急性脑血管病肿瘤坏死因子-α的临床研究

目的：探讨肿瘤坏死因子-α（TNF-α）在急性脑血管病（ACVD）中的作用及其变化的临床意义。方法：选取95例ACVD患者，并设性别及年龄相匹配的血清对照组（20例）及脑脊液对照组（10例）。应用酶联免疫吸附法（ELISA）于发病后第1、3、7、14d测定血清和脑脊液中TNF-α。结果：①三种脑血管病患者血清TNF-α动态变化存在差异，脑出血和脑梗死组的峰值单间为发病后第3d，而蛛网膜下腔出血（SAH）组为第1d。②脑梗死患者血清TNF-α水平与梗死面积、神经功能缺损程度及病情恶化与否相关。③SAH组于发病后第1d、3d、7d脑脊液TNF-α值高于血清，14d时降至对照组水平并与血清无差异。结论：①脑梗死患者血清TNF-α的动态观察，可为临床预测梗死灶大小、神经功能缺损程度及病情恶化与否提供依据。②发病早期的脑梗死患者若CT未能显示病灶时，血清TNF-α的明显升高有助于临床诊断和治疗。③SAH患者脑脊液中TNF-α水平明显高于血清，进一步提示脑内神经组织可产生TNF-α。脑脊液中TNF-α的持续明显升高可能与SAH后脑血管痉挛有关。④TNF-α参与了ACVD的炎性反应过程，早期抑制TNF产生及抗炎性反应的治疗可能具有潜在的临床价值。     

慢性老年精神分裂症患者认知功能及其与日常生活能力的比较研究

目的 :了解慢性老年精神分裂症患者认知功能和日常生活能力状况 ,探讨此类患者在额叶执行功能和记忆方面的神经心理功能障碍及其特征。方法 :采用简易智力状态检查 (MMSE)、日常生活能力量表 (ADL)、威斯康星卡片分类测验 (WCST)及韦氏记忆量表 (WMS)对 31例慢性老年精神分裂症和 31例正常对照组进行比较研究。结果 :慢性老年精神分裂症组MMSE得分明显低于正常对照组 (P <0 .0 1) ;而该组ADL总分明显高于正常对照组(P <0 .0 5 )。除非持续错误外 ,慢性老年精神分裂症患者的威斯康星卡片分类测验和韦氏记忆量表的各项测验成绩均差于对照组 (P <0 .0 5 )。结论 :慢性老年精神分裂症患者认知功能的障碍决定了患者日常生活能力的减退 ;这类患者有明显的额叶执行功能障碍和记忆障碍     

On the Edge: a drama‐based mental health education programme on early psychosis for schools

Aims: On the Edge is a mental health education programme designed to support early intervention by increasing knowledge and understanding of early psychosis, reducing the stigma associated with mental health issues and improving awareness of avenues of help. The target audience was young people aged 14–22 years in schools and colleges. Methods: An interactive drama programme was developed through collaborative working across psychiatry, applied drama and those with direct experience of psychosis. A national tour engaged 2500 students in 71 performances that took place in 51 schools and colleges. The programme was evaluated against its aims with data collected both during and after the tour. Results: Quantitative and qualitative evaluation found significant gains with respect to all three aims. Thirty‐one schools developed supportive links with local mental health services. Conclusions: This programme shows the value and effectiveness of delivering health education on early psychosis through the medium of applied drama, and offers a model for a programme that can be incorporated into early intervention services. Lessons learned through delivering this programme are a valuable contribution towards future developments of mental health education programmes for schools.     

Validating the eating disorder inventory (EDI‐2) in two danish samples: A comparison between female eating disorder patients and females from the general population

The Eating Disorder Inventory, Version 2 (EDI‐2) is a questionnaire used clinically and in research all over the world. EDI‐2 is cross‐culturally valid, yet normative values may depend on culture. Norms and reliability of the Danish version have to date been lacking, and will be presented in this article, comparing patients (N = 575) and controls (N = 881). Also, internal reliability of scales is tested for both groups. Differences between norms of the Danish and the North American version of EDI were small but significant for all scales except asceticism (eating disorder patients) and ineffectiveness, interpersonal distrust and maturity fears (normal controls). For both groups the internal consistency was >0.70 for all subscales except asceticism. Although differences across the eating disorder diagnostic groups were dubious, the EDI‐2 is useful to screen for eating problems in the general population as well as to rate progress and outcome among eating disorder patients. Copyright © 2009 John Wiley & Sons, Ltd and Eating Disorders Association.     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.