神经内科住院医师病历书写规范化培训探索

病历书写是住院医师规范化培训的基础.掌握神经内科疾病的病历书写和诊疗思路是住院医师必经的临床训练.结合首都医科大学宣武医院神经内科对住院医师培训的实践和经验,我们认为病历书写从基础到专病,从集中到个体化循序渐进的培训和考核、监控方法,有助于神经内科医师临床思维能力培养和临床水平的提高.     

神经内科住院医师规范化培训存在的问题与教学 改进

住院医师是医院人才梯队建设的基础,合理地安排培训工作,提高青年医师综合素质,对 培养高层次医学人才至关重要。宣武医院作为北京市首批神经内科住院医师规范化培训基地,近5年已 为社会培育出120名住院医师,取得北京市住院医师规范化培训合格证书。以宣武医院神经内科近5年 培训实践为例,探讨神经内科规范化培训的现状和管理实践,为持续改进培训工作提供参考。     

麻省总医院神经内科医师培训启示

美国住院医师制度相对成熟,我国虽然起步较晚,但也在不断完善。本文结合自身经历,分析美国神经内科住院医师培训的特点,旨在取长补短,为我国的医师培训提供参考。     

胜任力为导向的神经内科住院医师规范化培训的课程效果评价

目的 评价胜任力为导向的神经内科住院医师培训模式的效果。 方法 选取2016-2020年在北京大学第三医院神经内科完成或正在参加住院医师培训的研究生、 规范化培训的基地学生和住院医师,采取问卷调查或一对一访谈的形式对目前神经内科的系统模式 培训效果进行评价,包括神经内科知识和技能评价以及人文相关内容评价两方面。 结果 共纳入40名医师,培训总体满意度为85%。获益最大的带教方式是“学生为主体”的病例导入 学习（90%）,希望培训的内容包括神经影像学（82.5%）、心电图和胸片等内科基础知识（70%）、肌 电图和脑电图（65%）。最需要提升的疾病种类规培生更多希望掌握常见疾病的诊断和处理,八年制 及硕士研究生则把培训的需求放在罕见疾病的认识和提高。人文素质提升较大的方面包括同情心 和爱伤观念（75%）、职业自豪感（65%）、责任意识（62.5%）。 结论 胜任力为导向的神经内科住院医师培训模式有助于提高专业知识和技能以及人文素质。     

关于中美两国神经内科住院医师培训的一点思考

2011年笔者有幸获得北京市李桓英医学基金资助,到美国Baylor医学院神经内科和全美最大的私立医院Methodist医院的神经内科参观学习。期间主要在神经内科病房和运动障碍门诊学习,因此,有机会了解两院神经内科住院医师的培训情况,并对中美两国住院医师培训进行了一点比较和思考。     

多种教学方法在神经内科住院医师规范化培训中的应用

    针对神经内科住院医师规范化培训过程中存在的神经系统查体不规范,诊断方法认识不足、临床技能培训不够、带教科室管理和培训不得法,提出完善培训制度、改进培训方法等方面的对策,介绍多种教学方法,以便带教老师在有限时间内,高质量完成神经内科规范化培训目标。     

神经内科住院医师规范化培训“单位人”和“行业 内社会人”的临床教学实践

“单位人”和“行业内社会人”是住院医师规范化培训中不容忽视的两类人群，现从首都 医科大学宣武医院神经内科住院医师培训基地的教学实践出发，从临床基本功训练、多模式教学、绩效 考核、建立导师制等方面，探讨对上述两类人群如何进行针对性的教学培训。     

思维导图结合以问题为基础教学法在急诊神经内科住院医师卒中教学中的应用

将思维导图结合以问题为基础教学法（problem-based learning，PBL）应用于急诊神经内科 住院医师卒中培训的理论学习、急诊跟诊和全程诊治中，可以提高卒中诊疗的教学效果。思维导图结 合PBL的教学法有利于激发住院医师学习的主动性，提高学习效率，提升教学效果，对综合性教学医 院急诊卒中诊疗的培训工作有促进作用。     

