轻型缺血性卒中患者静脉溶栓治疗分析

目的探讨重组组织型纤溶酶原激活物(rt-PA)治疗急性轻型缺血性卒中的有效性和安全性。方法纳入2017年11月至2018年10月发病4.50 h内入院的252例急性轻型缺血性卒中患者,分别行rt-PA静脉溶栓(静脉溶栓组,84例)、阿司匹林联合氯吡格雷双联抗血小板(双抗组,108例),以及阿司匹林或氯吡格雷抗血小板(单抗组,60例)治疗,治疗后24 h采用CT或MRI观察有无颅内出血,比较治疗前后血清超敏C-反应蛋白(hs-CRP)和红细胞沉降率(ESR)表达变化,并于入院后7 d、发病后21和90 d行改良Rankin量表评分判断预后。结果入院后7 d,不同治疗组患者血清hs-CRP(均P=0.000)和ESR(均P=0.000)水平降低,其中双抗组和单抗组血清hs-CRP(P=0.000,0.000)和ESR(P=0.000,0.010)高于静脉溶栓组;治疗后24 h,静脉溶栓组与抗血小板组颅内出血发生率差异无统计学意义[1.19%(1/84)对0(0/168);χ~2=2.008,P=0.366]。入院后7 d,静脉溶栓组预后良好率高于双抗组(P=0.043)和单抗组(P=0.012);发病后21和90 d,静脉溶栓组预后良好率仅高于单抗组(P=0.021,0.037)。结论对于轻型缺血性卒中患者,尤其是症状轻微但可致残的患者应及时行rt-PA静脉溶栓,而因各种原因未能接受静脉溶栓治疗的患者则需在发病24小时内及时行阿司匹林联合氯吡格雷双联抗血小板治疗。     

ABCD3-Ⅰ评分在短暂性脑缺血发作预防与治疗中的应用

目的探讨ABCD3-Ⅰ评分系统评价阿司匹林单药及其与氯吡格雷联合治疗短暂性脑缺血发作的有效性和安全性。方法 122例短暂性脑缺血发作患者分别接受阿司匹林单药(单抗组)或阿司匹林与氯吡格雷联合(双抗组)治疗,并根据ABCD3-Ⅰ评分系统进一步分为低危组、中危组和高危组,评价各亚组患者缺血性卒中和药物不良反应发生率。结果治疗3周时,低危组无一例发生缺血性卒中,其他各组分别为:中危单抗组9/20例、中危双抗组2/19例,高危单抗组10/19例、高危双抗组3/20例,组间差异有统计学意义(P=0.031,0.019)。单抗组和双抗组患者药物不良反应均以恶心、反酸等消化道症状为主(χ2=0.000,P=1.000),无明显出血倾向、肝肾功能未见异常。结论 ABCD3-Ⅰ评分系统可以作为评价抗血小板药物安全性的指标。阿司匹林联合氯吡格雷可能较阿司匹林单药预防缺血性卒中更具优势。     

替罗非班在超时间窗非大血管闭塞性缺血性卒中中的应用价值

目的探讨超时间窗非大血管闭塞性缺血性卒中患者早期应用替罗非班的临床价值。方法对2017年4月至2019年4月的90例超时间窗非大血管闭塞性缺血性卒中患者临床资料进行回顾分析,根据不同治疗方案分为替罗非班联合双联抗血小板治疗组(治疗组,50例)和单纯双联抗血小板治疗组(对照组,40例);于治疗第1、3和7天进行神经功能缺损程度[美国国立卫生研究院卒中量表(NIHSS)]评价,入院当日与治疗3个月后进行神经功能恢复[改良Rankin量表(mRS)]和日常生活活动能力[日常生活活动能力量表(ADL)]评价,并记录两组患者治疗期间出血及严重血小板减少事件(血小板计数100×109/L)的发生情况。结果治疗后不同时间点两组NIHSS评分差异具有统计学意义(P=0.000)。对照组治疗第7天时,NIHSS评分低于第1天(P=0.000)和第3天(P=0.000);治疗组治疗后第1、3和7天NIHSS评分呈逐渐下降趋势(均P=0.000),且明显低于对照组(P=0.000)。两组治疗3个月后,mRS评分(P=0.000)低于、ADL评分高于(P=0.000)治疗前,且治疗组mRS评分低于(P=0.000)、ADL评分高于(P=0.003)对照组。治疗组与对照组患者出血及严重血小板减少事件发生率差异无统计学意义[26%(13/50)对35%(14/40);χ~2=0.483,P=0.439]。结论对于超时间窗非大血管闭塞性缺血性卒中患者,发病早期静脉应用替罗非班能够显著改善其神经功能,提高生活质量和日常生活活动能力。     

