注意缺陷多动障碍的分子遗传学进展

注意缺陷多动障碍（attention deficit hyperactivity disorder,ADHD）是常见的神经精神疾病,严重影响儿童、青少年和成人的学业、社交和工作技能。目前,儿童和青少年的患病率约为6％～9％。家系研究、双生子和寄养子研究结果显示遗传因素是ADHD的重要发病因素,平均遗传度约为76％。但是,ADHD病因与临床表现复杂,同时具有个体差异性,至今尚未阐明ADHD发病的生物学机制。对ADHD发病机制的分子遗传学研究主要集中于功能候选基因的关联分析领域。     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍大鼠模型的研究进展

人类注意缺陷多动障碍(attention deficit hyperactivity disorder,ADHD)是一种逐渐发展、影响终身的慢性疾病.目前认为,ADHD是由于遗传基础和环境因素共同作用的结果[1-2].由于人体研究的局限性,ADHD动物模型已成为研究其发病机制、药物治疗和科研预测的重要工具.目前,现有的各种模型虽具有不同的优缺点,但均以模仿ADHD的某-临床表现为主要行为学依据,从遗传、神经发育和社会应激等多个层面建立模型.本文就其中主要的ADHD大鼠模型的特点、研究现状和未来展望作一个综述.     

注意缺陷多动障碍与家庭因素

近年来,儿童注意缺陷多动障碍（ADHD）的研究在国内外受到广泛关注.美国儿科协会临床指南指出学龄儿童ADHD的患病率为4％～12％,是一种最常见的儿童心理行为疾病[1].我国选用DSM-Ⅳ的注意缺陷多动障碍诊断标准,近年调查学龄儿童检出率为3.94％～6.3％[2-4],调查数据普遍低于国外的数据,但总体呈上升趋势.儿童ADHD核心症状为注意力不集中、多动与冲动,它的病因目前仍不清楚,一般认为是由遗传和环境因素引起的一种心理行为性疾病.近年经许多回顾研究表明,ADHD儿童的不良行为与家庭环境因素和养育方式等具有一定的相关性,现在对此作一综述.关键词：注意缺陷多动障碍;家庭环境;教养方式;依恋     

注意缺陷多动障碍遗传学研究

注意缺陷多动障碍(Attention- deficit hyperactivity disorder,ADHD)是一种遗传性疾病,多与儿童行为障碍、酒精依赖、物质滥用、社会紊乱型人格障碍和情感障碍等共病.目前发现ADHD的某些症状,与孤独症类似.对双胞胎和家庭的研究发现其具有很高程度的遗传度,而与家庭环境基本无关.     

首发青少年抑郁症患者家庭环境及应付方式的研究

目的 探讨首发青少年抑郁症患者家庭环境、应付方式的特点及两者的关系.方法 采用家庭环境量表中文版(FES-CV)、应付方式问卷,对30例首发青少年抑郁症患者及30例正常对照者进行测评.结果 (1)青少年抑郁症患者家庭环境中亲密度、情感表达、知识性、娱乐性、宗教道德观等因子分低于正常对照组,矛盾性因子分高于正常对照组(P＜0.05);(2)青少年抑郁症组应付方式中的解决问题、求助因子分低于正常对照组,自责、退避因子分高于正常对照组(P＜0.05);(3)青少年抑郁症组应付方式中的解决问题因子与家庭环境中的控制性呈正相关(r=0.42);求助因子与情感表达呈正相关(r=0.41);自责因子与亲密度、情感表达呈负相关(r =-0.48,r =-0.44),与矛盾性呈正相关(r=0.47).结论 青少年抑郁症患者更多采用不成熟的应付方式,并与不良的家庭环境有关.     

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.     

难治性强迫症与非难治性强迫症临床特征比较

目的 比较难治性强迫症与非难治性强迫症的临床特征之间的差异.方法 分别用YBOCS量表评估51例难治性强迫症和59例非难治性强迫症患者的强迫症状,并比较两组临床症状特征的差异.结果 难治性强迫症组中的强迫思维分(11.18±3.07)、强迫行为分(7.35±4.92)及强迫总分(18.53±6.09)均显著性高于非难治性强迫症组(8.12±4.01,4.59±4.67,12.63±5.67;P＜0.05).难治性强迫症与非难治性强迫症两组中有无伴发其他精神症状(x2=0.016,P=0.899)、有无阳性家族史(x2=0.053,P=0.818)、发病年龄(20.29±8.72,20.56±8.00; t=0.113,P=0.911)及病程(7.56±3.23,8.56±3.52;t=0.486,P=0.629)无明显差异(P＞0.05).结论 难治性强迫症的临床症状严重程度(特别是强迫思维)显著性高于非难治性强迫症.     

躯体形式障碍与家庭环境和功能的关系

躯体形式障碍是一类以各种躯体症状为主要临床表现的神经症,其发病与社会心理因素关系密切,家庭因素是其中重要的因素之一.本文从家庭环境和家庭功能两方面加以综述,探讨躯体形式障碍和家庭因素之间的关系.     

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.     

高血压脑出血的显微外科治疗进展

高血压脑出血（Hypertensive intrac-rebral hemorrhage,HICH）是具有高发病率、高病死率、高致残率的急性脑血管疾病,占所有脑卒中患者的10%-20%,早期病死率可高达49.4%。随着人口老龄化,其发病率逐年提高;而外科手术的干预,使其病死率有所下降,但致残率居高不下。如何提高手术疗效和患者生存质量,一直是神经外科医师努力的方向。微侵袭血肿清除术因其手术创伤小,恢复快,是目前国内治疗高血压脑出血的重要手段。     

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.     

精神分裂症的家庭负担调查研究

目的评价精神分裂症的家庭负担情况。方法采用家庭负担会谈量表（familyinter-viewscheduleFIS）、抑郁自评量表（SDS）及焦虑自评量表（SAS）和自编量表为工具,符合ICD-10诊断标准的精神分裂症患者共900例,其中15例资料不完整者被剔除,余下885例中,男性534例,女性351例,调查其家庭照料及经济负担情况。结果照料者的负担明显,精神分裂症患者FIS的家庭经济负担、家庭日常活动、家庭休闲娱乐活动、家庭成员心理健康4个因子的阳性回答率较高,均超过60％,家庭成员生理健康、家庭关系两个因子的阳性回答率较低,均低于40％,男性患者照料者其家庭娱乐活动所受影响比女性患者照料者明显;男性患者照料者感到负担重,且直接照料时间越长,负担越重;885例患者亲属SAS的均分为（49．76±9．25）,明显高于正常人,经统计学处理两者有显著性差异（P〈0．01）,SDS均分为（51．27±9．97）,明显高于正常人,经统计学处理有显著性差异（P〈0．01）。结论精神分裂症造成严重的家庭和经济负担,应作为干预的对象,患者亲属焦虑、抑郁情绪明显高于正常人群。