脑血管病住院医师规范化培训方案思考——基于北京市神经内科住院医师规范化培训临床结业技能考核影响因素分析

目的 对北京市神经内科住院医师规范化培训结业技能考核成绩的影响因素进行分析,探讨脑血 管病住院医师培训方案的改进。 方法 收集2017-2020年北京市神经内科住院医师规范化培训临床结业技能考核成绩,对技能考 核是否通过,以及辅助检查、病例考核、技能操作及人文沟通等分项成绩的可能影响因素进行多因 素分析。 结果 二元logistic回归分析结果显示,性别、学历、专业基地规模是技能考核通过与否的影响因素。 多元逐步回归分析结果显示,性别、专业基地规模、学员类型、学历是辅助检查成绩的影响因素;专业 基地规模是影响病例考核成绩的影响因素;学员类型是技能操作成绩的影响因素。 结论 女性、大的培训基地学员及博士学历学员通过住院医师规范化培训结业技能考核率更高。 在制订脑血管病学员培养方案时,应充分考虑人员特点,针对其短板进行重点培训,并努力提高专业 基地的质量和同质性。     

思维导图结合以问题为基础教学法在急诊神经内科住院医师卒中教学中的应用

将思维导图结合以问题为基础教学法（problem-based learning，PBL）应用于急诊神经内科
住院医师卒中培训的理论学习、急诊跟诊和全程诊治中，可以提高卒中诊疗的教学效果。思维导图结
合PBL的教学法有利于激发住院医师学习的主动性，提高学习效率，提升教学效果，对综合性教学医
院急诊卒中诊疗的培训工作有促进作用。     

Environmental factors in the development and progression of late-onset Alzheimer＇s disease

Late-onset Alzheimer＇s disease （LOAD） is an age-related neurodegenerative disorder characterized by gradual loss of synapses and neurons, but its pathogenesis remains to be clarified. Neurons live in an environment constituted by neurons themselves and glial cells. In this review, we propose that the neuronal degeneration in the AD brain is partially caused by diverse environmental factors. We first discuss various environmental stresses and the corresponding responses at different levels. Then we propose some mechanisms underlying the specific pathological changes, in particular, hypothalamic-pituitary adrenal axis dysfunction at the systemic level; cerebrovascular dysfunction, metal toxicity, glial activation, and Aβ toxicity at the intercellular level; and kinase-phosphatase imbalance and epigenetic modification at the intracellular level. Finally, we discuss the possibility of developing new strategies for the prevention and treatment of LOAD from the perspective of environmental stress. We conclude that environmental factors play a significant role in the development of LOAD through multiple pathological mechanisms.     

Disrupted structural and functional brain connectomes in mild cognitive impairment and Alzheimer＇s disease

Alzheimer＇s disease （AD） is the most common type of dementia, comprising an estimated 60-80% of all dementia cases. It is clinically characterized by impairments of memory and other cognitive functions. Previous studies have demonstrated that these impairments are associated with abnormal structural and functional connections among brain regions, leading to a disconnection concept of AD. With the advent of a combination of non-invasive neuroimaging （structural magnetic resonance imaging （MRI）, diffusion MRI, and functional MRI） and neurophysiological techniques （electroencephalography and magnetoencephaJography） with graph theoretical analysis, recent studies have shown that patients with AD and mild cognitive impairment （MCI）, the prodromal stage of AD, exhibit disrupted topological organization in large-scale brain networks （i.e., connectomics） and that this disruption is significantly correlated with the decline of cognitive functions. In this review, we summarize the recent progress of brain connectomics in AD and MCI, focusing on the changes in the topological organization of large-scale structural and functional brain networks using graph theoretical approaches. Based on the two different perspectives of information segregation and integration, the literature reviewed here suggests that AD and MCI are associated with disrupted segregation and integration in brain networks. Thus, these connectomics studies open up a new window for understanding the pathophysiological mechanisms of AD and demonstrate the potential to uncover imaging biomarkers for clinical diagnosis and treatment evaluation for this disease.     

Edema and neuronal apoptosis in the hippocampus and cortex of elderly rats following transient cerebral ischemia/reperfusion injury