氯吡格雷联合奥扎格雷钠治疗急性缺血性卒中疗效评价

研究背景抗血小板治疗已经成为缺血性卒中的常规治疗方法,目前对其作用的肯定主要源于临床应用,迄今尚无一项能够准确评价其有效性的实验室指标。有研究证实,血小板活化程度与动脉粥样硬化和缺血性卒中相关,尤其是血小板α颗粒膜糖蛋白CD62p和溶酶体膜糖蛋白CD63均为血小板活化的重要指标。本研究旨在通过观察急性缺血性卒中患者血小板膜表面CD62p和CD63表达变化,探讨以血小板活化程度反映氯吡格雷(75 mg)、奥扎格雷钠(80 mg)与阿司匹林(0.15 g)的疗效差异。方法采用流式细胞术检测急性缺血性卒中患者氯吡格雷(75 mg)联合奥扎格雷钠(80 mg,联合治疗组)及阿司匹林单药(阿司匹林组)治疗前后血小板CD62p和CD63阳性表达率,美国国立卫生研究院卒中量表(NIHSS)评价神经功能改善程度。结果与正常对照组相比,治疗前急性缺血性卒中组患者血小板CD62p和CD63阳性表达率升高(P=0.001,0.032);治疗后CD62p和CD63阳性表达率、NIHSS评分逐步下降(均P=0.000)。与治疗前相比,治疗后联合治疗组和阿司匹林组患者血小板CD62p和CD63阳性表达率、NIHSS评分逐步下降(均P=0.000),但组间差异无统计学意义(均P>0.05)。CD62p和CD63阳性表达率在不同观察时间点与治疗分组之间不存在交互作用(F=1.403,P=0.250;F=2.830,P=0.063),但NIHSS评分在不同观察时间点与治疗分组之间存在交互作用(F=4.518,P=0.013)。结论抗血小板药物治疗急性缺血性卒中有效,但氯吡格雷与奥扎格雷钠联合治疗之疗效与阿司匹林单药治疗并无差异。缺血性卒中急性期测定血小板CD62p阳性表达率可以用于评价抗血小板药物的疗效,但CD63表达的临床价值尚待进一步研究。     

急性脑梗死患者微栓子信号的影响因素及其与近期预后的关系研究

目的 探讨急性脑梗死患者微栓子信号的影响因素及其与近期预后的关系。方法 前瞻 性连续纳入2019 年1 月至2020 年1 月皖南医学院第二附属医院神经内科接诊的118 例急性脑梗死患者 作为研究对象,均经颅多普勒监测微栓子信号,根据微栓子信号是否阳性,分为阳性组和阴性组。采用单因 素和多因素Logistic回归分析微栓子信号的影响因素;随访6个月,观察脑梗死复发情况,通过Kaplan-Meier 生存曲线分析微栓子信号阳性与脑梗死复发的关系。结果 118例急性脑梗死患者中,36 例（30.51%）微 栓子信号阳性;阳性组有颈动脉斑块占比［69.44%（25/36）］、颈动脉重度狭窄率［55.56%（20/36）］、血小 板［（278.84±26.93）×109/L］、超敏C 反应蛋白水平［（13.87±3.58）mg/L］、美国国立卫生研究院卒中量 表（NIHSS）评分［（5.93±1.17）分］均明显高于阴性组,高密度脂蛋白胆固醇水平［（0.91±0.33）mmol/L］ 低于阴性组［分别为29.27%（24/82）、20.73%（17/82）、（215.48±16.53）×109/L、（9.87±2.07）mg/L、（4.88± 0.58）分、（1.23±0.65）mmol/L］,差异均有统计学意义（均P ＜ 0.05）。经多因素Logistic 回归分析,颈动 脉斑块（OR=7.425,95%CI：2.892～28.882）、重度狭窄（OR=2.692,95%CI：1.362～8.736）、高水平血小板 （OR=8.462,95%CI：1.425～16.465）均是微栓子信号阳性的独立危险因素（均P＜ 0.05）。 所有患者获得 随访,脑梗死复发15 例,其中阳性组脑梗死复发率为22.22%（8/36）,高于阴性组的8.54%（7/82）,差异有 统计学意义（χ2=4.223,P=0.040）;经Kaplan-Meier 生存曲线分析和Log-rank 检验,阳性组较阴性组患者 更易出现脑梗死复发（P＜ 0.05）。结论 急性脑梗死患者微栓子信号阳性与颈动脉斑块、重度狭窄和高 水平血小板有关,提示这部分患者近期预后更差,需要更加密切的随访,严格控制危险因素。     

