帕金森病血抗氧化酶活性的研究

本文报道６７例帕金森病（ＰＤ）患者血超氧化物歧化酶（ＳＯＤ）．谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ），过氧化氢酶（ＣＡＴ）活性及脂质过氧化物（ＬＰＯ）量的测定结果。ＰＤ病人ＳＯＤ和ＧＳＨ－Ｐｘ活性高于正常对照组，但ＳＯＤ，ＧＳＨ－Ｐｘ和ＣＡＴ的活性及ＬＰＯ量与病程长短无明显关系，也与是否服用美多巴无关。研究结果提示，抗氧化酶活性的改变可能与ＰＤ病因有关。     

老年期痴呆患者血液和脑脊液的氧自由基反应相关指标研究

测定了１８例老年期痴呆患者和１５例正常老年人血液及脑脊液中ＳＯＤ，ＧＳＨ－Ｐｘ活力以及ＭＤＡ含量等氧自由基反应相关指标。发现：ＣＳＦ中平均Ｔ－ＳＯＤ活力及ＳＯＤ／ＭＤＡ比值老年期痴呆组显著低于正常老年组；而ＣＳＦ中ＭＤＡ含量两组之间无显著差别。血清Ｔ－ＳＤＯ活力和铨血ＧＳＨ－Ｐｘ活力以及血清ＭＤＡ含量在两组之间无明显差异。     

出血性卒中患者脑脊液微量元素和抗氧化酶含量的研究

本文测定３６例脑出血、３１例ＳＡＨ患者的脑脊液微量元素和抗氧化酶含量的变化，结果发现：脑出血和ＳＡＨ的脑脊液锌、硒、铬、铁、镁含量，ＧＳＨ－Ｐｘ活性和Ｇ／Ｍ比值明显低于对照组（Ｐ＜０．０５或Ｐ＜０．０１），铜、ＭＤＡ含量及ＳＯＤ活性明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）。提示：微量元素和抗氧化酶与出血性卒中有密切关系。     

羧乙基锗倍半氧化物对大鼠脑缺血再灌注损伤的保护作用

采用结扎双侧颈总动脉后再通的方法复制大鼠脑缺血再灌注损伤模型，通过测定再灌注后大鼠海马组织中脂质过氧化产物丙二醛（ＭＤＡ），超氧化物歧化酶（ＳＯＤ）与谷胱甘肽过氧化物酶（ＧＳＨ—Ｐｘ）及ＡＴＰａｓｅ的活性，观察了有机锗─羧乙基锗倍半氧化物（ＣＧＳ）对大鼠脑缺血再灌注后大鼠海马组织中ＭＤＡ水平，明显保护ＳＯＤ、ＧＳＨ─Ｐｘ、Ｎａ＋Ｋ＋─ＡＴＰａｓｅ及Ｃａ２＋─ＡＴ─Ｐａｓｅ活性。表明ＣＧＳ对大鼠脑缺血再灌注损伤具有保护作用。     

强迫症的临床特征

目的：探讨强迫症（ＯＣＤ）的临床表现。方法：对４０例符合ＤＳＭ－ⅣＯＣＤ诊断标准病人进行以下量表和问卷评定：强迫症量表（Ｙ－ＢＯＣＳ）,Ｈａｍｉｌｔｏｎ抑郁量表（ＨＡＭＤ）,Ｈａｍｉｌｔｏｎ焦虑量表（ＨＡＭＡ）,Ｍａｒｋｓ恐怖强迫量表（ＭＳＣＰＯＲ）,临床疗效总评量表（ＣＧＩ）和艾森克个性问卷（ＥＰＱ）;并对６５名正常人进行ＥＰＱ测试。结果：１５岁以前发病患者的ＭＳＣＰＯＲ的工作适应能力下降（ＷＤ）分显著高于１５岁以后发病患者;合病组病人的ＨＡＭＤ和ＥＰＱ的神经质分显著高于非合病组;洗涤／回避组的ＨＡＭＡ评分显著较高,迟缓／仪式化组的发病年龄显著较低,两组的ＭＳＣＰＯＲ的ＷＤ评分均显著高于强迫检查行为组。结论：１５岁以前发病,合病组,主要表现迟缓／仪式化或洗涤／回避症状的病人是ＯＣＤ较为严重的亚型。     

