缺血性脑血管病患者颅内外动脉狭窄分布研究

目的 研究缺血性脑血管病患者颅内外动脉狭窄分布特点.方法 本研究收集了1031例在院脑梗死和TIA患者的DSA资料,对其中资料完整的1000例患者进行分析.结果 DSA显示,1000例患者中有680例存在脑动脉狭窄,累计有1417条血管狭窄.发生部位依次为:大脑中动脉狭窄337条、椎动脉远端及基底动脉狭窄291条、颈内动脉颅外段狭窄280条、椎动脉起始段狭窄207条、颈内动脉虹吸段狭窄115条、大脑前动脉狭窄100条、大脑后动脉狭窄70条.大脑中动脉、椎基底动脉系统和颈动脉颅外段是最常见的动脉狭窄好发部位.颅内动脉狭窄331例,颅外动脉狭窄134例,颅内外动脉均见狭窄215例.结论 颅内动脉粥样硬化性狭窄仍是缺血性卒中的重要原因,最近三年,多发病变、颅外动脉病变检出率明显上升,值得关注,控制血压、血糖、血脂可预防脑动脉粥样硬化性狭窄的发生.     

缺血性脑血管病患者脑主要供血动脉狭窄分布的DSA分析

目的探讨缺血性脑血管病(ICVD)患者脑主要供血动脉狭窄分布特征。方法对2007-2009年诊治的脑主要供血动脉狭窄92例ICVD患者的临床和DSA资料进行回顾性分析。结果脑主要供血动脉颅外段病变发生率(82.6%)高于颅内段动脉(66.3%);多支动脉及前后循环同时病变的发生率较高(79.3%、57.6%);颈动脉系统常见狭窄部位是颈内动脉颅外段(57.6%)、大脑中动脉(34.8%),椎基底动脉系统常见狭窄部位是椎动脉颅外段(57.6%)、椎动脉颅内段(20.7%)。可干预危险因素越多,颅外合并颅内动脉狭窄的发生率越高,但无显著性差别(χ2=7.1;P=0.069)。结论 ICVD患者以颅外段动脉狭窄多见;颈动脉系统狭窄好发于颈内动脉颅外段、大脑中动脉,椎基底动脉系统好发于椎动脉颅外段。伴不同可干预危险因素组颅内合并颅内动脉狭窄的发生率无显著差异。     

400例缺血性脑梗死患者数字减影全脑血管造影分析

目的 分析缺血性脑梗死患者的脑血管病因和病变血管的分布情况.方法 回顾性分析400例缺血性脑梗死数字减影全脑血管造影(DSA)结果,分析脑梗死的血管病因,并对动脉粥样硬化脑梗死者总结分析动脉病变的部位、分布及血管狭窄形态.结果 脑血管造影结果提示88.25％缺血性脑梗死患者为不同程度的动脉粥样硬化引起血管狭窄或闭塞(353例),此外11.75％缺血性脑梗死患者病因是由于动脉夹层、Moyamoya病、椎基底动脉扩张延长症、鼻咽癌放疗后脑动脉病变、血管迂曲、微血管病变等原因引起.353例动脉粥样硬化性脑梗死中单纯前循环血管受累(45.61％)明显多于单纯后循环血管受累(34.27％),P＜0.01;前循环脑梗死中以颈内动脉(56.6％)和大脑中动脉(26.4％)受累最常见;后循环脑梗死中以椎动脉病变(33.0％)最多见.结论 脑血管造影显示缺血性脑梗死患者有最常见病因是动脉粥样硬化脑血管狭窄或闭塞,占88.25％.前循环脑梗死患者血管病变以颈内动脉起始部病变和大脑中动脉病变多见,后循环脑梗死中以椎动脉动脉病变多见.颅外血管狭窄以颈内动脉颅起始部和椎动脉起始部多见,颅内血管狭窄以大脑中动脉和椎动脉颅内段多见.     