奥扎格雷钠联合阿司匹林双重抗血小板治疗急性脑梗死疗效观察

目的观察奥扎格雷钠联合阿司匹林双抗血小板治疗急性脑梗死的临床疗效及安全性。方法将符合入选标准的120例急性脑梗死患者随机分为双抗组60例和单抗组60例。2组均给予相同的基础治疗和对症处理,双抗组给予奥扎格雷钠联合阿司匹林,单抗组单用阿司匹林抗血小板治疗。分别在治疗前及治疗后15d监测血小板参数、凝血指标并进行神经功能缺损评分(NIHSS)并记录出血等不良反应。结果治疗后2组PA均降低,双抗组降低更加明显,差异有统计学意义(P0.05);2组患者PT、APTT均延长,但2组比较差异无统计学意义(P0.05);治疗15d后,双抗组NlHSS评分较单抗组减少更明显,双抗组显效率及总有效率均显著高于单抗组,差异具有统计学意义(均P0.05)。2组均无严重出血事件发生。结论短疗程联合应用奥扎格雷钠及阿司匹林双重抗血小板治疗急性脑梗死,显著优于单用阿司匹林,可明显降低患者的血小板聚集率,显著提高临床疗效,且无明显不良反应发生。     

癌症相关缺血性卒中临床研究

目的探讨肿瘤患者发生缺血性卒中的影响因素、生化指标、病因,以及影像学特点,以提高临床认识。方法收集2018年4月至2019年1月收治的693例缺血性卒中患者临床资料,比较缺血性卒中伴活动性癌症组(癌症组,31例)与传统急性缺血性卒中不伴癌症组(对照组,662例)入院时社会人口学数据、脑卒中危险因素、入院时美国国立卫生研究院卒中量表(NIHSS)评分,血小板计数、D-二聚体、纤维蛋白原、C-反应蛋白水平,扩散加权成像(DWI)显示的梗死灶特点[急性多发性缺血病变(AMIMCT)],记录癌症组患者肿瘤类型及组织学分型差异。采用单因素和多因素后退法Logistic回归分析癌症相关缺血性卒中的影响因素。结果与对照组相比,癌症组患者年龄偏高(χ~2=2.148,P=0.032),高血压(χ~2=5.425,P=0.020)和高脂血症(Fisher确切概率法:P=0.000)比例低;血清D-二聚体(Z=2687.500,P=0.001)、纤维蛋白原(t=2.402,P=0.022)和C-反应蛋白(Z=3669.000,P=0.001)水平升高。两组TOAST分型差异具有统计学意义(Fisher确切概率法:P=0.000),与对照组相比,癌症组大动脉粥样硬化(LAA)型比例较低(Fisher确切概率法:P=0.000),不明病因(SUE)型比例较高(χ~2=175.418,P=0.000);而AMIMCT比例较高(χ~2=22.560,P=0.000)。多因素后退法Logistic回归分析显示,癌症组患者缺乏高脂血症病史(OR=0.188,95%CI:0.048～0.730;P=0.016),而SUE型(OR=29.854,95%CI:10.310～86.449;P=0.000)以及高水平的血清D-二聚体(OR=1.663,95%CI:1.294～2.137;P=0.000)和纤维蛋白原(OR=1.785,95%CI:1.294～2.137;P=0.000)是其危险因素。结论癌症相关缺血性卒中患者常缺乏大动脉粥样硬化证据,血清D-二聚体和纤维蛋白原水平升高,以及SUE型提示此类患者可能存在高凝状态和栓塞机制。     