BACKGROUND： Previous studies of cerebral ischemia have used young animals, with an ischemic time greater than 5 minutes （safe time limit）. Despite an increased understanding of neuronal apoptosis, it remains uncertain whether brief cerebral ischemic events of 5 minutes or less damage brain tissue in elderly rodents. OBJECTIVE： To investigate the effects of transient cerebral ischemia （5 minutes）/reperfusion injury on brain cortical and hippocampal edema, aquaporin-4 （AQP-4） expression, and neuronal apoptosis in aged rats, and to compare ischemic sensitivity between cortex and hippocampus. DESIGN, TIME AND SETTING： A randomized, controlled, animal experiment was performed at the Institute of Cerebrovascular Disease, Qingdao University Medical School from April 2008 to March 2009. MATERIALS： Rabbit anti-AQP-4 polyclonal antibody, TUNEL kit, and SABC immunohistochemistry kit were purchased from Wuhan Boster Bioengineering, China. METHODS： A total of 160 healthy, male, aged 19-21 months, Wistar rats were randomly assigned to 4 groups： sham-surgery, and ischemia 1-, 3-, and 5-minute groups, with 40 rats in each group. The global cerebral ischemia model was established using the Pusinelli four-vessel occlusion, and the three cerebral ischemia groups were subdivided into reperfusion 12-hour, 1-, 2-, 3-, and 7-day subgroups, with 8 rats in each subgroup. The sham-surgery group was subjected to exposure of the first cervical bilateral alar foramina and bilateral common carotid arteries. MAIN OUTCOME MEASURES： The dry-wet weight assay was used to measure brain water content and histopathology of the cortex and hippocampus was observed following hematoxylin-eosin staining. In addition, cortical and hippocampal AQP-4 expression was detected by streptavidin-biotin complex immunohistochemistry, and neuronal apoptosis was detected by the TUNEL method. RESULTS： There was no significant difference in brain water content or AQP-4 expression in the cortex and hippocampus between ischemia 1- and 3-minute groups and the sham-surgery group or brain water content or AQP-4 expression in the cortex between ischemia 5-minute group and sham-surgery group （P 〉 0.05）. However, brain water content and AQP-4 expression in the hippocampus after 5 minutes of cerebral ischemia were significantly increased compared with the sham-surgery group （P 〈 0.05 or P 〈 0.01）. Several TUNEL-positive cells were observed in the cortex and hippocampus of the sham-surgery group and ischemia 1-minute group, as well as in the cortex of the ischemia 3-minute group. In addition, the number of apoptotic neurons in the hippocampus of ischemia 3-minute group and in the cortex and hippocampus of ischemia 5-minute group was significantly increased （P 〈 0.05 or P 〈 0.01 ）. Neuronal apoptosis was increased after 12 hours of ischemia/reperfusion, and it reached a peak by 2 days （P 〈 0.01）. CONCLUSION： Transient cerebral ischemia （5 minutes） resulted in increased hippocampal edema, AQP-4 expression, and neuronal apoptosis. Moreover, cerebral ischemia had a greater effect on neuronal apoptosis than brain edema or AQP-4 expression, and the hippocampus was more sensitive than the cortex.     

Targeting 13-secretase with RNAi in neural stem cells for Alzheimer＇s disease therapy

There are several major pathological changes in Alzheimer＇s disease, including apoptosis of cho- linergic neurons, overactivity or overexpression of 13-site amyloid precursor protein cleaving enzyme 1 （BACE1） and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein （AI3） production, and introduced it into the pSilenCircle vector to construct a short hairpin （shRNA） expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing AI3 protein production. We anticipate that this technique combining cell transplantation and gene ther- apy will open up novel therapeutic avenues for Alzheimer＇s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.     

Total saponins of Panax ginseng effects on proliferation and differentiation of human embryonic neural stem cells and in a Parkinson’s disease mouse model

