颈动脉斑块稳定性相关因素研究进展

颈动脉粥样硬化是缺血性卒中常见病因。在西方国家,因颈动脉粥样硬化造成的缺血性卒中占19%￣35%[1]。Rothwell等[2]发现,颈动脉粥样硬化致颈动脉狭窄继发远端血流量减少者缺血性卒中的发生率并不高,提示动脉狭窄程度不再是单一预测缺血性卒中的发生指标。近年来该领域的相关研     

颈动脉粥样硬化与缺血性卒中

颈动脉粥样硬化是缺血性卒中的重要危险因素。研究颈动脉粥样硬化与缺血性卒中的关系对缺血性卒中发病机制的研究和缺血性卒中的预防都有重要意义。1　颈动脉粥样硬化引起缺血性卒中的机制颈动脉粥样硬化引起缺血性卒中的机制比较公认的有两种学说 ,即血栓 -栓塞学说和血流动力学性末梢低灌流学说。颈动脉粥样硬化斑块表面的微栓子受不稳定血流的冲击 ,可以被冲刷下来 ,形成微栓子阵雨 ,从而在颈动脉完全闭塞前发生分水岭性脑梗死或 TIA。栓子的另一来源是颈动脉血栓的扩散 ,血栓从颈内动脉起始部向远端扩展到第一条高流量旁支 (通常为眼…     

颈动脉粥样硬化与进展性缺血性脑卒中的关系

目的探讨颈动脉粥样硬化与进展性缺血性脑卒中的关系。方法采用彩色多普勒超声仪对564例缺血性脑卒中患者的颈动脉进行评估，比较进展性缺血性脑卒中和非进展性缺血性脑卒中患者的颈动脉粥样硬化特征和程度。结果564例缺血性脑卒中患者有135例为进展性缺血性脑卒中（23.8％）；在重度颈动脉粥样硬化110例中，有49例（44.5％）发展为进展性卒中；在重度颈动脉狭窄95例中，有48例（50．5％）发展为进展性卒中；在病理表现为溃疡斑86例中，有47例（54．7％）发展为进展性卒中：无颈动脉粥样硬化或伴轻度颈动脉粥样硬化的缺血性脑卒中患者，仅9％～10％发生进展性卒中。经Logistic回归分析发现，颈动脉粥样硬化程度、狭窄程度以及溃疡斑与进展性缺血性卒中的发生成正相关。结论颈动脉粥样硬化与进展性缺血性脑卒中的发生密切相关，颈动脉粥样硬化的严重程度可作为进展性缺血性脑卒中的预测指标。     

颈动脉粥样硬化与缺血性脑卒中

198 9年美国国立神经疾病和卒中研究所的资料中将 2 3%的脑梗死归因于颈动脉病变[1] ,近年来随着多普勒超声与磁共振血管造影的临床应用 ,颈动脉粥样硬化与缺血性卒中之间的密切关系越来越受到人们的重视。颈动脉粥样硬化对缺血性卒中病因学方面的重要意义主要在于它可能是脑栓子的一个重要来源以及它对脑血流动力学的影响。本文就近年来有关颈动脉粥样硬化的研究进展及其与缺血性卒中的关系综述如下 :1　颈动脉粥样硬化的危险因素动脉粥样硬化是一种全身慢性疾病 ,其病变主要累及体循环的大中型动脉 ,以主动脉、冠状动脉及脑动脉罹患最多。…     

颈动脉高分辨磁共振与缺血性卒中

正缺血性卒中占所有卒中的80%以上[1]。颅外颈动脉粥样硬化被认为是缺血性卒中的危险因素,约20%的缺血性卒中是由颈动脉粥样硬化性斑块引起[2],颈动脉斑块破裂形成栓子或者引起颈动脉狭窄均可导致缺血性卒中,颈动脉高分辨磁共振成像(high resolution magnetic resonance imaging,HRMRI)检查对预测早期缺血性卒中患者的预后,选择恰当的治疗方案,具有十分重要的意义。颈动脉的影像学检查有多种,包括超声     

颈动脉粥样硬化和缺血性脑卒中的相关性探讨

颈动脉粥样硬化是缺血性脑卒中的最重要病因和危险因素.为探讨颈动脉粥样硬化和缺血性卒中的关系,我们通过对72例经CT、MRI确诊的缺血性卒中患者颈动脉彩色多普勒超声检查作回顾性分析.     

