帕金森病患者血液抗氧化功能的变化及多巴制剂与VitE对 …

目的 探讨帕金森病（ＰＤ）的抗氧化酶（ＳＯＤ）活性和过氧化脂质（ＬＰＯ）代谢水平的变化和多巴药物及ＶｉＴ对其的影响，找出反映氧化异常的客观生化指标。方法 对９６例ＰＤ患者动态检测了服用Ｌ－多巴和ＶｔＥ前后的血浆及红细胞膜超氧化物岐化酶（Ｐ－ＳＯＤ、Ｅ－ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）活性，血浆及红细胞过氧化脂质（Ｐ－ＬＰＯ、Ｅ－ＬＰＯ）及丙二醛（ＭＤＡ）的变化，并与２０例正常３人对照。     

脑出血患者血总抗等指标的动态检测

本文对脑出血患者进行了血总抗氧化能力（总抗）、谷胱曾肽（血浆及血红蛋白ＧＳＨ）、血浆丙二醛（ＭＤＡ）的动态检测。结果提示，起病后（平均２．５小地）、总抗低于正常（Ｐ＜０．０１），血浆及血红蛋白ＧＳＨ、ＭＤＡ均高于正常（Ｐ＜０．０１），治疗１５天后，对存活者复查，总抗不仅低于正常，且低于治疗前，血浆ＧＳＨ低于治疗前（Ｐ＜０．００６５。血红蛋白ＧＳＨ统计学无意义（Ｐ＞０．０５）。ＭＤＡ低天治疗前，但仍高于正常（Ｐ＜０．０１）。我们认为脑出血患者自身的抗氧化能力不清除自由基较困难主张早期大量补充各种抗氧化剂。     

癫痫患者自由基代谢的变化及其与脑电图的关系

本文选择癫痫患者30例，分别于发作期和缓解期作血浆总抗氧化能力（GAA）、血浆谷胱甘肽（GSH1）、血红蛋白谷胱甘肽（GSH2）及血浆丙二醛（MDA）的检测及脑电图检查。结果提示：发作期，MDA明显高于正常，缓解期近于正常。MDA升高者，EEG多数异常。GAA、GSH的变化也具有显著意义。揭示自由基代谢参与癫痫的病理过程。     

合并多器官功能衰竭的急性脑血管病患者神经内分泌的改变

本实验动态测定了急性脑血管病（ＡＣＶＤ）并发多器官功能衰竭（ＭＯＦ）患者血清生长激素（ＧＨ）、泌乳素（ＰＲＬ）、促黄体生长素（ＬＨ）、促滤泡成熟激素（ＦＳＨ）、睾酮（Ｔ）、孕酮（Ｐ）、雌二醇（Ｅ２）、皮质醇（Ｆ）和血浆促肾上腺皮质激素（ＡＣＴＨ）水平的变化，并与ＡＣＶＤ各疾病组对比。结果发现：ＧＨ、ＰＲＬ、ＡＣＴＨ、Ｆ及ＦＳＨ水平显著升高；ＡＣＶＤ并发ＭＯＦ重型患者（ＭＯＦ积分＞４分）ＰＲＬ、ＧＨ、Ｆ水平显著高于轻型患者（ＭＯＦ积分≤４分）。结果提示ＰＲＬ、ＧＨ和Ｆ可能参与了ＡＣＶＤ并ＭＯＦ的病理生理过程     