BACKGROUND： Total saponins of Panax ginseng （TSPG） exhibits neuroprotection against Parkinson＇s disease in the substantia nigra. OBJECTIVE： To investigate the effects of TSPG on human embryonic neural stem cells （NSCs） proliferation and differentiation into dopaminergic neurons using in vitro studies, and to observe NSC differentiation in a mouse model of Parkinson＇s disease, as well as behavioral changes before and after transplantation. DESIGN, TIME AND SETTING： In vitro neural cell biology trial and in vivo randomized, controlled animal trial were performed at the Institute of Basic Medical Sciences, Chongqing Medical University between September 2004 and December 2007. MATERIALS： TSPG （purity 〉 95%） was isolated, extracted, and identified by Chongqing Academy of Chinese Materia Medica. Recombinant human basic fibroblast growth factor （bFGF） and recombinant human epidermal growth factor （EGF） were purchased from PeproTech, USA. A total of 25 C57/BL6J mice, aged 18-20 weeks were included. Twenty were used to establish a Parkinson＇s disease model with i.p. injection of MPTP （1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine） and TSPG alone or combined with interleukin-1 （IL-1）-treated NSCs prior to transplantation into the corpus striatum. The remaining five mice were pretreated for 3 days with TSPG prior to MPTP injection, serving as the TSPG prevention group. METHODS： Primary NSCs were isolated, cultured and purified from embryonic cerebral cortex. Immunocytochemistry was employed to detect specific antigen expression in the NSCs. In vitro experiment： （1） to induce proliferation, NSCs were treated with TSPG, EGF＋bFGF, or TSPG＋EGF＋bFGF, respectively; （2） to induce dopaminergic neuronal differentiation, NSCs were treated with TSPG, IL-1, or TSPG＋IL-1, respectively. MAIN OUTCOME MEASURES： In vitro experiment： the effects of TSPG on NSCs proliferation were evaluated with flow cytometry and MTT assay. Tyrosine hydroxylase expression was determined by immunocytochemistry assay to observe effects of TSPG on dopaminergic neuronal differentiation. In vivo experiment： differentiation of grafted NSCs in the mouse brain was determined by immunohistochemical staining. Behavioral changes were evaluated by spontaneous activity frequency, memory function, and score of paralysis agitans. RESULTS： （1） NSCs were cultured and passaged for more than three passages. Immunocytochemistry revealed positive nestin staining, as well as neurofilament protein and glial fibrillary acidic protein. （2） TSPG significantly increased NSC proliferation, in particular when combined with EGF and bFGF, which was twice as effective as FGF or bFGF alone. TSPG also induced dopaminergic differentiation in NSCs, in particular when TSPG was added together with IL-1, resulting in an effect five times greater than that of IL-1 alone. （3） At day 30 following transplantation, most NSCs in the TSPG prevention group differentiated into dopaminergic neurons, and the scores of paralysis agitans, spontaneous activity, and memory function were significantly increased compared with TSPG alone or TSPG＋IL-1 groups （P 〈 0.05）. CONCLUSION： TSPG stimulated NSC proliferation, in particular when combined with FGF and bFGF. TSPG significantly induced dopaminergic neuronal differentiation of NSCs, and the effect was greater when combined with IL-1. In addition, TSPG greatly improved behavior in the Parkinson＇s disease mouse model following NSC transplantation. Following NSC transplantation, TSPG pretreatment exhibited superior efficacy over either TSPG alone or TSPG in combination with IL-1, in terms of behavioral improvements in the Parkinson＇s disease mouse model.     

阿尔茨海默病治疗的研究进展

阿尔茨海默病（AD）是一种隐匿性起病,进行性恶化的神经退行性疾病,临床最初表现为认知功能障碍,并有可能在5～10年内完全衰退。患者往往伴随严重的记忆力丧失、精神行为异常、人格改变、言语功能障碍,无法独立生活,最终近乎于植物状态。Ferri等采用DISMOD软件在全球60岁以上人群中估计,全球的痴呆患者人数到2040年将达到8llO万左右。     

墨蝶呤还原酶基因与精神分裂症相关性的研究进展

墨蝶呤还原酶（SPR）催化四氢生物蝶呤（BH4）从头合成途径的最后一步反应。SPR基因遗传缺陷或突变可导致BH。的合成紊乱,影响单胺类神经递质（如多巴胺、5-羟色胺及谷氨酸等）的合成或释放,进而参与包括精神分裂症在内的多种神经精神系统疾病的发生发展过程。此外,SPR基因敲除小鼠表现出持续增强的自主活动等类精神分裂症症状,说明该基因在精神分裂症的发病中扮演重要的角色。进一步研究SPR基因及其单核苷酸多态性的功能,可为阐明精神分裂症的发病机制提供重要的线索,也为新一代抗精神病药物的研制及开发开拓新的视野。现对SPR基因与精神分裂症的相关研究做一综述。     

Neuronal failure in Alzheimer＇s disease： a view through the oxidative stress looking-glass

Considerable debate and controversy surround the cause（s） of AIzheimer＇s disease （AD）. To date, several theories have gained notoriety, however none is universally accepted. In this review, we provide evidence for the oxidative stress-induced AD cascade that posits aged mitochondria as the critical origin of neurodegeneration in AD.     

癫痫与自杀

自杀而导致死亡被为是增加癫痫患者死亡率的最重要原因之一。国外许多研究报道都表明癫痫患者的自杀率比普通人群的自杀率高几倍到二十几倍。可能导致癫痫患者自杀的危险性因素是有多方面的,本文将从5-HT、抗癫痫药及癫痫手术治疗、精神病理等方面对癫痫患者可能存在自杀危险因素进行综述,并希望在癫痫的综合治疗中对这些危险因素能加以考虑。     

Wnt信号通路与骨髓间充质干细胞增殖及分化的关系

骨髓间充质干细胞（bonemarrow—derived mesenchymal stem cells,BMSCs）是骨髓中不同于造血干细胞的一类细胞,其来源丰富,取材简便,易分离、纯化、培养,在一定的条件下可以迅速体外扩增,具有多向分化潜能,可以通过不同的方法被诱导分化成骨细胞、软骨细胞、肌细胞、神经胶质细胞、神经元细胞等,而且它具有低免疫源性,向病变部位迁移的能力,