急性缺血性脑卒中患者微栓子监测的研究进展

血液中微栓子的存在被认为是缺血性脑卒中的众多独立危险因素之一,而TCD又被认为能、甚至是唯一能侦测到血液中活动微栓子信号(MES)的无创性检查方法。TCD MES监测可预测无症状颈动脉狭窄发生卒中的风险,同时提示高危、不稳定的无症状斑块,或者斑块表面有血栓;还用于颈动脉内支架成形术后的MES监测与研究,使用抗凝药或抗血小板药的评估和疗效评价等。大面积脑梗死患者的MES阳性率显著高于小面积脑梗死和TIA的患者。对于隐源性卒中或复发性TIA,TCD MES是实时发现、定位、量化脑血栓形成的金标准,是卒中早期复发的独立预测因子。但是,TCD MES的检出率及其栓子负荷与急性缺血性脑卒中患者远期预后的关系的文献尚少,需要更多的研究加以证实。     

老年脑卒中患者主动脉弓粥样斑块与脑动脉微栓子信号的相关性

主动脉弓动脉粥样斑块(AAA)固有引起脑栓塞的潜在危险,已证实为老年人缺血性卒中的危险因素.然而AAA与脑循环中微栓子的关系并不十分清楚.本研究的目的是探讨老年缺血性卒中患者AAA是否与经颅多普勒(TCD)自动检测的脑动脉微栓子信号(MES)相关.     

进展性缺血性脑卒中危险因素分析及微栓子对卒中进展的预测价值

目的探讨进展性缺血性脑卒中(PIS)患者的危险因素及微栓子对进展性卒中的预测价值。方法纳入2016年3月至2018年3月就诊于内蒙古自治区人民医院神经内科的50例PIS患者及同时期非进展的缺血性卒中病人62例,所有纳入的患者均行头颅磁共振、颈动脉血管超声、心脏彩超、心电图、48 h内微栓子检查,并对纳入的患者进行问卷调查。结果微栓子阳性PIS患者病灶多位于皮质(P0.05)。PIS与微栓子、低密度脂蛋白异常、院前未服用阿司匹林、院前服用降压药物、颈动脉斑块等因素显著相关(P 0.05)。logistic回归分析提示微栓子(OR=7.246,P=0.001)、低密度脂蛋白异常(OR=3.879,P=0.007)、颈动脉斑块(OR=4.177,P=0.007)、院前未口服阿司匹林(OR=4.304,P=0.046)、院前服用降压药物(OR=3.734,P=0.01)为PIS的独立危险因素。结论微栓子、低密度脂蛋白异常、院前未口服阿司匹林、院前服用降压药物、颈动脉斑块是PIS危险因素,且微栓子更具预测价值。     

Tau-induced neurodegeneration: mechanisms and targets

The accumulation of hyperphosphorylated tau is a common feature of several dementias. Tau is one of the brain microtubule-associated proteins. Here we discuss tau’s functions in microtubule assembly and stabilization and with regard to its interactions with other proteins. We describe and analyze important post-translational modifications: hyperphosphorylation, ubiquitination, glycation, glycosylation, nitration, polyamination, proteolysis, acetylation, and methylation. We discuss how these post-translational modifications can alter tau’s biological function. We analyze the role of mitochondrial health in neurodegeneration. We propose that microtubules could be a therapeutic target and review different approaches. Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and propose a mechanism of neurodegeneration.     

The effect of risperidone on reward‐related brain activity is robust to drug‐induced vascular changes

Dopamine (DA) mediated brain activity is intimately linked to reward‐driven cerebral responses, while aberrant reward processing has been implicated in several psychiatric disorders. fMRI has been a valuable tool in understanding the mechanism by which DA modulators alter reward‐driven responses and how they may exert their therapeutic effect. However, the potential effects of a pharmacological compound on aspects of neurovascular coupling may cloud the interpretability of the BOLD contrast. Here, we assess the effects of risperidone on reward driven BOLD signals produced by reward anticipation and outcome, while attempting to control for potential drug effects on regional cerebral blood flow (CBF) and cerebrovascular reactivity (CVR). Healthy male volunteers (n = 21) each received a single oral dose of either 0.5 mg, 2 mg of risperidone or placebo in a double‐blind, placebo‐controlled, randomised, three‐period cross‐over study design. Participants underwent fMRI scanning while performing the widely used Monetary Incentive Delay (MID) task to assess drug impact on reward function. Measures of CBF (Arterial Spin Labelling) and breath‐hold challenge induced BOLD signal changes (as a proxy for CVR) were also acquired and included as covariates. Risperidone produced divergent, dose‐dependent effects on separate phases of reward processing, even after controlling for potential nonneuronal influences on the BOLD signal. These data suggest the D2 antagonist risperidone has a wide‐ranging influence on DA‐mediated reward function independent of nonneuronal factors. We also illustrate that assessment of potential vascular confounds on the BOLD signal may be advantageous when investigating CNS drug action and advocate for the inclusion of these additional measures into future study designs.     

