戊巴比妥对^32P胶体兔脑组织间质内放疗损伤保护作…

在建立＾３２Ｐ胶体间质内放疗动物模型实验的基础上，间质内放疗剂量４００Ｇｙ时腹腔内应用氯胺酮和戊巴比妥，以观察内放疗周围脑组织损伤的保护作用。结果表明：在ＭＲＴ２ＷＴ像上水肿范围以及多胺ＳＰｄ含量上，氯胺酮处理组与正常对照组无显著差异，而戊巴比妥处理组和正常对照组以及氯胺酮组存在差异，提示氯胺酮对＾３２Ｐ胶体间质内放疗脑组织损伤无明显保护作用，而戊巴比妥具有明显保护作用，并和多胺中ＳＰｄ减少有关。     

戊巴比妥对~(32)P胶体兔脑组织间质内放疗损伤保护作用实验研究

戊巴比妥对３２Ｐ胶体兔脑组织间质内放疗损伤保护作用实验研究李爱民朱凤清我们用氯胺酮和戊巴比妥对３２Ｐ胶体兔脑组织间质内放疗损伤保护作用程度比较，观察非麻醉剂量戊巴比妥对３２Ｐ胶体兔脑组织间质内放疗脑保护效果，了解其临床可用性。首先将家兔２６只随机分组...     

脑卒中患者血浆超氧化物歧化酶（SOD）的变化及意义

为探讨脑卒中时颅内病变组织与血液中ＳＯＤ的改变的相关性，测定了２０例脑出血的脑组织与血液，及４８例脑梗塞、３２例脑出血血液内ＳＯＤ。结果脑出血脑组织中ＳＯＤ较正常对照组减少４２．３％（Ｐ＜０．０１），血浆内ＳＯＤ：梗塞组较正常对照组减少７８．９％，出血组减少７７．１％。各组与正常对照组问呈显著差异（Ｐ＜０．０１）。患者血液ＳＯＤ与脑组织ＳＯＤ的改变经相关分析ｒ＝０．６５２３（Ｐ＜０．０５），表明脑卒中时，血液内ＳＯＤ的变化，反映了颅内病变情况，为临床提供了一个诊断与观察病情变化的客观指标。     

静脉内注射乙醇对基底动脉痉挛作用的实验研究（摘要）

静脉内注射乙醇对基底动脉痉挛作用的实验研究（摘要）傅震，陈华辉，吴幼章，侯金稿材料和方法ＳＤ大鼠３０只，随机分成对照组和治疗组。戊巴比妥３０ｍｇ／ｋｇ腹腔麻醉后，开放一侧股静脉，气管切开插Ｔ形管维持呼吸道通畅。用自动牵开器使嘴张大，将舌与下颌尽可能向...     

丹参对大鼠脑颞叶梗死后空间认知障碍的改善和HSP32表达的影响

目的　探讨丹参对单侧颞叶缺血性损害大鼠空间认知能力的改善作用及与热休克蛋白３２（ＨＳＰ３２）表达的关系。方法　采用立体定向光化学技术导致大鼠左侧颞叶皮层梗死,术前３０ 分钟及术后第３ 天分别给丹参组大鼠腹腔注射丹参１０ｇ／ｋｇ,用Ｍｏｒｒｉｓ 水迷宫监测大鼠行为。然后取脑进行ＨＥ染色及ＨＳＰ３２ 免疫组化分析。结果　丹参组大鼠在Ｍｏｒｒｉｓ 迷宫中搜索目标的反应时和行程较单纯梗死组显著缩短,且较多地使用了正常的认知策略,其由随机式过渡到趋向和直线式策略的进程也与正常对照组无明显差异。丹参治疗组颞叶梗死体积较单纯梗死组显著缩小,ＨＳＰ３２ 表达明显减少。结论　丹参可以明显改善单侧颞叶缺血性损害大鼠的空间认知能力障碍。ＨＳＰ３２ 表达与颞叶损害有关联。     