缺血性脑卒中患者的数字减影脑血管造影的研究

目的探讨缺血性脑卒中患者全脑血管造影的特点。方法对243例缺血性脑卒中患者进行全脑血管造影检查,回顾性分析脑动脉颅内动脉狭窄、颅外动脉狭窄的发生率及其分布情况。结果在243例缺血性脑卒中180例（74.07%）存在脑动脉狭窄或闭塞,前循环动脉狭窄或闭塞82例（45.46%）,后循环52例（28.89%）,前后循环均有46例（25.56%）。颅内动脉狭窄或闭塞48例（26.67%）,颅外动脉86例（47.78%）,颅内、外动脉均有46例（25.56%）。180例中共发现狭窄血管356支,单支血管病变82例,多支血管病变98例。颅外血管狭窄以颈内动脉颅外段最多,颅内血管狭窄以椎动脉颅内段和大脑中动脉为多。结论脑血管造影可以准确地评价缺血性脑卒中患者脑动脉狭窄的分布情况及其程度,为临床提供了诊治依据。     

中青年与老年脑梗死患者脑动脉狭窄分布的DSA分析

目的应用数字减影血管造影对中青年与老年脑梗死患者脑动脉狭窄的分布特征进行分析。方法选择脑梗死患者86例,根据患者年龄分为中青年组（年龄〈60岁）48例,老年组（年龄≥60岁）患者38例,应用数字减影血管造影技术（DSA）对患者脑动脉病变血管狭窄程度及分布进行分析。结果 1老年组患者在颅外动脉病变以及前循环狭窄发生率明显高于中青年组（P〈0.05）,而颅内动脉病变以及后循环狭窄发生率却明显低于中青年组（P〈0.05或P〈0.01）,在脑血管病变及颅内外动脉同时受累发生率上,两组差异无统计学意义（P〉0.05）;2中青年组最常见为重度狭窄,发生率高于轻度及中度狭窄（P〈0.05）,好发部位为椎动脉开口处,发生率高于颈内动脉起始段及大脑中动脉MI段（P〈0.05）;老年组最常见为重度狭窄（P〈0.05）,好发部位为椎动脉开口处及颈内动脉起始段,发生率高于大脑中动脉MI段（P〈0.05）。结论中青年患者最常受累血管为颅内血管,病变发生部位多以椎动脉起始处居多;老年患者最常受累血管为颅外血管,最常受累血管为椎动脉起始处及颈内动脉。     

特发性脑动脉夹层28例致缺血性卒中机制分析

目的 通过回顾分析特发性脑动脉夹层（cerebral artery dissection,CAD）患者影像学和血管学资料研究其缺血性卒中机制,为治疗策略提供依据。方法 选取28例特发性CAD所致急性缺血性卒中患者,根据缺血性卒中病灶形态和分布来确定CAD致缺血性卒中机制;根据夹层病变的位置分为颅内组和颅外组,对两组患者夹层致缺血性卒中机制进行比较。结果 共28例患者纳入研究,男19例,女9例。颅外组17例,其中颈内动脉夹层15例,椎动脉V1段夹层2例。颅内组11例,其中大脑中动脉M1段夹层3例,基底动脉夹层2例,椎动脉V4段夹层6例。颅内组高血压和糖尿病患者分别为7例（63.6%）和5例（45.5%）,颅外组均为1例（5.9%）,颅内组高血压和糖尿病患病比例多于颅外组（P =0.002,0.022）。颅外组和颅内组单纯栓塞性缺血性卒中分别有12例（70.6%）和2例（18.2%）,两组比较差异有统计学意义（P =0.018）。颅内组由夹层病变闭塞局部穿支动脉所致缺血性卒中7例（63.6%）,由夹层闭塞穿支合并血流动力学机制所致1例（9.1%）,单纯血流动力学机制所致1例（9.1%）。结论 颅外CAD致缺血性卒中机制与颅内CAD有所不同,前者主要导致栓塞性缺血性卒中,而后者致缺血性卒中机制主要为夹层病变闭塞局部穿支动脉。     

