急性脑梗死患者血清YKL-40、hs-CRP水平与颈动脉粥样硬化斑块的相关性研究

目的 探讨急性脑梗死患者颈动脉粥样硬化性斑块与人类软骨糖蛋白-39(YKL-40)、超敏C-反应蛋白(hs-CRP)含量的关系.方法 选取130例急性脑梗死患者和30例正常对照者检测血清YKL40、hs-CRP水平.对急性脑梗死患者结合颈动脉超声检查结果,分为颈动脉IMT正常组30例、颈动脉IMT增厚组30例、颈动脉斑块组70例,其中稳定斑块37例,不稳定斑块33例,测定并比较各组血清YKL40、hs-CRP水平.结果 急性脑梗死组血清YKL40、hs-CRP水平显著高于正常对照组(P＜0.01);在急性脑梗死患者中,有颈动脉粥样硬化组血清YKL-40、hs-CRP水平较颈动脉IMT正常组明显升高(P＜0.01),颈动脉IMT斑块形成组血清YKL-40、hs-CRP水平较颈动脉IMT增厚组明显升高(P＜0.01),颈动脉粥样硬化不稳定斑块组血清YKL-40、hs-CRP水平显著高于稳定斑块组;线性相关分析表明YKL-40水平和hs-CRP水平无明显相关性(r=0.04,P＞0.05);Logistic回归分析结果显示:YKL-40、hs-CRP是发生颈动脉粥样硬化的危险因素(OR=1.128,95％C1 1.21～1.87;OR=2.62,95％ CI1.76 ～4.47).结论 YKL-40、hs-CRP可能反映急性脑梗死患者颈动脉粥样硬化斑块的炎症程度以及斑块的不稳定程度,病变越重,斑块越不稳定,YKL-40、hs-CRP水平越高,且YKL-40水平独立于hs-CRP水平.     

急性脑梗死患者颈动脉粥样硬化与血清高敏C反应蛋白水平的关系

目的 探讨颈动脉粥样硬化与高敏C反应蛋白(hs-CRP)、急性脑梗死之间的关系.方法 应用彩色多普勒超声检测仪对58例急性脑梗死患者及35例健康对照者进行颈动脉超声检查,观测颈动脉内膜-中膜厚度(IMT)、粥样斑块类型,同时检测血清hs-CRP水平.结果 脑梗死组患者血清hs-CRP、颈动脉IMT及粥样斑块发生率较对照组明显增加(P＜0.05);脑梗死患者中不稳定斑块、稳定斑块、无斑块组血清hs-CRP水平差异有统计学意义(P＜0.05);血清hs-CRP水平与颈动脉IMT呈正相关.结论 颈动脉IMT、粥样硬化斑块、血清hs-CRP与脑梗死有密切的关系,hs-CRP能反映颈动脉粥样硬化的程度及斑块的稳定性.     

可溶性CD40L、MMP-9与颈动脉粥样硬化及急性脑梗死的关系

目的探讨可溶性CD40L(sCD40L)、基质金属蛋白酶-9(MMP-9)与颈动脉粥样硬化及急性脑梗死(ACI)的关系。方法选取首次发病的ACI患者90例和健康对照组30例,采用双抗体夹心酶联免疫吸附试验(ELISA)测定血清sCD40L、MMP-9的水平。应用颈动脉超声检测颈动脉内膜状况。比较不同程度颈动脉粥样硬化及不同面积脑梗死患者血清sCD40L、MMP-9的水平变化,并对所有脑梗死患者进行神经功能缺损评分。结果 ACI患者血清sCD40L、MMP-9的水平显著高于对照组(P0.01);大梗死组血清sCD40L、MMP-9水平高于中、小梗死组,中梗死组高于小梗死组,差异均有统计学意义(均P0.01);随着颈动脉粥样硬化程度加重,脑梗死病情越重及脑梗死面积越大,血清sCD40L、MMP-9的水平也越高;血清sCD40L与MMP-9的水平呈正相关(r=0.887,P0.01)。结论 ACI患者血清sCD40L、MMP-9水平可以反映颈动脉粥样硬化斑块的性质和稳定性、脑梗死面积与病情的严重程度;CD40-CD40L系统可能通过上调MMP-9导致颈动脉粥样硬化斑块不稳定。     