大鼠蛛网膜下腔出血后脑组织P53基因表达与细胞损伤

目的　探索防治蛛网膜下腔出血（ Ｓ Ａ Ｈ）引起的脑血管痉挛（ Ｃ Ｖ Ｓ）的新途径。方法　利用大鼠 Ｓ Ａ Ｈ 模型，设立对照组、 Ｓ Ａ Ｈ 组、放线菌素酮治疗组（ Ｃ Ｈ Ｘ 组）。经 Ｄ Ｉ Ｇ Ｒ Ｔ Ｐ Ｃ Ｒ 对不同时间大鼠脑组织 Ｐ５３基因进行检测。结果　对照组、 Ｃ Ｈ Ｘ 组 Ｐ５３基因表达相近， Ｓ Ａ Ｈ 组 Ｐ５３基因表达增高。显微镜下见 Ｃ Ｈ Ｘ 组病理形态学变化近似正常， Ｓ Ａ Ｈ 组神经细胞损伤严重。结论　大鼠 Ｓ Ａ Ｈ 后 Ｃ Ｖ Ｓ所致的脑缺血，脑组织 Ｐ５３基因表达明显增高。大鼠 Ｓ Ａ Ｈ 模型 Ｐ５３基因表达与脑神经元细胞损伤明显相关。放线菌素酮通过抑制 Ｐ５３基因表达从而抑制其诱导的损伤。     

甲基强的松龙对颅脑损伤后血清S-100B蛋白变化的影响

1材料与方法将72只成年SD大鼠随机分为正常组、对照组、治疗组,用3%戊巴比妥30mg/kg腹腔内注射麻醉。正常组8只,只行开颅手术,不作头颅打击;对照组和治疗组各32只,分别分为伤后1h、6h、12h、24h4个小组。对照组和治疗组大鼠麻醉后,采用Feeney法造成鼠脑挫裂伤模型。治疗组大鼠致伤后即刻腹腔内注射30mg/kg甲基强的松龙,对照组则即刻腹腔内注射同等体积生理盐水。对照组和治疗组大鼠分别在伤后1h、6h、12h、24h时间点断头取血3ml,离心后取上清液1ml用ELISA检测技术定量检测血清S-100B蛋白水平。2结果正常组血清S-100B蛋白(0.35±0.029)…     

局灶性脑缺血再灌注损伤模型大鼠与促红细胞生成素的神经保护作用

背景：近年来动物实验和体外细胞培养研究证实促红细胞生成素对脑缺血具有神经保护作用，有关促红细胞生成素脑保护的作用机制目前尚未阐明。 目的：通过观察缺血损伤区域脑组织细胞学形态，检测脑组织超氧化物歧化酶、丙二醛浓度，探讨促红细胞生成素对脑缺血再灌注损伤的保护作用。 方法：采用线栓法建立Wistar大鼠局灶性缺血再灌注损伤模型，分别于缺血后2 h腹腔注射生理盐水3 000 U/kg、促红细胞生成素3 000，1 000 U/kg，并设假手术组。缺血再灌注损伤24 h后，应用苏木精-伊红染色法检测大鼠脑组织病理学变化，应用黄嘌呤氧化酶法和硫代巴比妥酸法分别测定超氧化物歧化酶活性和丙二醛浓度。 结果与结论：形态学结果显示促红细胞生成素高剂量组较生理盐水组皮质神经细胞存活数量增多，损伤程度减轻；促红细胞生成素高、低剂量组超氧化物歧化酶活性均明显高于假手术组和生理盐水组(P < 0.05)，丙二醛浓度明显低于假手术组和生理盐水组(P < 0.05)；促红细胞生成素高剂量组超氧化物歧化酶活性明显高于促红细胞生成素低剂量组，丙二醛含量明显低于促红细胞生成素低剂量组(P < 0.05)。提示经腹腔注射促红细胞生成素，可使大鼠脑缺血再灌注损伤区神经细胞存活数量明显增加，可显著改善组织的病理学改变，其保护作用可能是通过促红细胞生成素清除自由基，拮抗过氧化损伤实现的。     