106例缺血性脑血管病患者全脑血管造影分析

目的分析缺血性脑血管病患者颅内外动脉狭窄的分布。方法对我院实施DSA检查的106例缺血性脑血管病的结果进行分析,均经头颅CT排除脑出血,TCD及颈动脉彩超检查后怀疑有动脉狭窄的缺血性脑血管病。所有患者均实施选择性全脑血管造影术,椎动脉和颈动脉均有正侧位血管造影像;根据患者的DSA检查结果,分析动脉狭窄的部位、受累血管数目及血管狭窄形态;重度狭窄的病例予以支架治疗和球囊成型术。结果血管造影结果提示89.6%患者有不同程度的血管狭窄或闭塞,其中75.5%为前循环受累,37.7%为后循环受累。前循环受累血管中以颈内动脉(56.6%)和大脑中动脉(26.4%)受累最常见,后循环受累血管中以椎动脉(33.0%)最多见。支架治疗和球囊成型术临床疗效显著。结论缺血性脑血管病造影显示大部分患者有肯定的脑血管狭窄和闭塞。脑梗死患者血管病变以颈内动脉病变为主,椎基底动脉供血不足亦以颈内动脉病变多见,支架治疗和球囊成型可作为重度狭窄的治疗方法。     

青年缺血性脑卒中患者脑血管病变的特点

目的 应用数字减影血管造影（DSA）了解青年缺血性脑卒中脑血管病变的特点。方法 选择连续行主动脉弓＋全脑血管造影检查的青年（年龄15～44岁）缺血性脑卒中患者136例，并分成15～30岁、31～44岁2组，分析血管病变的类型、数目和部位。结果 136例患者中有68．4％异常，38．8％患者存在2支或2支以上的血管病变，且在30～44岁组中常见（2组比较P＜0．05）；61．2%患者为单支血管病变，后者主要分布在颅内血管，但2组无差异（P＞0．05）；血管病变的部位依次为颈内动脉颅外段、大脑中动脉、椎动脉、颈内动脉颅内段、大脑前动脉等。同时发现MoyaMoya病8例，动脉夹层5例，动脉发育不良4例。结论 青年人缺血性脑卒中的血管病变异常率高，颅内、颅外段大血管狭窄均较常见，动脉夹层和变异也是缺血性脑卒中的原因之一。     

265例缺血性脑卒中患者DSA结果分析

目的对265例缺血性脑血管病患者的DSA资料进行分析,进一步评价DSA在缺血性脑血管病诊治中的意义。方法对265例确诊为缺血性脑血管病的患者于发病后2h~6个月行全脑血管造影,明确有无脑供血动脉狭窄或闭塞,明确血管狭窄部位及责任动脉,并测定狭窄长度及狭窄程度。结果 265例缺血性脑血管病患者脑供血动脉狭窄或闭塞的发生率为72.1%。缺血性脑血管病患者脑血管狭窄或闭塞的好发部位依次为颈内动脉起始部(16.4%)、大脑中动脉水平段(13.9%)、椎动脉开口处(12.3%)。单发脑供血动脉狭窄或闭塞88例(46.1%),多发脑供血动脉狭窄或闭塞103例(53.9%),其中颅内外动脉串联病变43例(41.7%),颅内外非串联病变60例(58.3%)。责任动脉的检出率为77%。结论对反复卒中及患糖尿病的缺血性卒中患者应行DSA以明确患者有无颅内外脑供血动脉狭窄,以制定包括药物及支架置入术等更为有效的二级预防。     

84例缺血性脑卒中患者的CTA结果分析

目的 研究缺血性卒中患者脑血管病变的严重程度、分布以及相关危险因素,为缺血性脑卒中的发病机制、临床诊断、治疗及预防提供可靠的依据.方法 对84例缺血性脑卒中患者的CTA(Computer Tomography angiograph)检查结果进行分析.结果 在84例缺血性脑卒中患者中,颅内动脉狭窄率高于颅外动脉狭窄率,颅内动脉斑块检出率明显多于颅外动脉斑块检出率,颈内动脉颅内段狭窄率(17.5％)大于颈内动脉颅外段(6.6％),两者存在明显差异(P＝0.001),颅内动脉中基底动脉的狭窄率最低(12.2％),大脑后动脉狭窄率最高(42％),两者存在明显差异(P＜0.000).此外,颅内血管发生钙化斑多于颅外动脉,其狭窄率也高于颅外动脉.结论 CTA在诊断和评估方面价值已经逐渐得到重视,对颅内动脉病变及其危险因素进行及时有效的干预,可使缺血性卒中患者的预后得到明显的改善.     

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