阿苯达唑与吡喹酮治疗脑囊虫病的对比观察

目的：比较阿苯达唑与吡喹酮治疗脑囊虫病短期和近期的临床疗效及不良反应。方法：６３例脑囊虫病人，随机分为两组，治疗组３２例，阿苯达唑２００ｍｇ，Ｐｏ，ｑ８ｈ，１０ｄ为一疗程，以后间隔１５ｄ再进行下一个疗程。对照组３１例，砒喹酮２００ｍｇ，Ｐｏ，ｑ８ｈ。以两组短期和近期疗程结束后为统计界限。结果：两组短期疗效人数变化比较差异显著（Ｐ＜０．０５）；近期疗效人数变化比较差异不显著（Ｐ＞０．０５）；近期基本治愈率两组比较差异较显著（Ｐ＜０．０１）；近期两组不良反应人数比较差异显著（Ｐ＜０．０５）。结论：短期阿苯达唑治疗脑囊虫病病人较砒喹酮临床疗效突出，近期安全性优于砒喹酮。     

阿苯达唑与吡喹酮治疗脑囊虫病的对比观察

目的：比较阿苯达唑与砒喹酮治疗脑囊虫病短期和近期的临床疗效及不良反应。方法：63例脑囊虫病人，随机分为两组，治疗组32例，阿苯达唑200mg,Po,q8h,10d为一疗程，以后间隔15d再进行下一个疗程，对照组31例，砒喹酮200mg,Po,q8h，以两组短期和近期疗程结束后为统计界限，结果：两组短期疗效人数变化比较差异显著（P＜0．05）；近期疗效人数变化比较差异不显著（P＞0．05），近期基本治愈率两组比较差异较显著（P＜0．01），近期两组不良反应人数比较差异显著（P＜0．05），结论：短期阿苯达唑治疗脑囊虫病病人较砒喹酮临床疗效突出，近期安全性优于砒喹酮。     

实质型脑囊虫病的MRI分期诊断与临床病理研究

目的 探讨实质型脑囊虫病的MRI表现与病理改变的对应关系，旨在提高其诊断水平。方法 对50例临床、病理证实的脑囊虫病患者的MRI表现进行了分析。结果 （1）活虫期：MRI表现为囊状长T1长T2信号，囊壁光滑且与头节均呈等T1等T2信号；（2）变性死亡早期：MRI表现为虫体周围见长T1长T2信号水肿带，囊壁增厚、头节可见，增强后可出现环状增强；（3）变性死亡后期：MRI表现水肿范围缩小或消失，头节消失，囊壁增厚；（4）钙化纤维化期：虫体死亡并钙化，MRI表现为长T1短T2信号灶。结论 实质型脑囊虫病的MRI分期诊断对临床治疗有其重要的指导意义。     

脑实质型脑囊虫病的诊断与治疗

目的探讨单纯脑实质内泡型脑囊虫病的诊断与治疗。方法对9例脑实质型脑囊虫病患者的临床资料及手术效果进行分析总结。结果单囊患者7例,双囊患者2例。术前误诊5例。7例患者病灶全部摘除（头节＋囊壁）,另2例患者行囊虫结节囊壁大部分摘除,无新的神经功能障碍产生,无手术死亡。随访3个月～6年,有癫痫的5例患者术后癫痫均控制良好,术前肌力障碍的1例患者术后肌力恢复正常,有共济失调症的1例患者术后该症状亦明显减轻。结论脑实质型脑囊虫病误诊率较高,其显微手术治疗效果良好。     

脑囊虫病有效药物治疗:吡喹酮

目的:研究脑囊虫病的临床特点及有效的治疗措施。方法:对495例脑囊虫病患者进行回顾性研究,总结其临床特征,实验室检查数据,影像学指标及治疗方法。结果:495例脑囊虫病患者中59.2%为男性,40.8%为女性;82.0%为农村人口,18.0%为城市人口。患者中癫痫发作340例,头痛171例。血液和脑脊液免疫检查囊虫阳性率分别为67.8%和46.9%。CT和MRI检查显示,患者中包括了四种类型脑囊虫病。其中437例给予吡喹酮治疗,41例手术治疗。23.7%患者痊愈;71.5%患者临床症状明显改善。结论:脑囊虫病流行趋势农村高于城市,癫痫发作和颅压升高为主要临床症状。绝大多数患者应用吡喹酮有效。     

