超敏C反应蛋白、同型半胱氨酸在急性脑梗死患者血清中的水平及其与颈动脉狭窄的相关性研究

目的观察超敏C反应蛋白(hs-CRP)、同型半胱氨酸(Hcy)在急性脑梗死(ACI)患者血清中的水平,并探讨其与颈动脉狭窄(CAS)的相关性。方法 132例ACI合并CAS患者,根据颈动脉狭窄程度分为,轻度狭窄组(n=47例)、中度狭窄组(n=44例)和重度狭窄组(n=41例);根据临床神经功能缺损程度评分标准分为轻型(n=40例)、中型(n=45例)和重型(n=47例);根据脑梗死病灶面积分为腔隙性梗死组(n=42例)、小面积梗死组(n=46例)和大面积梗死组(n=44例);根据斑块性质分为分为软斑组(n=43例)、硬斑组(n=43例)和其他类型组(n=46例)。比较各组血清hs-CRP、Hcy表达水平。结果各狭窄组ACI患者血清hs-CRP、Hcy表达水平均明显高于对照组(P0.05),且随着颈动脉狭窄程度加重,血清hs-CRP、Hcy表达水平显著性升高(P0.05);不同病情程度组ACI患者血清hs-CRP、Hcy表达水平均明显高于对照组(P0.05),且随着病情程度加重,血清hs-CRP、Hcy表达水平显著性升高(P0.05);不同病灶面积组ACI患者血清hs-CRP、Hcy表达水平均明显高于对照组(P0.05),且随着病灶面积增大,血清hs-CRP、Hcy表达水平显著性升高(P0.05);不同斑块性质组ACI患者血清hs-CRP、Hcy表达水平均明显高于对照组(P0.05),且随着斑块性质逐渐加重,血清hs-CRP、Hcy表达水平均明显升高(P0.05)。结论血清Hcy、hs-CRP表达水平随CAS程度、病情程度、病灶面积及斑块性质加重而升高,可作为判断ACI患者病情严重程度的实验室指标。     

急性脑梗死患者循环血小板微颗粒和内皮细胞微颗粒水平的研究

目的分析急性脑梗死(ACI)患者循环血小板微颗粒(PMP)及内皮细胞微颗粒(EMPs)水平。方法 300例ACI患者分为大面积梗死组72例和小面积梗死组228例,另取健康对照组60例。采集空腹外周静脉血,测定血浆PMP、EMPs及血清心型脂肪酸结合蛋白(H-FABP)、S-100β蛋白(S-100β)、神经元特异性烯醇化酶(NSE)、基质金属蛋白酶原(MMP-9)水平。分析PMP、EMPs与H-FABP、S-100β、NSE、MMP-9的相关性。结果大面积梗死组的血浆PMP和EMPs水平高于小面积脑梗死组,健康对照组最低,差异有统计学意义(P<0.05)。大面积梗死组的血清H-FABP、S-100β、NSE、MMP-9水平高于小面积脑梗死组,对照组最低,差异均有统计学意义(P<0.05)。ACI患者PMP和EMPs水平与H-FABP、S-100β、NSE、MMP-9水平均呈正相关(P<0.05)。结论高水平的PMP及EMPs可能参与了ACI的发生和发展,有望成为疾病诊断、病情评估和预后的新指标。     

三七总皂苷对急性脑梗死患者血清NSE水平及功能恢复的影响

目的观察三七总皂苷对急性脑梗死(ACI)患者血清神经元特异性烯醇化酶(NSE)水平及神经功能缺损程度评分的影响。方法将100例ACI患者随机分为2组,对照组50例给予常规治疗,观察组50例在对照组基础上加用三七总皂苷注射液,比较2组临床疗效及治疗前后的血清NSE水平和神经功能缺损程度评分。结果观察组临床总有效率显著高于对照组(P0.05),治疗后的血清NSE水平、神经功能缺损程度评分改善程度均显著优于对照组(P0.05)。结论三七总皂苷治疗ACI疗效明显,对促进神经功能缺损恢复有一定价值。     