脑缺血再灌注脑内纹状体区细胞外液谷胱甘肽的动态变化及丹参的影响

采用脑内微透析技术，应用高压液相色谱电化学检测方法（ＨＰＬＣ－ＥＤ），活体动态观察沙土鼠全脑缺血３０分钟，再灌注１２０分钟的细胞外液中的谷胱甘肽（Ｇｌｕｔａｔｈｉｏｎｅ，ＧＳＨ）的变化及丹参对它的影响。结果显示：全脑缺血后，细胞外液ＧＳＨ水平迅速升高（Ｐ＜０．０１），缺血３０分钟达高峰为缺血前的５。８２倍。再灌注后ＧＳＨ水平明显降低，于３０分钟趋于正常。脑缺血前３０分钟给予丹参注射液不影响细胞外液ＧＳＨ水平。表明脑缺血及再灌注期，ＧＳＨ反应性增高。ＧＳＨ作为内源性抗氧化剂及ＮＭＤＡ受体拮抗剂在脑缺血损伤中起重要作用。     

伴与不伴注意缺陷多动障碍的抽动秽语综合征患儿动态脑电图的 …

目的 探讨与不伴注意缺陷多动障碍（ＡＤＨＤ）的抽动微语综合征（ＴＳ）患儿间脑电图的差异。方法 对８６例伴与不伴ＡＤＨＤ的ＴＳ患儿进行２４ｈ动态脑电图（ＡＥＥＧ）监测。结果 伴ＡＤＨＤ的ＴＳ组（４０例）ＡＥＥＧ异常率为７５％,单纯ＴＳ组（４６例）异常率为３０％,２组差异有显著性（Ｐ〈０．０５）;ＡＥＥＧ异常的主要表现为慢波异常以及癫痫样波,伴ＡＤＨＤ的ＴＳ组的ＡＥＥＧ局部异常多于广泛异常,且以额叶受     

缺血性脑血管病伴OSAS患者的血压和血管舒缩功能观察

目的 观察缺血性脑血管病（ＩＣＶＤ）伴阻塞型睡眠呼吸暂停综合征（ＯＳＡＳ）患者平均动脉压（ＭＡＢＰ）、血浆降钙素基因相关肽（ＣＧＲＰ）和内皮素（ＥＴ）的变化及相互关系。方法 应用放免方法测量３１例患者血浆ＣＧＲＰ和ＥＴ含量,静息状态下测量血压;多元相关分析。结果 ＩＣＶＤ伴ＯＳＡＳ患者组ＭＡＢＰ、ＥＴ均炕于正常对照组（均Ｐ〈０．００１）,ＣＧＲＰ明显低于对照组（Ｐ〈０．００１）;ＣＧＲＰ与ＭＡＢＰ     

伴与不伴多动的Tourette综合征脑电图对比分析

目的 探讨伴与不伴注意缺陷多动障碍（ＡＤＨＤ）的Ｔｏｕｒｅｔｔｅ综合征（ＴＳ）之间的脑电图变化差异。方法 对８６例患儿进行常规ＥＥＧ描记研究分析。结果 伴ＡＤＨＤ的ＴＳ患儿ＥＥＧ异常率显著高于单纯ＴＳ，主要表现为慢波异常以及癫痫样波。结论ＴＳ在神经生理学上存在异质性。ＴＳ与ＡＤＨＤ之间在解剖生理及生化上的关联有待进一步探讨。     

Alzheimer病与老年精神分裂症的脑电地形图研究

目的：为探讨Ａｌｚｈｅｉｍｅｒ病（ＡＤ）和老年精神分裂症患者（ＳＳ）在定量脑电地形图（ＢＥＡＭ）检查中特点。方法：应用丹麦ＳＥＥＧ－１６道脑电地形图仪，对符合ＤＳＭ－Ⅲ－Ｒ诊断标准的３２例ＡＤ、２４例ＳＳ和３９例正常老人作了ＢＥＡＭ检查。结果：ＢＥＡＭ－ＥＥＧ图象上ＡＤ患者和ＳＳ患者均出现低密度带，前者为横行形，后者趋向凹字形。与正常老人相比，ＡＤ患者和ＳＳ患者ＢＥＡＭ－ＥＥＧ变化特征是，δ和θ波功率上ＡＤ在所有点、ＳＳ在主要点均增高，绝大部分脑区增高程度在统计学上有显著意义。α波功率下降，ＡＤ患者在后颞、前颞、顶区，ＳＳ患者在额区、顶区有显著差异。β波功率ＡＤ患者在前额、后颞，ＳＳ患者在额极、中颞、后颞、枕区增高，且有显著性。结论：ＡＤ患者和ＳＳ患者的ＢＥＡＭ－ＥＥＧ具有不同于正常老人的变异，且ＡＤ和ＳＳ患者在脑区记录点异常分布上明显不同，提示ＢＥＡＭ－ＥＥＧ对ＡＤ患者和ＳＳ患者鉴别上有一定参考意义。     