H型高血压并发急性脑梗死同型半胱氨酸水平升高的危险因素分析

目的 探讨H型高血压并发急性脑梗死同型半胱氨酸(Hcy)与炎症因子、颈动脉粥样硬化及斑块形成的相关性。方法 选取许昌市中心医院103例高血压并发急性脑梗死患者,均行Hcy水平检测,依据Hcy水平分为观察组53例(Hcy15μmol/L),对照组50例(Hcy≤15μmol/L),比较2组性别、年龄、超敏C反应蛋白(hs-CRP)、单核细胞趋化蛋白1(MCP-1)、氧化型低密度脂蛋白(ox-LDL)、血管内皮细胞钙黏蛋白(VE-cadherin)水平、颈动脉内膜中层厚度(IMT)、颈动脉斑块形成率等。结果观察组血清hs-CRP、MCP-1、ox-LDL、VE-cadherin水平及IMT均高于对照组,不稳定斑块形成率60.38%(32/53),高于对照组40.00%(20/50),差异有统计学意义(P0.05);经Logistic回归分析,血清hs-CRP、MCP-1、ox-LDL、VE-cadherin及IMT、颈动脉斑块形成为诱发高血压并发急性脑梗死患者血清Hcy水平升高的危险因素(P0.05);经Spearman相关性分析,高血压并发急性脑梗死患者血清Hcy水平升高与炎症因子、颈动脉粥样硬化及颈动脉粥样斑块形成率呈正相关(P0.05)。结论 炎症因子、颈动脉粥样硬化及斑块形成是高血压并发急性脑梗死患者血清同型半胱氨酸水平升高的高危因素,与血清同型半胱氨酸水平升高呈正相关。     

急性缺血性脑血管病患者血清ox-LDL及PAPP-A水平与颈动脉粥样硬化的相关性研究

目的探讨急性缺血性脑血管病患者颈动脉粥样硬化与血清氧化型低密度脂蛋白(ox-LDL)、妊娠相关血浆蛋白A(PAPP-A)水平的关系。方法随机选取急性脑梗死患者90例和短暂性脑缺血发作(TIA)患者60例作为研究对象,随机选取健康体检者30例作为对照组。入选者均检测血清ox-LDL、PAPP-A水平。对急性脑梗死和TIA患者进行颈动脉超声检查,发现颈动脉内-中膜厚度(IMT)正常者22例,IMT增厚者47例,颈动脉斑块形成者81例,其中稳定斑块者49例,不稳定斑块者32例。比较各组血清ox-LDL及PAPP-A水平。结果急性脑梗死组血清PAPP-A及ox-LDL水平显著高于TIA组(P<0.01),后者显著高于正常对照组(P<0.01);在缺血性脑血管病患者中,颈动脉粥样硬化斑块形成者血清PAPP-A及ox-LDL水平较颈动脉IMT增厚组明显升高(P<0.01),后者高于IMT正常组(P<0.01);在颈动脉斑块形成者中,其血清PAPP-A及ox-LDL水平在不稳定斑块组高于稳定斑块组(P<0.01)。Spearman分析显示,血清PAPP-A与ox-LDL水平之间存在明显相关性(r=0.839,P<0.05);logistic回归分析显示,血清PAPP-A与ox-LDL水平是发生颈动脉粥样硬化的危险因素(OR=2.549,95%CI1.12~3.79;OR=1.317,95%CI1.15~2.11)。结论急性缺血性脑血管病患者颈动脉粥样硬化的发生和进展与ox-LDL、PAPP-A水平相关,血清ox-LDL及PAPP-A水平可在一定程度上反映急性缺血性脑血管病患者颈动脉粥样硬化的程度。两者在颈动脉甚至颅内动脉粥样硬化的形成过程中产生协同作用。     

急性脑梗死患者颈动脉粥样硬化斑块稳定性与血清YKL-40水平的相关性研究

目的探讨急性脑梗死患者颈动脉粥样硬化斑块稳定性与血清YKL-40水平之间的相关性,为颈动脉粥样硬化及脑梗死的早期诊治提供临床依据。方法选取95例急性脑梗死患者为研究对象,按照颈动脉彩超检查结果将脑梗死组分为不稳定斑块组、稳定斑块组和无斑块组。选取同期健康体检人员50例为对照组。采用双抗体夹心酶联免疫法检测急性脑梗死患者入院48 h、入院14 d及对照组血清YKL-40水平,比较不同时期不同性质颈动脉斑块血清YKL-40的差异。结果脑梗死组患者血清YKL-40水平明显高于正常对照组,且不稳定斑块组血清YKL-40的水平>稳定斑块组>无斑块组,差异均具有统计学意义(P<0.05),脑梗死各亚组入院14 d血清YKL-40水平均低于入院48 h血清值,差异有统计学意义(P<0.05)。YKL-40的水平与梗死面积、NIHSS、胆固醇、血压、GLU、LDL-C、TG呈正相关(P<0.05)。结论血清YKL-40是AS形成的重要标志物,与动脉粥样硬化斑块的稳定性相关。血清YKL-40可以监测动脉粥样硬化的程度,从一定程度上预测脑梗死发生的风险。     