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。     

东菱克栓酶对全脑缺血再灌流损伤脑保护作用的实验研究

本文采用Ｐｕｌｌｓｉｎｅｌｌｉ的４ＶＯ方法制作了大鼠全脑缺血再灌流动动物模型，采用ＴＢＡ法、ＤＴＮＢ直接法测定全脑缺血１０ｍｉｎ再灌流后４８ｈ海马区的过氧化脂质（ＬＰＯ）和谷光甘肽过氧化物酶（ＧＳＨ－Ｐｘ）含量变化，计量病理和电子显微镜观察病理变化及东菱精纯克栓酶对其含量变化和病理改变的影响。结果显示：（１）东菱克栓酶可降低海马区ＬＰＯ含量（Ｐ〈０．０１），使ＧＳＨ－Ｐｘ活性上升（Ｐ〈０．０１）。     

神经症患者超氧化物歧化酶、谷胱甘肽超氧化物酶及脂质超氧化物含量的变化

为研究氧自由基与神经症之间的关系，分别采用邻苯三酚自氧化法、二硫对硝基苯甲酸直接法、硫代巴比妥酸比色法，测定了８７例神经症和５５名健康人超氧化物歧化酶（ＳＯＤ）、谷胱甘肽超氧化物酶（ＧＳＨ－Ｐｘ）和脂质超氧化物（ＬＰＯ）含量。结果显示，神经症组ＳＯＤ与ＧＳＨ－Ｐｘ两种酶含量均低于对照组，神经症组治疗前低于治疗后；ＬＰＯ为治疗前高于治疗后，差异均有显著性。从单胺类的代谢与生成氧自由基的生化联系以及机体内ＳＯＤ、ＧＳＨ－Ｐｘ、ＬＰＯ之间的相互关系上对结果进行了分析，提示体内单胺类物质代谢过程中产生的氧自由基在神经症的病理过程中可能发挥一定的作用。     

氧化、脂质过氧化与脑梗死关系的探讨

目的:探讨一氧化氮、氧化、脂质过氧化与脑梗死的关系。方法:检测了１４６例急性脑梗死患者(ＣＩ)和１００例健康志愿者(ＨＶ)血浆中的一氧化氮(Ｐ－ＮＯ)、维生素Ｃ(Ｐ－ＶＣ)、维生素Ｅ(Ｐ－ＶＥ)、β－胡萝卜素(Ｐ－β－ＣＡＲ)和过氧化脂质(Ｐ－ＬＰＯ)含量及红细胞中的超氧化物歧化酶(Ｅ－ＳＯＤ)、过氧化氢酶(Ｅ－ＣＡＴ)、谷胱甘肽过氧化物酶(Ｅ－ＧＳＨ－Ｐｘ)活性和过氧化脂质(Ｅ－ＬＰＯ)含量并作分析比较;同时,检测了其中４４例患者治疗前后的上述生化指标,并作分析比较。结果:与ＨＶ组比较,ＣＩ组的Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著升高(Ｐ＜０．００１),Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ平均值均显著降低(Ｐ＜０．００１);与治疗前比较,治疗后的Ｐ－ＮＯ、Ｐ－ＬＰＯ、Ｅ－ＬＰＯ平均值均显著降低(Ｐ＜０．００１),Ｐ－ＶＣ、Ｐ－ＶＥ、Ｐ－β－ＣＡＲ、Ｅ－ＳＯＤ、Ｅ－ＣＡＴ、Ｅ－ＧＳＨ－Ｐｘ平均值均显著升高(Ｐ＜０．００１)。结论:脑梗死患者体内ＮＯ代谢异常,一系列自由基连锁反应病理性加剧,氧化抗氧化平衡严重失调,ＮＯ、氧化和脂质过氧化损伤加剧。     