Wilson病患者血清氧化物和抗氧化物水平与内脏损伤的关系

目的 探讨Ｗｉｌｓｏｎ病（ＷＤ）患者血清氧化物和抗氧化物水平与内脏损伤的关系。方法 应用化学比色法和反相高效液相色谱法（ＲＰ－ＨＰＬＣ）测定２９例ＷＤ患者和２１名正常人血清丙二醛（ＭＤＡ）、谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）、谷胱甘肽（ＧＳＨ）和维生素Ｅ（ＶｉｔＥ）的水平。结果 ＷＤ组与对照组相比ＭＤＡ显著增高（Ｐ〈０．０１）,ＧＳＨ－ＰＸ显著下降（Ｐ〈０．０１）。且两者呈负相关;血清ＶｉｔＥ和ＧＳＨ在肝型ＷＤ患者显著减少（分别Ｐ〈０．０１和Ｐ〈０．０５）。非肝型患者与对照组比,差别无显著性（Ｐ〉０．０５）。结论 ＷＤ患者轿清中存在着自由基系统的代谢紊乱,氧化物水平升高,抗氧化物水平下降,这可能是该病患者内脏损伤的重要原因之一。     

血小板活化因子与癫痫关系初探

本文对30例癫痫患者，分别于发作后72小时内及发作缓解期进行血小板活化因子（PAF）的检测，发现发作后72上时内，高于正常对照组，发作缓解期近于正常，提示PAF参与癫痫的病理过程，对其在癫痫中的作用进行讨论。     

Guanidino compound levels in the serum of healthy adults and epileptic patients.

Some guanidino compounds are known to be convulsants and to change in the brain during seizures. In this study, we examined the serum levels of guanidino compounds in healthy adults (controls), non-epileptic neurological patients (NENP) and epileptic neurological patients (ENP). In healthy adults, serum levels of guanidinoacetic acid (GAA), creatinine (CRN) and homoarginine (HArg) were significantly lower in women than in men. Serum levels of GAA in ENP and NENP were significantly lower than in controls, with the exception of female NENP. In the male patients, CRN levels were significantly lower in ENP and NENP compared to the controls. Significantly higher arginine (Arg) levels were observed in both male and female ENP and NENP. HArg levels in the male patients were significantly lower in ENP compared with both controls and NENP. With regard to serum levels of guanidino compounds in ENP with symptomatic generalized epilepsy and with symptomatic partial epilepsy, significantly lower levels of HArg were observed in male ENP with symptomatic generalized epilepsy than in NENP. Serum levels of GAA and HArg in uncontrolled female ENP were significantly lower than those in controlled ENP. Furthermore, Arg and HArg levels in uncontrolled male ENP were significantly lower than in controlled ENP. Serum levels of Arg in male ENP and HArg in both sexes of ENP taking valproic acid were significantly lower than those in ENP not taking valproic acid. These results suggest that some metabolic disorder of guanidino compounds may exist in ENP and NENP and that guanidino compounds may be affected by seizure types, seizure severity and anticonvulsants.     