急性脑梗死患者血清内脂素含量的变化及对颈动脉粥样硬化斑块形成和稳定性的影响

目的观察急性脑梗死(ACI)患者血清内脂素水平,探讨其与颈动脉粥样硬化斑块形成和稳定性的关系。方法对68例ACI患者及45例健康人群(对照组)进行颈动脉彩色多普勒超声检查,根据血管超声检查颈动脉粥样硬化斑块结果,对ACI患者分组并检测血清内脂素水平。结果 68例ACI患者中,稳定斑块组31例,不稳定斑块组25例,无斑块形成(无斑块组)12例;3组内脂素水平分别为(28.25±8.06)μg/L、(34.25±8.75)μg/L、(16.58±6.02)μg/L,对照组为(14.56±6.12)μg/L;不稳定斑块组高于稳定斑块组,稳定斑块组高于无斑块组及对照组,组间比较差异有统计学意义(P0.05)。结论血清内脂素与ACI患者颈动脉粥样硬化斑块的形成及不稳定性的形成关系密切。     

急性脑梗死患者血清甲壳质酶蛋白40水平与颈动脉粥样硬化的关系

目的 探讨急性脑梗死(ACI)患者血清甲壳质酶蛋白40(YKL-40)水平与颈动脉粥样硬化的关系.方法 采用酶联免疫吸附(ELISA)法对78例ACI患者(ACI组)和34名健康体检者(正常对照组,NC组)进行血清YKL-40水平检测;并对ACI患者采用彩色多普勒超声仪进行颈动脉超声检查,测定其颈动脉内膜-中层厚度(IMT)及颈动脉粥样硬化斑块的性质.结果 ACI组患者血清YKL-40水平明显高于NC组(P＜0.001) 共有74例(94.9％) ACI患者存在颈动脉IMT异常.其中,管腔狭窄组(颈动脉IMT＞ 1.4 mm)的血清YKL-40水平明显高于斑块形成组(IMT 1.2 ～1.4 mm)及内膜增厚组(IMT 1.0～1.1 mm)(均P＜0.05);而斑块形成组与内膜增厚组比较差异无统计学意义.有64例患者(82.1％)存在颈动脉粥样硬化斑块(不稳定斑块40例,稳定斑块24例),12例患者(15.4％)表现为颈动脉内膜粗糙.其中,不稳定斑块组血清YKL-40水平明显高于稳定斑块组和内膜粗糙组(均P＜0.01);而稳定斑块组与内膜粗糙组的差异无统计学意义.结论 ACI患者血清YKL-40水平明显升高,并且与颈动脉粥样硬化程度有关.     

急性脑梗死患者血清sdLDL-C与PTX-3水平与颈动脉粥样硬化斑块性质的关系

目的通过联合测定血清小而密低密度脂蛋白胆固醇(sdLDL-C)、正五聚蛋白3(PTX3)水平探讨与急性脑梗死发生及颈动脉粥样硬化斑块性质的关系。方法纳入急性脑梗死患者150例为观察组,根据颈动脉粥样硬化斑块稳定性分为稳定型斑块组64例、易损斑块组86例,另取体检健康者102例为对照组。采用(ELISA)法检测血清sdLDL-C、PTX3水平。应用非条件多因素Logistic回归分析sdLDL-C、PTX3与急性脑梗死患者颈动脉粥样硬化斑块性质的关系。结果观察组血清sdLDL-C及PTX3水平明显高于对照组(P 0. 01);易损斑块组TG、LDL-C、sdLDL-C、PTX3均高于稳定斑块组(P 0. 01),但HDL-C水平低于稳定斑块组(P 0. 05);非条件多因素Logistic回归分析显示LDL-C、sdLDL-C、PTX3为急性脑梗死患者颈动脉粥样斑块稳定性的独立危险因素(P 0. 05)。结论血清sdLDL-C和PTX-3水平升高是急性脑梗死发生及不稳定颈动脉粥样硬化斑块形成的危险因素。     