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     

Elevated plasma superoxide dismutase in first-episode and drug naive patients with schizophrenia: inverse association with positive symptoms

Excessive free radical production or oxidative stress may be involved in the pathophysiology of schizophrenia as evidenced by increased superoxide dismutase (SOD) activities, a critical enzyme in the detoxification of superoxide radicals. This study compared plasma SOD activities in 78 never-medicated first-episode and 100 medicated chronic schizophrenia patients to 100 healthy control subjects and correlated these SOD activities with the Positive and Negative Syndrome Scale (PANSS) among the schizophrenic patients. We found that both first-episode and chronic patients had significantly increased plasma SOD activities compared to controls, and that chronic schizophrenic patients on antipsychotic medication had significantly higher SOD activities than first episode schizophrenic patients. Plasma SOD activities were also negatively correlated with positive symptoms of schizophrenia, but only in first-episode patients. Thus, oxidative stress appears to be greater in first episode schizophrenic patients with fewer positive symptoms and may become greater as schizophrenia becomes more chronic, although we cannot exclude the possibility that chronic antipsychotic treatment may increase SOD activities and presumed oxidative stress in schizophrenia.     

Serum Oxidative Stress Marker Levels in Unmedicated and Medicated Patients with Schizophrenia

Oxidative stress has been suggested to be involved in schizophrenia, but studies have demonstrated inconsistent results on oxidative stress marker level/activity in patients with schizophrenia. In order to clarify the circulating oxidative stress marker level/activity in patients with schizophrenia, this study recruited 80 schizophrenia patients (40 first-episode, drug-free and 40 chronically medicated patients) and 80 controls to analyze serum activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC), and levels of lipid peroxidation marker malondialdehyde (MDA) in schizophrenia patients, and whether they associate with the severity of the disease. We showed that only serum GSH-Px activity was significantly reduced in unmedicated patients with schizophrenia when compared with control subjects, whereas the other three analyzed oxidative stress markers did not show significant differences between cases and controls. Moreover, our results demonstrated that chronic medication increased GSH-Px activity and MDA levels in patients with schizophrenia, but reduced SOD activity in the patients. We also found that short-term antipsychotic treatments on the patients with schizophrenia reduced the SOD activity. Correlation analyses indicated that the oxidative stress marker activity/level is not significantly associated with the severity of schizophrenia, except that SOD level correlated with PANSS positive score significantly. Taken together, the data from the present study suggested that the dysfunctions of oxidative stress markers in patients with schizophrenia were mainly caused by antipsychotics, emphasizing increased oxidative stress as a potential side effect of antipsychotics on the patients.     

Changes in oxidative stress markers in patients with schizophrenia: The effect of antipsychotic drugs

The aim of this study was to investigate the serum levels or activities of oxidative stress markers in patients with schizophrenia in acute phase and evaluate the changes in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH) and thiobarbituric acid-reactive substances (TBARS) after treatment. We consecutively enrolled 41 patients with schizophrenia in acute phase, and 27 patients were followed up with a 4-week antipsychotic treatment. Serum oxidative stress markers were measured with assay kits. We found that Positive and Negative Syndrome Scale (PANSS) total scores were significantly negatively correlated with serum GPx activity and GSH levels and positively correlated with serum SOD activity in patients with schizophrenia in acute phase. In addition, serum GPx activity had a positive correlation with GSH levels and negative correlation with SOD activity. We also found that serum SOD activity was significantly negatively correlated with TBARS levels in patients in acute phase. Furthermore, we found significantly increased changes only in GPx activity in female patients receiving the 4-week treatment (P=0.006). In conclusion, our results suggest that SOD, GPX and GSH might be indicators of schizophrenia severity in acute phase. Furthermore, antipsychotic drugs might affect serum GPx activity in female patients receiving the 4-week treatment.     