星形胶质细胞对天冬氨酸特异性半胱氨酸蛋白酶介导β淀粉样蛋白早期突触毒性作用的影响

目的探讨星形胶质细胞(astrocyte,AS)对天冬氨酸特异性半胱氨酸蛋白酶(cysteinyl aspartate specific proteinase,caspase)介导β淀粉样蛋白(β-amyloid,Aβ)早期突触毒性作用的影响,以期为进一步研究与血管性痴呆(vascular dementia,Va D)的发病机制奠定基础。方法以原代培养大鼠海马纯神经元体系(NE-S)及混合培养体系(MIX-S,主要包含神经元及AS)为研究对象,各体系分为6组:对照组、caspase-8抑制剂组、caspase-9抑制剂组、Aβ处理组、caspase-8抑制剂预处理加Aβ组和caspase-9抑制剂预处理加Aβ组。免疫荧光检测各组近胞体10μm段树突中突触后密度蛋白(postsynaptic density-95,PSD95)表达量的变化。结果 1在NE-S与MIX-S中,与对照组相比,caspase-8抑制剂组、caspase-9抑制剂组PSD95的表达量均无明显差异,Aβ处理组PSD95的表达量均显著降低(P均0.001)。2在NE-S中,与Aβ处理组相比,caspase-9抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,caspase-8抑制剂预处理加Aβ组则无显著改变;在MIX-S中的结果则相反,即caspase-8抑制剂预处理加Aβ组PSD95的表达量显著回升至对照组水平,而caspase-9抑制剂预处理加Aβ组则无显著改变。3MIX-S与NE-S两种培养系统间相比较,对照组间及Aβ处理组间PSD95的表达量均无显著差异,而caspase-8抑制剂预处理加Aβ组间及caspase-9抑制剂预处理加Aβ组间PSD95的表达量差异有显著性。结论在Aβ早期突触毒性作用中,AS参与caspase-8介导的死亡受体通路激活过程,且参与抑制神经元的线粒体通路。     

Ultrastructure of non-myelinated neurons during energy deprivation

Summary This paper examines the neuropathology of oxygen-glucose deprivation uncomplicated by stagnant conditions. Rabbit vagus nerves were pulled into asmulti-compartment perfusion chamber, stimulated five times per second and deprived of energy by substituting nitrogen and deoxyglucose for oxygen and glucose in the Locke's perfusate. After incubation the compartments were perfused with gluteraldehyde solution, and the nerves were prepared for electron microscopy. Fixation in the compartments ensured precise cross and longitudinal sections which permitted quantitative comparisons. Although the action potentials ceased in 45 min, 1 h of energy deprivation did not significantly affect the ultrastructure. After 2 h of deprivation the axons were smaller and flattened and microtubules appeared packed together. In the smallest axons the microtubules were gone, the neurofilaments were compacted and the few mitochondria had a dense, homogenous appearance. By 4 h the shrinking was extreme, yet 8% were swollen much larger than any of the controls. Longitudinal views showed these balloned areas were greatly expanded regions of the smallest axons. Both tiny and huge regions were devoid of microtubules and the swollen axons contained expanded mitochondria.Calcium is indirectly implicated in the pathogenesis by the concurrence of mitochondrial alteration as the microtubules disappear coupled with the known role of mitochondria in calcium regulation and the reported effect of high calcium on microtubual dissociation. In is suggested that axons first shrink as osmotially active molecules are used or washed out. After a time without energy the mitochondria can no longer regulate the intracellular calcium, microtubules dissociate, and calcium-activated phospholipases create osmotically active molecules. Finally, high-amplitude, disruptive swelling occurs.Supported, in part, by a Grant-in-aid from the American Heart Association with funds contributed by the American Heart Association, Kansas Affiliate and by the University of Kansas Biomedical Sciences Support Grant RR0737     