Myotonic dystrophy: investigation of the proposed defect in guanidoacetic acid synthesis

No significant abnormality was detected in plasma levels or urinary excretion of guanidoacetic acid (GAA) in patients with myotonic dystrophy. It therefore seems unlikely that there is defective synthesis of GAA in this disorder. It was confirmed that arginine-glycine amidinotransferase (AGA), the enzyme responsible for GAA synthesis, is present in renal cortical tissue, but no enzyme activity could be detected in a variety of other, more accessible tissues taken from healthy controls.     

Lipid peroxidation in women with epilepsy

Background:

Lipid peroxidation is an indicator of free radical metabolism and oxidative stress in human beings and other organisms. Malondialdehyde (MDA), an end product of lipid peroxidation, is a metabolite that can be readily estimated in serum samples. Excess oxidative stress may be a final common pathway through which anti epileptic drugs may exert their teratogenic potential in pregnant women with epilepsy. Our objective in this study was to ascertain the variations in malondialdehyde (MDA) in women with epilepsy.

Material and Methods:

This study was carried out in the Kerala Registry of Epilepsy and pregnancy after obtaining clearance from the Institutional Ethics Committee. Informed consent was obtained from all the subjects. The quantitative examination of MDA was performed according to standard procedures. The ideal plasma level of MDA is below 2 nmol/ml.

Results:

Fifteen women with confirmed epilepsy (mean age 26.9 ± 3.5) were included in the study. Two women were pregnant. MDA levels ranged from 1.7 to 2.8 nmol/ml (mean level = 2.13 ± 0.37 nmol/ml). Eight women (53 %) had MDA levels above the upper limit of normal. Three patients had levels above 2.5 nmol/ml, which corresponded to the 75 centile.

Conclusions:

This study had shown that the estimation of MDA levels in plasma is a convenient method to study lipid peroxidation and thereby oxidative stress in women with epilepsy. Over half of Women With Epilepsy (WWE) have excess oxidative stress as indicated by high levels of MDA in the plasma. Correlations between MDA level and characteristics of epilepsy, AED therapy, nutritional status and other medical conditions need to be observed in a larger cohort.     

Free radicals in patients with post-traumatic stress disorder

There is mounting evidence indicating that reactive free radical species (FRs) are involved in initiation and development of many different forms of human pathologies including psychiatric disorders. In the present study, we aimed to determine whether antioxidant enzyme (glutathione peroxidase, GSH-Px; superoxide dismutase, SOD and catalase, CAT) activities and malondialdehyde (MDA) levels, a product of lipid peroxidation, were associated with post-traumatic stress disorder (PTSD). The study comprised 14 patients who had been diagnosed with PTSD according to DSM-IV criteria and met the admission criteria and 14 healthy controls. The activities of GSH-Px SOD, CAT and MDA were measured in both the patients and controls. In addition, all patients were assessed using the Clinician Administered PTSD Scale (CAPS). The mean GSH-Px, SOD, CAT activities and MDA levels of the patient group did not differ from those of the controls. However, in patients, the GSH-Px and SOD activities were significantly and positively correlated with CAPS scores, while there was a trend toward positive correlations between CAPS scores and MDA or CAT. In conclusion, our results suggest that the production of FRs does not seem to be related to PTSD.     

癫痫患者血浆丙二醛及红细胞超氧化物歧化酶的检测

本文采用硫巴比妥酸法及肾上腺素法测定52例癫痫患者血浆MDA含量及红细胞SOD活力。发现各型癫痫患者MDA含量均显著升高(P<0.01),而SOD活力除4例单纯部分性发作患者较对照组明显升高外其余各型未见明显改变(P>0.05)。病程5年以内患者的SOD活力明显升高(P<0.001),随病程延长逐渐降低。提示脂质过氧化物的增加和一些自由基清除酶类的相对缺少是癫痫发生、发展的一个重要原因。     

Plasma asymmetric dimethylarginine (ADMA) concentrations in patients with first and multiple episode schizophrenia