血清MMP-9与NSE在ACI患者中检测的意义

目的探讨血清基质金属蛋白酶-9(MMP-9)与神经烯醇化酶(NSE)水平检测在急性脑梗死(ACI)患者中的临床价值。方法分析2014-12-2015-09在开封市中心医院神经内科接受诊治的94例ACI患者的临床资料。根据病灶面积的大小分为A组(大面积脑梗死,21例)、B组(中等面积脑梗死,46例)和C组(小面积脑梗死,27例)。另选取同期健康体检的92例健康者为对照组。比较2组基线资料、血清MMP-9与NSE的表达水平,并分析ACI患者血清MMP-9与NSE的关系。结果ACI组血清MMP-9与NSE浓度明显较对照组高(P0.05)。其中,ACI组血清MMP-9与NSE水平随着梗死面积的增大而逐渐上升,A、B、C 3组组间比较有显著性差异(P0.05)。ACI患者血清MMP-9与血清NSE水平存在正相关性(r=0.568,P0.05)。结论血清MMP-9与NSE水平的检测可用于判断ACI患者病情严重程度及其预后情况,具有重要的临床价值。     

合并OSAHS的老年急性脑梗死患者同型半胱氨酸和胰岛素抵抗临床分析

目的研究合并阻塞性睡眠呼吸暂停综合征(OSAHS)的老年急性脑梗死(ACI)患者血清同型半胱氨酸(Hcy)及稳态模型胰岛素抵抗指数(HOMA-IR)水平,分析老年ACI患者OSAHS、Hcy和HOMA-IR相互关系。方法根据年龄和睡眠呼吸监测数据,将患者分为老年ACI+OSAHS组(n=21)、老年ACI组(n=30)、中年ACI+OSAHS组(n=28)和中年ACI组(n=34),检测并比较各组血清Hcy、胰岛素抵抗指数(HOMA-IR)等各指标。结果老年ACI+OSAHS组较其余3组的Hcy和HOMA-IR均升高,差异有统计学意义(P0.05);中年ACI+OSAHS组较中年ACI组Hcy和HOMA-IR增高,差异有统计学意义(P0.05)。Hcy与年龄、AHI、平均腰围、BMI、HOMAIR均呈正相关;多元线性回归分析显示AHI与年龄、Hcy、HOMA-IR、BMI呈正相关。结论随年龄的增加,合并OSAHS的急性脑梗死患者Hcy和HOMA-IR水平随之升高;OSAHS可能通过升高Hcy及增加胰岛素抵抗导致ACI。     

检测Hcy hs-CRP与IL-6水平对急性脑梗死患者的诊断价值

目的探讨检测同型半胱氨酸(homocysteine,Hcy)、超敏C反应蛋白(high sensitivity C-reactive protein,hsCRP)与白细胞介素-6(interleukin-6,IL-6)水平对急性脑梗死(acute cerebral infarction,ACI)患者的诊断价值。方法选择2012-03—2013-03在我院接受治疗的ACI患者46例为研究对象,纳入观察组。另选同期于我院接受健康体检的志愿者46例为对照组。对比2组治疗前后Hcy、hs-CRP及IL-6水平,不同程度脑梗死患者Hcy、hs-CRP及IL-6水平,以及分析各指标间的相关性。结果观察组治疗前Hcy、hs-CRP及IL-6水平均显著高于对照组,差异均有统计学意义(均P0.05)。但治疗后与对照组相比,差异均无统计学意义(均P0.05)。中型脑梗死患者的Hcy、hs-CRP及IL-6水平均显著高于轻型脑梗死者,而重型脑梗死患者Hcy、hs-CRP及IL-6水平亦均显著高于中型脑梗死者,差异均有统计学意义(均P0.05)。随脑梗死程度的逐渐加重,患者Hcy、hs-CRP及IL-6水平均呈现上升趋势,Hcy与hs-CRP、Hcy与IL-6及hs-CRP与IL-6均呈正相关。结论 Hcy、hs-CRP与IL-6水平的检测对于ACI患者的临床诊断具有较大价值,临床上应予以重视。     

