difference in test performance was demonstrated in only 1 of 4 tests. There was no significant correlation between the number of DCS and test performance. In both groups, DCS occurrence was independent of age, whereas in the MI group, but not in the CI group, test performance was inversely related to age. In the CI group, DCS occurrence was not significantly related to size or site of the infarction. The results indicate that an organic brain damage cannot be the sole cause of DCS, and it is suggested that some of the symptoms are manifestations of a stress response syndrome provoked by insufficient coping with the consequences of the disease.     

糖尿病脑梗死及非糖尿病高血压脑梗死患者的临床研究

目的 探讨糖尿病脑梗死与非糖尿病高血压脑梗死患者的临床特点.方法 糖尿病并发脑梗死患者85例,其中糖尿病高血压脑梗死组57例,糖尿病正常血压脑梗死组28例;同期住院的无糖尿病高血压脑梗死组40例;正常对照组40例.观察血压、血糖、血脂、肾功能及预后.结果 高血压脑梗死组的舒张压(DBP)及平均动脉压(MAP)明显高于糖...