聚合牛血红蛋白对缺血再灌注脑组织氧自由基和SOD的影响

目的探讨聚合牛血红蛋白（ＰＢＨｂ）在缺血再灌注后脑损伤的治疗作用。方法采用大鼠全脑缺血再灌注损伤模型，观察缺血前后应用ＰＢＨｂ对脑组织氧自由基和超氧化物歧化酶（ＳＯＤ）含量的影响。结果与缺血再灌注组相比，脑保护及复苏ＰＢＨｂ组均能有效减少氧自由基产生，其中脑复苏ＰＢＨｂ组比白蛋白对照组作用更强。同时，ＳＯＤ含量相应降低，尤以脑复苏ＰＢＨｂ组显著。结论ＰＢＨｂ能有效地抑制氧自由基产生而表现出良好的脑保护及复苏作用，这种作用不是通过增强ＳＯＤ活力产生的。     

脑梗塞患者血清中LPO,SOD水平与巴曲酶的影响

本文应用硫代巴比妥酸显色比色法和邻苯三酚自氧法测定８７例脑梗塞患者血清中ＬＰ０、ＳＯＤ含量，随机分组分别用巴曲酶和低分子右旋糖酐＋丹参治疗，并测定治疗后血清中ＬＰＯ、ＳＯＤ含量，研究证明脑梗塞患者血清中ＬＰＯ显著高于非脑血管病及健康对照者（Ｐ＜０．０１），而ＳＯＤ显著低于非脑血管病及健康对照者（Ｐ＜０．０１）。巴曲酶治疗后血清中ＬＰＯ明显低于治疗前（Ｐ＜０．０１），ＳＯＤ高于治疗前（Ｐ＜０．０５），而对照组无差异（Ｐ＞０．０５）。提示巴曲酶可抑制脑梗塞患者血清中ＬＰＯ产生，提高ＳＯＤ活性，具有保护神经细胞作用。     

Treatment Considerations in Anticonvulsant Monotherapy

Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.     

Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity

Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.     

Pediatric Epilepsy Surgery

Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.     

Un nouveau cadre conceptuel de travail pour une psychiatrie revisitée ? Introduction à deux articles de E. Kandel

In two articles which appeared in the American Journal of Psychiatry and that were subsequently translated for Évolution Psychiatrique, E. Kandel examines the bases for a reinterpreted psychiatry that is prepared to confront the major challenge of the 3rd millenium: that of insight into the mind and brain. This requires a major reorganization of the discipline, which involves a reinvestment of the scientific approach and a critical  assessment of the data provided by psychoanalytical psychiatry and cognitive neurosciences. Seven concepts have therefore been proposed for interactive re-examination: consciousness, the unconscious, memory, emotion, development, desire, impulse. The dynamic relations existing between genetics and the environment allow one to see how evolutions are possible from actions at different levels, both psychotherapeutic and pharmacological. Imaging and other techniques provide additional objective information to the process of human interaction which remains the basis of psychiatry. A common framework for psychiatry and the neurosciences, a reconsideration and renewal of the psychoanalytical approach are both possible and necessary.     

Opioids and the developing organism: A comprehensive bibliography, 1984–1988

A comprehensive bibliography of the literature concerned with opioids and the developing organism for 1984-1988 is presented. Utilized with companion papers (Neurosci. Biobehav. Rev. 6:439-479; 1982; 8:387-403; 1984), these articles cover the clinical and laboratory references beginning in 1875. For the years 1984, 1985, 1986, 1987, and 1988, a total of 877 citations were recorded. A series of indexes accompanies the citations in order to make the literature more accessible. These indexes are divided into clinical and laboratory topics, and subdivided into such topics as the type of opioid explored and the general area of biological interest (e.g., physiology).     