脑卒中高危人群颈动脉斑块与血清sCD40L之间的关系

目的观察血清可溶性CD40配体(s CD40L)与高危人群颈动脉斑块性质之间的关系,为高危人群早期服用阿司匹林预防缺血性脑血管病提供依据。方法根据入选条件选取145例作为高危组,选取健康体检者40例作为对照组,据颈动脉超声检查结果将高危组分为无斑块组(Ⅰ)67例、稳定斑块组(Ⅱ)21例和不稳定斑块组(Ⅲ)57例3个亚组,采用酶联免疫吸附法(ELISA)测定所有研究对象血清s CD40L水平。结果高危组血清s CD40L水平明显高于对照组,差异有统计学意义P<0.05;高危组各亚组间血清s CD40L水平比较:Ⅰ组<Ⅱ组<Ⅲ组[(3.489±0.820)mg/ml<(3.600±0.697)mg/ml<(4.011±1.074)mg/ml],差异有统计学意义P<0.05;经Logistic回归分析结果显示:血清s CD40L(OR=1.788,P=0.037)是影响颈动脉斑块性质的危险因素。结论血清s CD40L是颈动脉粥样硬化斑块形成的危险因素;血清s CD40L可能影响颈动脉粥样硬化斑块的性质,促使其由稳定斑块向不稳定斑块的方向发展;对于脑卒中高危人群血清s CD40L水平较高者,应早期给予阿司匹林药物治疗,以此来预防缺血性脑血管病的发生、发展。     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Effects of prevention of afferentation of the development of the chick optic lobe

BONDY, S. C., M. E. HARRINGTON AND C. L. ANDERSON. Effects of prevention of afferentation on the developmentof the chick optic lobe. BRAIN RES. BULL. 3(5) 411–413, 1978.—The effects of unilateral extirpation of the right optic cup of the three-day incubated chick embryo upon the rate of synthesis and the stability of DNA in the non-innervated optic lobe, have been studied. This surgical procedure prevents innervation of the optic lobe contralateral to the removed eye, while the other optic lobe is normally innervated by retinal ganglion cells of the remaining eye. At the 20th day of incubation, the DNA content of the non-innervated lobe was below that of the paired lobe receiving normal innervation. This deficiency of cell number was caused by two events; death of an excess number of neurons formed early in embryogenesis and a reduced rate of glial proliferation in the later stages of incubation.     

帕金森病运动症状进展分析

目的分析帕金森病(PD)患者运动症状进展特点。方法采用PD统一评分量表(UPDRS)Ⅲ对912例PD患者进行评估。结果与病程1年的患者比较,除病程1~2年的患者外,其他病程患者的UPDRSⅢ评分、强直分、姿势或步态异常分、轴性症状总分、言语分、步态分显著升高(均P0.05),病程5~6年及14年患者的震颤分,病程5~6年、7~8年、9~13年、14年患者的运动迟缓分、姿势分显著升高(P0.05~0.01)。轴性症状进展速度高于UPDRSⅢ评分。结论 PD患者病程早期UPDRSⅢ评分进展快,震颤症状进展独立于其他症状,轴性症状评分较UPDRSⅢ更敏感地反映疾病加重趋势。     

Frequency of accumulation of filaments in adaxonal cytoplasm of Schwann cells of myelinated fibers of rat spinal roots

Summary The frequency of accumulation of 6-nm filaments in the adaxonal cytoplasm of Schwann cells in the 6th lumbar dorsal and ventral roots was evaluated in 4-, 8-, 26- and 45-week-old Sprague-Dawley rats. The frequency was higher in 4- and 8-week-old (growing) rats than in 26- and 45-week old (mature) rats, and also higher in ventral than in dorsal roots in 4-, 8- and 26-week old rats. There were no clusters on certain groups of myelinated fibers according to the size of transverse axonal area, in both the ventral and dorsal roots. Therefore, this accumulation may reflect certain functions of the adaxonal cytoplasm of Schwann cell during natural growth and maturation of the axon and myelin sheath.     