An increasing number of reports in the literature indicate that asymmetric dimethylarginine (ADMA) regulates nitric oxide generation in numerous disease states. ADMA has been less studied in psychiatric disorders. The purpose of this study was to determine plasma ADMA concentrations in patients with schizophrenia compared to healthy controls. The study was conducted in 49 male patients with schizophrenia and 30 healthy male control subjects. The patient group was 24 first episode and 25 multiple episode schizophrenia participants. All schizophrenic patients were administered the Scale for the Assessment of Negative Symptoms, the Scale for the Assessment of Positive Symptoms (SAPS) and the Brief Psychiatric Rating Scale. Measurement of plasma concentrations of ADMA was accomplished by HPLC. There was a significant increase in the plasma ADMA concentrations in patients with schizophrenia when compared to healthy controls. There were no significant correlations between the plasma concentrations of ADMA and scores of psychiatric rating scales. In the multiple episode schizophrenia subgroup, the mean plasma ADMA concentration was significantly higher than in the first episode schizophrenia subgroup. The study indicate that plasma ADMA concentrations in patients with schizophrenia are elevated.     

Plasma urea and ammonia in epileptic patients and their relatives.

The plasma levels of urea and ammonia were examined in patients with primary generalized epilepsy, patients with partial epilepsy and in the first-degree relatives of these subjects. The results show a significant decrease in plasma urea in both groups of patients and their first-degree relatives as compared to the non-epileptic controls. The plasma ammonia concentrations were significantly higher in both groups of patients and in the relatives of generalized epilepsy patients as compared to the controls. The observed changes in plasma urea and ammonia were found not to be due to the effect of anticonvulsant drugs. The data suggest that a metabolic defect in urea synthesis may constitute one of the genetic components in the multifactorial etiologies of primary generalized and partial epilepsies.     

Phenytoin Levels in Catamenial Epilepsy

We studied the fluctuations in phenytoin (PHT) levels during ovulatory and menstrual phases of the cycle, in eight patients with catamenial epilepsy and in eight age-matched controls. Pharmacokinetic studies of PHT were done in five patients with catamenial epilepsy. The difference in PHT levels during menstrual and ovulatory phase in catamenial group was 3.44 +/- 3.25 micrograms/ml as compared with 0.91 +/- 2.03 micrograms/ml in controls. The mean fall during menstrual phase was significant (p less than 0.05) in the catamenial group. There was also rapid though statistically nonsignificant clearance of PHT during menses as compared with the ovulatory period. It is presumed that the fall in plasma PHT levels during menses, though still within therapeutic range, may be responsible for catamenial exacerbation of epilepsy.     

Evaluation of the mechanism underlying the inhibitory effect of guanidinoacetate on brain Na, K-ATPase activity

Guanidinoacetate methyltransferase deficiency (GAMT-deficiency) is an inherited neurometabolic disorder clinically characterized by epilepsy and mental retardation and biochemically by accumulation of guanidinoacetate (GAA) and depletion of creatine. Although the neurological symptoms are predominant, the pathogenesis of the brain dysfunction in this disorder is not yet established. In the present study we investigated the in vitro effect of GAA on Na+, K+-ATPase and Mg2+-ATPase activities in synaptic plasma membrane from hippocampus of young rats. Results showed that GAA significantly inhibited Na+, K+-ATPase activity without affecting Mg2+-ATPase activity. We also evaluated the effect of glutathione (GSH), trolox, Nomega-nitro-L-arginine methyl ester (L-NAME) and taurine (Tau) on the inhibition elicited by GAA on Na+, K+-ATPase activity. GSH, trolox, L-NAME and Tau per se did not alter Na+, K+-ATPase activity. However, L-NAME and taurine prevented the inhibitory effect of GAA on this enzyme activity. Our findings suggest that the inhibition of Na+, K+-ATPase activity caused by GAA is possibly mediated by nitric oxide (NO) formation and/or synaptic membrane alteration. The present data may contribute to the understanding of the neurological dysfunction characteristic of GAMT-deficient patients.