Development of 18F-labeled radiotracers for neuroreceptor imaging with positron emission tomography

Positron emission tomography (PET) is an in vivo molecular imaging tool which is widely used in nuclear medicine for early diagnosis and treatment follow-up of many brain diseases. PET uses biomolecules as probes which are labeled with radionuclides of short half-lives, synthesized prior to the imaging studies. These probes are called radiotracers. Fluorine-18 is a radionuclide routinely used in the radiolabeling of neuroreceptor ligands for PET because of its favorable half-life of 109.8 min. The delivery of such radiotracers into the brain provides images of transport, metabolic, and neurotransmission processes on the molecular level. After a short introduction into the principles of PET, this review mainly focuses on the strategy of radiotracer development bridging from basic science to biomedical application. Successful radiotracer design as described here provides molecular probes which not only are useful for imaging of human brain diseases, but also allow molecular neuroreceptor imaging studies in various small-animal models of disease, including genetically-engineered animals. Furthermore, they provide a powerful tool for in vivo pharmacology during the process of pre-clinical drug development to identify new drug targets, to investigate pathophysiology, to discover potential drug candidates, and to evaluate the pharmacokinetics and pharmacodynamics of drugs in vivo.     

Norharman-induced motoric impairment in mice: neurodegeneration and glial activation in substantia nigra

Summary. The β-carboline norharman is present in cooked food and tobacco smoke and show structural resemblance to the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. C57BL/6 mice were injected subcutaneously with norharman (3 and 10 mg/kg) twice per day for five consecutive days. Eighteen hours after the last dose an increased expression of glial fibrillary acidic protein and fluoro-jade staining were demonstrated whereas the number of tyrosine hydroxylase positive cells were unchanged in the substantia nigra. Two weeks after the last treatment a decreased motor activity was observed whereas cognitive functions remained intact. In cultured PC12 cells norharman treatment induced mitochondrial dysfunction and increased the number of caspase-3 and TUNEL-positive cells. The results demonstrate that norharman induced apoptosis in cultured cells as well as early neurodegeneration, glial activation and sustained motor deficits in mice and suggest that exposure to norharman may contribute to idiopathic Parkinson’s disease.     

轻型缺血性卒中静脉溶栓后双重抗血小板疗效观察

目的 观察rt-PA静脉溶栓联合双重抗血小板治疗轻型缺血性卒中的有效性及安全性。 方法 以2013年12月-2016年12月在石家庄市第一医院连续住院治疗的轻型缺血性卒中患者为研究 对象,将其随机分为对照组、溶栓+单抗组和溶栓+双抗组。对照组不进行静脉溶栓,长期口服阿 司匹林（100 mg/d）抗血小板治疗;溶栓+单抗组在rt-PA静脉溶栓（0.9 mg/kg,最大剂量90 mg）基 础上长期单用阿司匹林（100 mg/d）抗血小板治疗;溶栓+双抗组在溶栓后单抗基础上加用氯吡格雷 （75 mg/d）双重抗血小板治疗,双抗治疗21 d后改为阿司匹林长期单抗治疗。随访3个月,有效性指标 为3个月时NIHSS 0～1分、Barthel指数（Barthel index,BI）95～100分和mRS 0～1分的比例,3个月时缺 血性卒中的复发率;安全性指标为治疗24 h出血转化和症状性出血转化的发生率。另外比较三组间 基线和3个月时血清hs-CRP和IL-6的水平差异。 结果 研究共纳入85例患者,对照组28例,溶栓+单抗组28例,溶栓+双抗组29例,全部患者均完 成3个月随访,无死亡患者。对照组、溶栓+单抗组和溶栓+双抗组3个月随访时NIHSS 0～1分比例分 别为46.43%、78.57%和93.10%,BI 95～100分比例分别为53.57%、82.14%和89.66%,mRS 0～1分 的比例分别为50.00%、82.14%和93.10%,三组上述有效性指标差异均有统计学意义,两两比较显 示,溶栓+双抗组高于溶栓+单抗组和对照组,溶栓+单抗组高于对照组,差异均有统计学意义;对 照组、溶栓+单抗组和溶栓+双抗组3个月时缺血性卒中复发率分别为32.14%、7.14%和3.45%,差异 有统计学意义。安全性指标方面,三组均无出血转化事件。对照组、溶栓+单抗组和溶栓+双抗组3 个月时的hs-CRP水平分别为11.92±3.58 mg/L、9.04±2.85 mg/L和6.04±2.65 mg/L,IL-6水平分别为 26.18±4.65 ng/L、16.11±6.93 ng/L和12.84±2.57 ng/L,三组上述炎症因子水平差异均有统计学意 义,其中溶栓+双抗组低于溶栓+单抗组和对照组,溶栓+单抗组低于对照组。 结论 对于急性轻型缺血性卒中患者,rt-PA静脉溶栓治疗后短期双重抗血小板治疗可显著改善患 者神经功能,降低炎症因子水平,降低复发率,且不增加出血风险。     