颈动脉粥样硬化和缺血性脑卒中的相关性探讨

颈动脉粥样硬化是缺血性脑卒中的最重要病因和危险因素。为探讨颈动脉粥样硬化和缺血性卒中的关系，我们通过对72例经CT、MRI确诊的缺血性卒中患者颈动脉彩色多普勒超声检查作回顾性分析。     

他汀类药物与颈动脉粥样硬化斑块

卒中,尤其是缺血性卒中的发病率居高不下,颈动脉粥样硬化斑块作为缺血性卒中的重要危险因素,成为近年研究的热点,积极治疗颈动脉粥样硬化斑块成为防治缺血性卒中的重要手段之一。他汀类药物的调脂、稳定及逆转斑块的作用,得到了多项临床试验的肯定,并在临床应用上逐渐推广：下面结合动脉粥样硬化的发病机制,对他汀类药物治疗颈动脉粥样硬化斑块的机制进行综述。     

颈动脉粥样硬化与缺血性卒中

颈动脉粥样硬化的研究大约经历了对其病因和临床的认识、外科治疗、药物治疗和对卒中的特殊预防4个主要阶段。颈动脉与脑梗塞关系的研究虽然已有20多年的历史,但仍然是临床病理学探讨的重要课题。随着脑血管病检查新技术的不断开展,颈动脉粥样硬化的研究也日渐广泛和深入。本文就颈动脉粥样硬化与缺血性卒中关系的几个问题作如下综述。颈动脉粥样硬化与缺血性卒中的关系颈动脉粥样硬化是脑实质缺血性病变的主要原因之一。颈动脉粥样硬化是否引起脑的缺血性病变与其病变类型、狭窄程度、有无伴随血栓、栓塞及血液动力学改变等因素有关。颈动脉内膜溃疡及狭窄:颈动脉粥样斑块和内膜溃疡是TIA和卒中的潜在病因。临床病理学结果     

40例缺血性脑血管病与颈动脉内膜病变关系分析

缺血性脑血管病是致残率和病死率较高的疾病之一,国内位居第三,其特点是反复发病.故对其病因探寻预防疾病发生突显重要.颈动脉粥样硬化是缺血性卒中常见病因,在西方国家,因颈动脉粥样硬化造成的缺血性卒中占19%～35%[1].颈动脉超声检查具有安全、无创、简便易行及准确的特点,在临床广泛应用.下面将40例均经CT或MRI确诊的脑梗死病例的颈动脉超声检查情况分析如下.     

Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine

By reducing neuronal excitability through selective binding to the α(2)δ subunit of voltage-dependent calcium channels, pregabalin effectively treats epilepsy, chronic pain, and anxiety disorders. To evaluate if pregabalin coadministration affects pharmacokinetics of other antiepileptic drugs, population pharmacokinetic analyses using NONMEM software were performed on data from three epilepsy trials involving seven antiepileptic drugs with pregabalin as add-on therapy. Results demonstrated that pregabalin did not alter the steady-state plasma concentrations of carbamazepine, lamotrigine, phenobarbital, phenytoin, tiagabine, topiramate, and valproate. Furthermore, the small percent change in the population estimate of antiepileptic drug plasma clearance values (-2% to +7%) suggests that pregabalin coadministration exerted no significant effect on the pharmacokinetics of these antiepileptic drugs, with the possible exception of tiagabine (+34.9%). These findings are in agreement with those of previously published reports. A further clarification study is necessary for tiagabine. In conclusion, it appears that pregabalin can be coadministered with other antiepileptic drugs without concern for significantly altering their pharmacokinetic profiles.     

Consecutive Gas Chromatographic Determination of Phenytoin, Phenobarbital, Primidone, Phenylethylmalondiamide, Carbamazepine, Trimethadione, Dimethadione, Ethosuximide, and Valproate from the Same Serum Specimen

A quantitative gas-liquid chromatographic procedure is described for the consecutive determination of phenytoin, phenobarbital, primidone, phenylethylmalondiamide, carbamazepine, trimethadione, dimethadione, ethosuximide and valproate from a single serum specimen of 1.2 ml. After extraction from serum by two different procedures, the anticonvulsants are chromatographed without further purification on a 3% OV 17 column either with or without derivative formation by means of "on-column" methylation. Multiple internal standards are employed in order to enhance the reproducibility of drug-concentration measurement.     