La biologie et le futur de la psychanalyse : un nouveau cadre conceptuel de travail pour une psychiatrie revisitée

The American Journal of Psychiatry has received a number of letters in response to my earlier “Framework” article (1). Some of these are reprinted elsewhere in this issue, and I have answered them briefly there. However, one issue raised by some letters deserves a more detailed answer, and that relates to whether biology is at all relevant to psychoanalysis. To my mind, this issue is so central to the future of psychoanalysis that it cannot be addressed with a brief comment. I therefore have written this article in an attempt to outline the importance of biology for the future of psychoanalysis.     

Facteurs de risque environnementaux à la schizophrénie

Schizophrenia is currently a major concern, its prevalence being estimated at around 1% and its social consequences being severe. The elucidation of the pathophysiology of the disease is difficult due to the great variability of clinical expressions, the instability of the clinical symptoms during the evolution and the absence of reliable biological markers. The existence of a familial aggregation in schizophrenia is well known, the risk of presenting the disease for first-degree relatives of patients being 5 to 10 times higher than the risk observed in the general population. The genetic component was further confirmed by twin and adoption studies. Although the concordance for the disease is higher (40 to 70%) among monozygotic twins as compared with dizygotic twins (15%) it does not reach 100%, which implies that environmental factors modulate the effects of the genotype. However, the role of these factors and especially their interaction with genetic factors remain unclear but the implications of some specific environmental factors are well documented by recent research data. The current literature on sex differences in schizophrenia is consistent. Several studies have suggested that male and female patients may differ in age at the onset and expression of clinical symptoms. Complications during pregnancy or birth-giving may increase the risk of developing schizophrenia later in life. The major complications are oxygen deprivation during pregnancy, bleeding, maternal malnutrition or infection (exposure to influenza, for example). A low birth weight is associated with an increased risk of schizophrenia. Psychoses are more common among people living in an urban environment and among those born during winter months. Schizophrenia is probably more prevalent in people who are living promiscuously, are subject to toxic abuse, poor nutrition and stress but here more precise data are needed. Moreover, immigrants have a higher risk of developing psychotic disorders. In addition, head traumas are associated with an increased risk of schizophrenia. Though they are contentious, some studies suggest that substance abuse (cannabis use in European countries) is related to the development of schizophrenia, especially in people with genetic vulnerability. Moreover, substance misuse may worsen the symptoms. If the environment is sufficiently stressful, people with a high genetic vulnerability will develop some degree of mental illness, including schizophrenia. Conversely, a less stressful or a protective environment may decrease the risk of its onset in persons with a predisposition to schizophrenia.     

Introduction: Goals

Summary: Epilepsy is characterized by recurrent seizures. Many epilepsies with focal seizures as well as convulsive generalized seizures respond satisfactorily to antiepileptic drugs (AEDs) that reduce repetitive firing (e.g., phenytoin, carbamazepine, and valproate) or that augment GABA_A-mediated inhibition (e.g., phenobarbital and benzodiazepines). A number of drugs presently under development, such as NMDA receptor antagonists, loreclezole, losigamone, meth-ysticine, and dextromethorphan, are promising in acute animal models of otherwise drug-resistant convulsant activity. As a result of recent studies in both experimental models and surgically resected human epileptic brain, the prospects for development of AEDs have significantly improved. Several new AEDs recently have reached the commercial market or are in experimental or clinical trials. A comparative presentation of the standing of the new AEDs with respect to their efficacy and side effects is necessary, but still very difficult. Because initial experience with new AEDs is restricted to populations with severe drug-resistant epilepsy, the crucial question whether potential new AEDs can alter prognosis is not yet definitively answered. There is a clear need to compare the effects of standard AEDs and new AEDs in naive patients and over longer follow-up periods. Moreover, because of the strong desire to develop antiepileptic therapy that directly treats the primary etiology of a given epileptic syndrome , or modifies the neurobiological processes that cause recurrent seizures, better experimental epilepsy models for chronic epilepsy and further clinical studies are necessary to increase the knowledge on the pathophysiology of distinct epileptic syndromes. In this respect, studies on the differences between responders and nonresponders to a given AED treatment are extremely valuable.