血清NSE、IMA及LPA对急性脑梗死患者预后的评估价值

目的探讨血清神经元特异性烯醇化酶(NSE)、缺血修饰白蛋白(IMA)及溶血磷脂酸(LPA)对急性脑梗死(ACI)患者预后的评估价值。方法分析149例ACI患者临床资料,根据治疗后3个月患者改良Rankin评分(mRS)分为预后良好组(85例,mRS≤2分)和预后不良组(64例,mRS> 2分)。对比两组临床资料,Logistic回归分析确定影响ACI患者预后的危险因素,分析血清NSE、IMA及LPA与美国国立卫生院卒中表(NIHSS)评分的相关性,绘制受试者工作特征曲线(ROC)曲线分析血NSE、IMA、LPA水平对ACI患者预后的预测价值。结果预后不良组患者后循环梗死发生率、入院NIHSS评分、发病至给药时间及血清NSE、IMA、LPA水平明显高于预后良好组(P<0.05)。Logistic回归分析显示,后循环梗死、入院NIHSS评分、发病至给药时间长及血清NSE、IMA、LPA水平升高是ACI患者预后不良的重要危险因素(P<0.05)。ACI患者血清NSE、IMA、LPA水平与NIHSS评分均呈显著正相关(P<0.05)。血清NSE、IMA及LPA评估ACI患者预后的ROC曲线下面积分别为0.806、0.803、0.819。结论血清NSE、IMA及LPA水平与ACI患者神经功能损伤情况密切相关,其水平升高预示患者预后不良,检测血清三项指标水平有助于判断ACI患者预后状况。     

动态检测血清S100B蛋白与同型半胱氨酸对急性脑梗死的诊断价值

目的探讨动态检测血清S100B蛋白和Hcy水平对急性脑梗死(ACI)的诊断价值。方法选取72例ACI患者按病情分为轻、中、重型损伤3组各24例,于患者发病后首日及第3、6、14天采样进行血清S100B和Hcy检测,并对患者进行NIHSS评分,同期选择正常人24例测定血清S100B和Hcy,4组结果进行比较并分析S100B和Hcy与病情、NIHSS之间的相关性。结果除发病第14天轻型组血清S100B、Hcy水平与对照组无明显差异外,其他时间点测定结果均为S100B、Hcy水平重型组中型组轻型组对照组(P均0.05);血清Hcy、S100B与患者病情严重程度、同期NIHSS评分均呈正相关。结论血清Hcy、S100B联合检测是诊断ACI早期、特异、准确的检查方法,值得临床推广。     

新生儿缺氧缺血性脑病S-100B与NSE的检测及临床意义

目的探讨新生儿缺氧缺血性脑病(HIE)血清S-100B与NSE的检测及临床意义。方法选取我院2013-01—2016-01收治的90例HIE患者为观察组,另选取同期健康新生儿30例为对照组。观察组根据病情程度分为轻度、中度与重度组,分别采用酶联免疫吸附(ELISA)法和电化学发光法测定研究对象各时期血清S-100B与NSE的水平,对比各组S-100B与NSE水平的变化情况。结果观察组血清S-100B与NSE水平明显高于对照组,差异有统计学意义(P0.05)。观察组各亚组血清S-100B与NSE水平比较,差异有统计学意义(P0.05),随着病情程度的加重,S-100B与NSE水平均呈升高趋势。动态监测显示,出生后1、3d,观察组S-100B与NSE含量逐渐升高,至第7天时S-100B与NSE含量降低(P0.05),血清S-100B与NSE浓度高峰出现于出生后第3天。结论临床检测S-100与NSE有助于HIE的早期诊断,且可作为判断HIE病情程度的敏感指标。     

急性脑梗死患者血清NSE分析

目的探讨急性脑梗死(ACI)患者血清中神经元特异性烯醇化酶(NSE)水平及其与脑梗死面积大小的关系。方法对210例ACI患者按脑梗死面积大小进行分组,采用双抗体夹心ELISA法进行血清NSE水平测定。结果ACI患者各亚组间血清NSE水平有显著性差异(F值=16.2,P0.05),且与梗死灶体积呈显著正相关(r=0.72,P0.05)。结论ACI患者血清NSE水平可反应ACI患者的脑梗死状态,对判断病情和预后有重要价值。     

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.