Alteration of proteins regulating apoptosis, Bcl-2, Bcl-x, Bax, Bak, Bad, ICH-1 and CPP32, in Alzheimer''s disease

Recently, apoptosis has been implicated in the selective neuronal loss of Alzheimer's disease (AD). Apoptosis is regulated by the B cell leukemia-2 gene product (Bcl-2) family (Bcl-2, Bcl-x, Bax, Bak and Bad) and the caspase family (ICH-1 and CPP32), with apoptosis being prevented by Bcl-2 and Bcl-x, and promoted by Bax, Bak, Bad, ICH-1 and CPP32. In the present study, we examined the levels of these proteins in the membranous and cytosolic fractions of temporal cortex in AD and control brain. In the membranous fraction, the levels of Bcl-2, Bcl-x_L, Bcl-x_β, Bak and Bad were increased in AD. In the cytosolic fractions, the level of Bcl-x_β was increased, while Bcl-x_L, Bax, Bak, Bad and ICH-1_L were unchanged. CPP32 was not detected in AD or control brain. These findings demonstrate a differential involvement of cell death-regulatory proteins in AD and suggest that Bak, Bad, Bcl-2 and Bcl-x are upregulated in AD brains.     

Mass spectrometric identification of Cu, Zn, Fe, Co, Mn, Mg, and Pb in mammalian brain.

Combining the techniques of thin-layer chromatography (TLC) and mass spectrometry, we unambiguously identified the trace metals Cu, Zn, Fe, Pb, Mn, Co, and Mg in the brain of a female human who had no evidence of any pathologic disease in the central nervous system, and in brains from mouse, rat, guinea pig, and rabbit. These trace metals were also found in anatomic regions of human brain: cortex (gray), cortex (white), caudate nucleus, putamen, hippocampus, and thalamus, and in anatomic regions of rat brain: hypothalamus, cerebellum, stem striatum, and "the rest." The metals were characterized from the color and Rf values of their tetraphenylporphyrin chelates on TLC and from the mass and pattern of molecule ion cluster of the mass spectrum. The unexpected presence of lead in the brain is discussed.     

中国汉族人群SCA1、2、3、6、7、8、10、12、17亚型和齿状核-红核-苍白球-路易体萎缩亚型频率分布

目的 研究中国汉族人群中脊髓小脑性共济失调(SCAs)不同基因亚型的频率分布.方法 运用聚合酶链反应、变性聚丙烯酰胺凝胶电泳、Southern blot、T载体克隆重组DNA技术结合直接测序等技术对559例临床诊断为SCA的患者(363例常染色体显性遗传先证者,196例散发患者)进行了SCA1、SCA2、SCA3/MJD、SCA6、SCA7、SCA8、SCA10、SCA12、SCA17和齿状核-红核-苍白球-路易体萎缩(DRPLA)致病基因多核苷酸病理重复突变检测分析.结果 在363个常染色体显性遗传的SCA(AD-SCA)家系中,发现有15个SCA1家系(4.13%),26个SCA2家系(7.16%),187个SCA3/MJD家系(51.52%),6个SCA6家系(1.65%),7个SCA7家系(1.93%),1个SCA12家系(0.28%)和1个SCA17家系(0.28%),120个SCA家系未明确基因分型(33.06%);在196例散发SCA患者中,发现有2例SCAI患者(1.02%),3例SCA2患者(1.53%),15例SCA3/MJD患者(7.65%),3例SCA6患者(1.53%),173例SCA患者未明确基因分型(88.27%);未发现SCA8、SCA10和DRPLA型患者.结论 在中国汉族人群中SCA3/MJD为最常见的SCA亚型,其次为SCA2、SCA1、SCA7和SCA6,SCA12和SCA17比较少见,SCA8、SCA10和DRPLA罕见,SCA17亚型为国内首次报道.部分AD-SCA家系存在其他致病基因的作用,大部分散发SCA患者除遗传因素外还存在其他致病因素.