脑囊虫病的MR误诊分析(6例报告)

目的 探讨脑囊虫病的磁共振表现及误诊原因,提高对脑囊虫病的认识.方法 经病理活检或临床确诊的曾经误诊的脑囊虫病6例,回顾分析其MR影像学表现.结果 多发病灶4例、12个,单发病灶2例,均位于额顶叶皮髓质交界区,5个病灶T1WI囊液信号高于脑脊液,T2WI呈高信号,9个病灶T2WI显示囊内容物呈低信号,或高低混杂信号.病灶周围均可见水肿带,并呈环形强化.4例误诊为转移瘤,2例误诊为脑脓肿.结论 MR是诊断脑囊虫病的重要检查方法,重视流行病学,提高对MR征象的认识,可以避免误诊.     

高颅压型脑囊虫病术后服吡喹酮的组织病理学研究

目的从组织病理学方面研究手术并服吡喹酮治疗高颅压型脑囊虫病的优越性。方法对从1984年-2002年收治的230例高颅压型脑囊虫病人进行手术并手术后服吡喹酮治疗,对摘出囊虫进行病理观察。结果随访6个月,脑室型囊虫术后复查CT示:脑室系统对称性扩大,梗阻脑积水影像消失,皮肌内囊虫阴影消失90%以上者92例,血常规及血生化检查正常,癫癎发作减少75%以上,高颅压症状完全消失。总有效率96.7%,死亡率3.3%。结论术后服吡喹酮是治疗高颅压型脑囊虫病较为有效的方法。     

脑实质型囊性囊虫病的显微手术治疗

目的 探讨脑实质型囊性囊虫病的诊断与显微手术治疗效果.方法 对11例行显微手术治疗的脑实质型囊性囊虫病患者的手术效果进行分析总结.结果 病灶内有头节的患者头节均被摘除,9例患者囊壁全部摘除,2例患者囊壁大部分摘除,术后病理均证实为脑囊虫.随访3个月-6年,有癫痫的6例患者术后癫痫均控制良好,术前有颅高压的5例患者术后症状立即明显改善,术前有肌力障碍的2例患者术后6个月内肌力均恢复正常,有共济失调症的1例患者该症状亦明显减轻.失访1例.结论 脑实质型囊性囊虫病误诊率较高,但显微手术治疗效果良好.     

大剂量肠虫清治疗脑囊虫病临床观察

观察大剂量肠虫清治疗脑囊虫病的临床效果。方法：５４例脑囊虫病患者,随机分为二组,观察组应用肠虫清６０ｍｇ／ｋｇ／ｄ,分三次口服;对照组应用吡喹酮２０ｍｇ／ｋｇ／ｄ,分二次口服,采用全国脑囊虫病学订会议制定的标准出疗效评价。     

高颅压型脑囊虫病术后服吡喹酮的组织病理学研究

目的 从病理组织学厅面研究手术并服毗喹酮治疗高颅压型脑囊虫病的优越性。方法 对1984-2002年收治的230例高颅胝型腑囊虫病人进行手术并服吡喹酮治疗，摘出囊虫后进行病理观察。结果 随访89例6个月，癫痫发作减少75％以上；高颅压症状完全消失；腰穿脑脊液压力正常；血常规及血生化检查正常；复查CT示脑室系统对称性扩大及梗阻性脑积水影像消失，皮肌内囊虫消失90％者72例。结论 术后服用吡喹酮是治疗高颅压型脑囊虫病较为有效的方法。     

25例大面积脑梗死的外科治疗临床分析

目的 评价大面积脑梗死的外科治疗方法 及疗效.方法 回顾性分析我院2005年7月～2009年12月脑系科收治的25例大面积脑梗死病例外科救治方法 及疗效.结果 恢复良好15例,中残2例,重残3例,植物状态生存2例,死亡3例.结论 开颅去骨瓣减压术加颞肌贴敷不仅可明显降低大面积脑梗死患者的病死率,而且可以获得较好的功能预后.对高度怀疑大面积脑梗死的患者,应急时行CT或MRI检查,以便得到更积极的抢救性治疗.     

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。     

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.     

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.     

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.     