他汀类药物的使用和颅内动脉瘤破裂相关性分析

目的 探讨他汀类药物对颅内动脉瘤破裂的影响。方法 2010年3月至2014年3月收治颅内囊状动脉瘤67例,其中破裂者32例,未破裂者35例。采用多变量Logistic回归评估他汀类药物的使用和颅内动脉瘤破裂的关系。结果 破裂组术前使用他汀类药物4例（12.5%,4/32）,未破裂组16例（45.7%,16/35）。破裂组服用他汀类药物的百分比显著低于未破裂组（P<0.01）。纠正潜在的混杂干扰后（or值: 0.30,95%可信空间:0.12~="" 0.64）显示,颅内动脉瘤破裂与他汀类药物的使用呈显著负相关,也与高血清总胆固醇浓度有关。结论 本结果提示他汀类药物对颅内动脉瘤破裂有一定的预防效果。     

Impact of our understanding of the genetic aetiology of epilepsy

A genetic contribution to aetiology is estimated to be present in up to 40% of patients with epilepsy. It is useful to categorise genetic epilepsies according to the mechanisms of inheritance into Mendelian disorders, non-mendelian or ‘complex’ disorders, and chromosomal disorders. Over 200 Mendelian diseases include epilepsy as part of the phenotype, and the genes for a number of these have been identified recently. These include autosomal recessive progressive myoclonic epilepsies such as Unverricht-Lundborg disease, Lafora disease and the neuronal ceroid lipofuscinoses, and three autosomal dominant idiopathic epilepsies. The last named have been shown to arise from mutations in ion channel genes. Autosomal dominant nocturnal frontal lobe epilepsy is caused by mutations in CHRNA4, benign familial neonatal convulsions by mutations in KCNQ2 and KCNQ3, and generalised epilepsy with febrile seizures plus by mutations in SCN1B. ‘Complex’, familial epilepsies are more difficult to analyse, but evidence has been obtained for loci predisposing to juvenile myoclonic epilepsy on chromosome 6p and 15q. Lastly, the genes underlying several spike-wave epilepsies in mice have been cloned, and three of these encode sub-units of voltage-gated calcium channels. Received: 29 September 1999/Accepted: 7 December 1999     

Function of circle of Willis

Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.     

肌萎缩侧索硬化三例误诊分析

目的掌握肌萎缩侧索硬化(ALS)的诊断标准,以便早期准确诊断,避免误诊。方法分析3例ALS患者早期被误诊的临床资料。结果 3例患者均以下肢无力发病,逐渐波及上肢或对侧肢体,脊柱MR I示颈部或腰部椎间盘突出压迫硬膜囊,手术治疗后,症状无缓解,病情仍进行性加重,经肌电图检查证实为ALS。结论临床医师应熟知ALS的诊断标准,对患者详细询问病史、认真查体和电生理检查是减少ALS误诊的关键。     

失匹配负波在意识障碍评估中的临床价值探讨

自失匹配负波(MMN)于20世纪70年代被发现以来,我们对规律性声音被打破后所诱发的前注意检测有了进一步认识,而MMN成为了开启认知大门的钥匙。至今为止,MMN的研究范围从产生机制发展到神经精神疾病相关的临床试验,特别是对于急性脑损伤(ABI)昏迷以及进展后的慢性意识障碍(DoC)患者,MMN被认为是一个可靠的预后预测指标。然而,由于MMN难以用于个体评估,目前在临床实践中的应用仍十分有限,广大临床医师对MMN的了解甚少。因此,本文就MMN的产生机制、在意识障碍中的临床意义、判读方法及其影响因素做一综述。     

腺垂体功能减退症临床特征变化分析

目的探讨腺垂体功能减退症患者的病因结构变化及临床表现。方法回顾性分析我院2013-01—2016-12住院及门诊78例腺垂体功能减退症患者的临床资料。结果男32例(41.03%),女46例(58.97%);诊断时年龄11~89岁,平均62.5岁;鞍区占位(包括术前及术后)52例(66.67%),席汉综合征8例(10.26%),空泡蝶鞍9例(11.65%),病因不明8例(10.26%),垂体-下丘脑发育不良1例(1.28%)。首次就诊科室:纳差厌食、恶心呕吐就诊于消化内科36例(46.15%)最常见。ACTH+TSH+Gn+G激素缺乏为19例最多,占24.36%,ACTH+TSH+Gn缺乏15例,占19.23%。结论腺垂体功能减退症病因结构发生变化,发病人群、首发症状及受累激素也不同,患者女性多于男性,发病年龄偏高,症状不典型,分布于临床多个科室,其中以低钠血症为首发临床表现就诊消化内科最多。