The ENIGMA‐Epilepsy working group: Mapping disease from large data sets

Epilepsy is a common and serious neurological disorder, with many different constituent conditions characterized by their electro clinical, imaging, and genetic features. MRI has been fundamental in advancing our understanding of brain processes in the epilepsies. Smaller‐scale studies have identified many interesting imaging phenomena, with implications both for understanding pathophysiology and improving clinical care. Through the infrastructure and concepts now well‐established by the ENIGMA Consortium, ENIGMA‐Epilepsy was established to strengthen epilepsy neuroscience by greatly increasing sample sizes, leveraging ideas and methods established in other ENIGMA projects, and generating a body of collaborating scientists and clinicians to drive forward robust research. Here we review published, current, and future projects, that include structural MRI, diffusion tensor imaging (DTI), and resting state functional MRI (rsfMRI), and that employ advanced methods including structural covariance, and event‐based modeling analysis. We explore age of onset‐ and duration‐related features, as well as phenomena‐specific work focusing on particular epilepsy syndromes or phenotypes, multimodal analyses focused on understanding the biology of disease progression, and deep learning approaches. We encourage groups who may be interested in participating to make contact to further grow and develop ENIGMA‐Epilepsy.     

缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布特点的超声造影研究

目的 应用超声造影观察缺血性卒中并发2型糖尿病患者颈动脉斑块内新生血管分布情况,明确其 斑块内新生血管分布特征。 方法 病例组选取因急性缺血性卒中住院的糖尿病患者40例（入组前未服用降糖药）,卒中同侧颈 动脉斑块形成;对照组为同期门诊就诊的颈动脉斑块形成患者,无卒中病史,性别及年龄匹配的非 糖尿病患者32例。两组患者行弓上计算机断层扫描血管造影（computed tomography angiography,CTA） 检查排除主动脉弓斑块及颅内动脉病变,排除卵圆孔未闭及心房颤动等。对所有患者均行常规超声 及超声造影检查。常规超声观察斑块厚度及内部回声,超声造影观察斑块增强情况,横切面多角度 观察,将超声造影结果分为近内膜处有增强（代表新生血管）及近内膜处无增强两种。 结果 两组患者颈动脉斑块厚度及回声情况差异无统计学意义。超声造影结果显示病例组颈动脉 斑块近内膜处增强者34例（85%）,对照组近内膜处增强12例（37.5%）,差异有统计学意义（χ 2=17.38, P＜0.01）。 结论 未服用降糖药的2型糖尿病并发急性缺血性卒中的患者颈动脉粥样硬化斑块内近内膜处新生 血管增生多于无糖尿病患者,提示血糖升高与颈动脉斑块内血管新生有关。     

Yohimbine increases the binding potential for [11C]flumazenil in the monkey brain

Summary. We evaluated the impact of yohimbine administration on benzodiazepine (BDZ) receptor binding in the central nervous system of non-human primates (rhesus monkeys). Estimates of the binding potential (B_max/K_d) of BDZ receptors were made following intravenous administration of yohimbine, an α₂-adrenoceptor antagonist. Positron emission tomography was used in conjunction with [¹¹C]flumazenil (Ro 15-1788), a tracer for central BDZ receptor binding activity. The effects of yohimbine were compared with a control condition in which saline was administered. Yohimbine significantly increased the binding potential in the hippocampus, as assessed using a Student's t-test with Bonferroni correction. The result that the administration of yohimbine readily induces an increase in the binding potential for BDZ receptors in the primate brain suggests that the presence of an anxiety state potentiates the effect of anxiolytics. Accepted August 10, 2001