良性阵发性位置性眩晕的治疗进展及心理评估

良性阵发性位置性眩晕（BPPV）是在头位改变时出现的以短暂眩晕发作为主要特征的外周前庭性疾患,耳石复位治疗具有独特的疗效。体位限制对耳石复位后的治疗及预后是否有效尚未明确。前庭康复对反复发作的BBPV及其预后有一定疗效。BPPV引起的眩晕／头晕、姿势不稳等不适症状明显影响患者心理状态,更多表现为焦虑状态,因此心理评估及心理干预在BPPV的康复治疗中愈显重要。现对良性阵发性位置性眩晕的复位手法、体位限常】、前庭康复及心理评估作一综述。     

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.     

血浆谷胱甘肽过氧化物酶研究进展

谷胱甘肽过氧化物酶（glutathione peroxidases,GPX）是在哺乳动物中发现的,可通过还原性谷胱甘肽催化还原过氧化物和有机过氧化氢物,从而保护细胞和其他如DNA、蛋白及脂质体等敏感生物分子免受氧自由基的损伤。血浆谷胱甘肽过氧化物酶（GPx-3）是1987年Takahashi等从人的血浆中纯化得到的,是目前已知的GPX家族8个成员中唯一的细胞外亚型。研究发现有多种因素影响GPx-3的表达,并参与了多种疾病的发生、发展,本文就GPx-3的结构、功能、基因表达及其与疾病的关系作一综述。     

蝙蝠葛酚性碱与褪黑素对缺血再灌注损伤神经元的作用比较

BACKGROUND： Recent studies have demonstrated that phenolic alkaloids from Menispermum dauricum （PAMD） can protect the heart and brain from ischemia/reperfusion injury, and promote neuron survival by inhibiting neuronal Bax and upregulating Bcl-2 expression following ischemia/reperfusion.
OBJECTIVE： To investigate the neuroprotective effects of PAMD versus exogenous melatonin against ischemia/reperfusion injury.
DESIGN, TIME AND SETTING： Observation and comparison experiments at a cellular level were performed at the Department of Biochemistry and Molecular Biology, Tongji Medical College of Huazhong University of Science and Technology between February 2007 and February 2008.
MATERIALS： PAMD （95% purity） was provided by Kunming Institute of Botany, Chinese Academy of Sciences; melatonin was provided by Sigma, USA.
METHODS： N2a mouse neuroblastoma cells were cultured in vitro deprived of glucose, serum and oxygen for 90 minutes, then cultured in normal medium containing different concentrations of PAMD （0.1, 1.0, 10 mg/L） or melatonin （1, 10, and 100 μmol/L）. Cells cultured in normal conditions served as a control.
MAIN OUTCOME MEASURES： The culture solution was collected to determine the content of ex- citatory neurotransmitters such as glutamic acid and aspartic acid; cell viability was detected by MTT methods; reactive oxygen species production was determined by fluorescence spectroscopy; mito- chondrial transmembrane potential （？Ψm） was detected by laser confocal scanning; cytochrome C was measured by western blotting; and caspase-3 activity was determined by visible spectropho- tometry.
RESULTS： Melatonin and PAMD both promoted oxygen-glucose-serum deprivation-mediated N2a cell survival （P 〈 0.01） and inhibited glutamic acid release （P 〈 0.01）, but melatonin did not inhibit aspartic acid production. The protective effects were the strongest using melatonin 100 μmol/L and PAMD 10 mg/L, so subsequent experiments were the performed at those doses. Although PAMD could no longer maintain mitochondrial transmembrane potential 6 hours after reperfusion, its in- hibitory effects on cytochrome C release from mitochondria and scavengers of reactive oxygen species were stronger than those of melatonin （P 〈 0.01）. However, its inhibitory effect on caspase-3 activity was weaker than that of melatonin： PAMD could inhibit caspase-3 activity 12 hours after reperfusion （P 〈 0.01）, but melatonin inhibited caspase-3 activity 28 hours after reperfusion （P 〈 0.01）.
CONCLUSION： The results show that melatonin and PAMD have neuroprotective effects, but that the mechanisms are varied. Melatonin can maintain mitochondrial transmembrane potential, but its inhibitory effects on cytochrome C release, caspase-3 activity, and reactive oxygen species scav-enging are different from those of PAMD.     

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。