精神分裂症患者机体抗氧化功能指标的实验研究

目的 探讨机体抗氧化能力在精神疾病发病机理中的作用及其临床意义。方法 采用化学比色法检测176例精神分裂症患者血清中SOD、MDA、GSH－Px、VC、VE和NO含量。结果 精神分裂症患者血清中SOD、MDA、NO含量均高于对照组（P＜0．05或0．01）;GSH－Px、VC含均低于对照组（P＜0．01）;VE两者无显著差异（P＞0．05）;精神分裂症家族史阳性者血清中NO高于精神分裂症阴性家族史者（P＜0．05）;精神分裂症患者抗氧化能力含量可因病程、性别、年龄的不同而不同;精神分裂症患者治疗后SOD、MDA低于治疗前（P＜0．01）。结论 精神分裂症患者体内自由基代谢异常可能是精神分裂症发病的生物学因素之一。     

Evidence for impaired cortical inhibition in schizophrenia using transcranial magnetic stimulation

BACKGROUND: Cortical inhibition (CI) deficits have been proposed as a pathophysiologic mechanism in schizophrenia. This study employed 3 transcranial magnetic stimulation (TMS) paradigms to assess CI in patients with schizophrenia. Paired-pulse TMS involves stimulating with a lower-intensity pulse a few milliseconds before a higher-intensity pulse, thereby inhibiting the size of the motor evoked potential produced by the higher-intensity pulse. In the cortical silent period paradigm, inhibition is reflected by the silent period duration (ie, the duration of electromyographic activity cessation following a TMS-induced motor evoked potential). Transcallosal inhibition involves stimulation of the contralateral motor cortex several milliseconds prior to stimulation of the ipsilateral motor cortex, inhibiting the size of the motor evoked potential produced by ipsilateral stimulation. METHODS: We measured CI using these 3 paradigms in 15 unmedicated patients with schizophrenia (14 medication-naive and 1 medication-free for longer than 1 year) (13 were in the transcallosal inhibition paradigm), 15 medicated patients with schizophrenia (11 taking olanzapine, 1 risperidone, 1 quetiapine, 1 methotrimeprazine + perphenazine, 1 quetiapine + loxapine), and 15 healthy controls. RESULTS: Unmedicated patients demonstrated significant CI deficits compared with healthy controls across all inhibitory paradigms whereas medicated patients did not (at all inhibitory intervals, paired-pulse TMS: controls = 59.9%, medicated = 44.3%, unmedicated = 28.7%; cortical silent period: controls = 55.0 milliseconds, medicated = 60.4 milliseconds, unmedicated = 39.7 milliseconds; transcallosal inhibition: controls = 33.6%, medicated = 23.7%, unmedicated = 10.4%; P<.05). CONCLUSIONS: These results suggest that schizophrenia is associated with deficits in CI and that antipsychotic medications may increase CI.     

Auditory event-related potentials and electrodermal activity in medicated and unmedicated schizophrenics.

Event-related potentials (ERPs) and electrodermal activity were studied in 14 medicated schizophrenics, 17 unmedicated schizophrenics, and 23 age- and education-matched controls. Subjects were run in three auditory stimulus paradigms differing from the usual ERP paradigms in having interstimulus intervals greater than 12 sec to permit measurement of the longer latency skin conductance response (SCR). In every paradigm medicated but not unmedicated schizophrenics had smaller N120 amplitudes and fewer SCRs than controls. In addition, medicated schizophrenics showed reduced P200 amplitude and latency, longer P320 latency, and reduced skin conductance levels in certain paradigms. These effects cannot easily be attributed to different mental states of medicated and unmedicated patients, since their Brief Psychiatric Rating Scale scores were almost the same. It is more probable that antipsychotic and antiparkinsonian drugs reduced electrodermal activity through anticholinergic mechanisms and that the antipsychotic drugs attenuated N120 through other biological mechanisms.     

男性精神分裂症患者抗精神病药治疗前后血浆MicroRNA-181b表达水平

目的:研究血浆中microRNA-181b(miR-181b)在男性精神分裂症患者抗精神病药治疗过程的不同阶段表达水平的变化。方法:40例精神分裂症患者和40例正常对照,均为成年男性。以实时荧光定量PCR(RT-PCR)技术检测患者组(用药前、治疗2周和治疗4周)和对照组血浆miR-181b的表达水平。结果:和正常对照组相比,精神分裂症组在治疗前、治疗2周和治疗4周血浆miR-181b的表达水平均显著上调(P<0.001)。随着抗精神病药的治疗,病情逐渐好转,男性精神分裂症患者血浆miR-181b表达水平逐渐下降(治疗2周、治疗4周与治疗前比较,P均<0.001)。结论:血浆miR-181b可能参与精神分裂症的发病机制,其表达水平受抗精神病药影响。     

The effects of antipsychotic medication on factor and cluster structure of neurologic examination abnormalities in schizophrenia

This study extends a previous study of the factor structure of the neurologic examination in unmedicated schizophrenia, utilizing cluster analysis and adding a medicated condition. We administered a modified version of the Neurologic Evaluation Scale (NES) on two occasions to 80 patients with schizophrenia or schizoaffective disorder, once while on antipsychotic medications and once while off medication. Data were distilled by combining right- and left-side scores, and by excluding rarely abnormal and unreliable items from the analysis. Principal components analysis yielded an intuitive four-factor solution in the unmedicated condition, but an inscrutable five-factor solution during medication. Cluster analysis revealed three groups: normal, cognitively impaired, and diffusely impaired. These results were also less interpretable with data from the medicated condition. Neurologic performance was better in the medicated than in the unmedicated condition. As is the case with other domains of symptoms and performance in schizophrenia, relationships among neurologic exam variables are altered by the presence of antipsychotic medication.     

The deceleration capacity – a new measure of heart rate variability evaluated in patients with schizophrenia and antipsychotic treatment

BackgroundSchizophrenia is associated with increased cardiac mortality. A disturbed autonomic modulation of heart rate (HR) has been described in patients with schizophrenia in whom antipsychotic medication may represent an additional cardiac risk. The novel measure deceleration capacity (DC) of heart rate predicts cardiac mortality in patients with cardiovascular illnesses. The aim of the present paper was to calculate DC in patients with schizophrenia and to compare this measure with established parameters of heart rate variability (HRV).MethodsHRV and DC were calculated in 24-hour electrocardiogram (ECG) recordings of 20 unmedicated, 40 medicated patients with schizophrenia and 40 controls. As activity has a major influence on HRV, 4-hour periods of “sleep-” and “wake-” ECG were evaluated as additional parameters. Actigraphy was used to ensure comparable levels of activity in patients and controls.ResultsThe DC as well as the other established HRV measures were not significantly different comparing unmedicated patients with schizophrenia to healthy controls. However, medicated patients showed a significant reduction of DC calculated from ECG recordings during 4 hour over night periods.ConclusionCalculation of DC might contribute to a better monitoring and identification of an increased risk of cardiac mortality in patients with schizophrenia undergoing antipsychotic treatment.     

Taurine and glutathione in plasma and cerebrospinal fluid in olanzapine treated patients with schizophrenia

Oxidative stress has been implicated in the pathophysiology of schizophrenia. Taurine and glutathione (GSH) have antioxidant and central nervous system protective properties, and are proposed to be involved in the pathology of schizophrenia. The aim of this study was to compare the blood and cerebrospinal fluid (CSF) levels of taurine and GSH in patients with schizophrenia, medicated with oral olanzapine, compared with controls. In total, 37 patients with schizophrenia and 45 healthy volunteers were recruited. We found the plasma taurine levels to be elevated in patients compared with controls. No differences were, however, found between patients and controls regarding taurine in CSF or GSH concentrations in plasma and CSF. Moreover, in the patient group no correlations between taurine and GSH levels and the symptoms or function of the disorder were found. The higher levels of plasma but not CSF taurine in patients with schizophrenia treated with OLA may implicate the involvement of taurine in the pathophysiology of the disease. The absence of GSH differences both in plasma and CSF between patients and controls is interesting in the perspective of earlier research proposing a dysregulation of GSH metabolism as a vulnerability factor for the development of schizophrenia.