脑出血大鼠脑内bFGF蛋白和mRNA的表达

目的 探讨脑出血大鼠脑内bFGF蛋白和mRNA表达的规律，从而为脑出血后神经功能的修复提供理论依据。方法 用VII型胶原酶诱导大鼠脑出血模型、行为学计分、免疫组化及表达的光密度图像分析、Northern blot及光密度扫描。结果 在行为学计分方面，脑出血大鼠在出血7d时有明显降低，免疫组化结果显示，bFGF蛋白在脑内表达广泛，主要位于海马，皮质有少量表达。吸光度扫描结果显示，脑出血大鼠脑内bFGF蛋白和mRNA的表达在3d时达到高峰，7d时逐渐减弱。结论 随着脑出血大鼠脑内bFGF蛋白和mRNA表达的增强，其行为学得到改善，这可能是神经功能修复的主要机制之一。     

脑出血大鼠脑内bFGF mRNA和TNF蛋白的表达

目的 研究脑出血大鼠脑内碱性成纤维生长因子(bFGF) mRNA和肿瘤坏死因子(TNF)蛋白表达的规律，探讨脑出血后神经功能修复的内源性机制。方法 用Ⅵ型胶原酶诱导大鼠脑出血模型，采用Northem blot、Western blot及吸光度扫描分析bFGF和TNF表达。结果 脑出血大鼠脑内bFGF‘mRNA和TNF蛋白的表达在3d时达到高峰，7d时逐渐减弱。结论 随着脑出血大鼠脑内损伤因子TNF蛋白表达的增强，保护因子bFGF mRNA的表达也相应增强，这可能是脑出血过程中神经功能修复的主要机制之一。     

脑微血管内皮细胞缺氧模型转化生长因子β1表达与脑溢安的干预

背景：临床及动物实验证实脑溢安能促进脑出血急性期血肿吸收及神经功能恢复，提高生活质量。 目的：观察脑溢安血清对体外缺氧培养的大鼠脑微血管内皮细胞转化生长因子β1 mRNA表达的影响。 方法：用分离培养的大鼠脑微血管内皮细胞移入厌氧培养箱培养18 h建立缺氧损伤模型，并随机分为正常组、模型组、正常血清组及含脑溢安血清组。正常组为同一批正常培养的脑微血管内皮细胞；模型组将正常培养的细胞放入厌氧培养箱内培养18 h；正常血清对照组细胞在培养液中加5%正常血清后，放入厌氧培养箱中培养18 h；脑溢安血清组细胞在培养液中加5%脑溢安血清后，放入厌氧培养箱内培养18 h。 结果与结论：缺氧培养使脑微血管内皮细胞存活数量减少，其表达的转化生长因子β1 mRNA增强，而脑溢安血清能明显增加脑微血管内皮细胞存活数量，降低转化生长因子β1 mRNA表达水平(P < 0.05)。说明脑溢安血清下调转化生长因子β1mRNA的表达可能是其抑制脑微血管内皮细胞的凋亡对缺氧损伤脑微血管内皮细胞的保护作用机制之一。     

脑出血大鼠脑红蛋白表达与脑含水量变化

目的：观察脑出血大鼠脑组织内脑红蛋白（Ngb）的表达,探讨其与脑出血后脑水肿之间的关系。方法：将大鼠随机分为3组：正常对照组,假手术组和脑出血组。脑出血组和假手术组动物在模型建立后1、6、24、48、72h5个时间点各随机分为5个亚组。采用立体定向技术将自体血注入大鼠尾状核建立脑出血模型（假手术组注入生理盐水）,用干湿重法测定脑出血后脑含水量的变化,用Western blot检测脑出血后不同时间脑组织内Ngb的表达。结果：与假手术组或正常对照组比较,脑出血组1h时血肿周围脑组织内Ngb表达开始增高（P〈0.05）,24h时脑含水量开始升高（P〈0.05）,二者均在48h时达到高峰并持续至72h（P〈0.01）。结论：脑出血后脑组织内Ngb表达上调。脑出血后Ngb表达水平的变化与脑水肿的发生、发展在时间上不完全同步。     

康复训练联合促红细胞生成素对脑出血大鼠神经 修复及海马胶质原纤维酸性蛋白表达的影响

目的 康复训练联合促红细胞生成素（EPO）对脑出血大鼠神经修复及海马组织胶质原纤 维酸性蛋白（GFAP）表达的影响。方法 健康雄性SD 大鼠30 只随机分成3 组：模型组、EPO 组和训练组， 每组各10 只大鼠。3 组均建立脑出血模型，EPO 组与训练组在造模成功24 h 后均腹腔注射EPO，训练组 大鼠给予康复训练，模型组注射与EPO 组及训练组所注射EPO等量的生理盐水。观察与检测大鼠神经 修复及海马GFAP表达情况。结果 所有大鼠均造模成功，EPO 组与训练组造模后7 d、14 d 和28 d 的 Tarlov 评分高于模型组（P＜ 0.05），训练组也显著高于EPO 组（P ＜ 0.05）。造模后28 d，EPO 组与训练组 的脑含水量、血清IL-6 和TNF-α 值、海马组织GFAP蛋白相对表达水平显著低于模型组（P＜ 0.05），训练 组也低于EPO 组（P ＜ 0.05）。结论 康复训练联合EPO在脑出血大鼠中的应用能抑制海马GFAP表达 与血清炎性因子的释放，减轻脑水肿，从而促进神经功能恢复正常。     

脑出血大鼠脑内bFGF和TNF蛋白的表达

在脑出血引起的缺血损伤过程中,存在着多种细胞因子的表达,其中一些是脑保护因子,另一些是脑损伤因子,它们在脑出血的过程中既共存又对立,碱性成纤维生长因子（basic　fibroblastgrowth　factor bFGF）和肿瘤坏死因子（tumor necrosis factor　TNF）是这种因子的代表。因此本实验选用bFGF和TNF作为研究对象,观察在脑出血过程中两者的表达情况,以探讨脑出血后神经功能的修复机理。     

安脑丸对实验性脑出血大鼠的保护作用

目的通过观察安脑丸对大鼠脑出血后NF-kBp65、GAP-43、Caspase3表达的影响,探讨安脑丸对脑出血的保护作用机制。方法将190只Sprague-Dawley雄性大鼠随机分为正常组、假手术组、模型组、安脑丸组,后三组组内又随机分为术后12 h、1、2、4、7、10 d六个时间点;按Rosenberg法建立脑出血模型,安脑丸组每天上午下午各灌胃1mg/ml安脑丸10 ml/kg1次;采用免疫组化法观察NF-kBp65、GAP-43、Caspase3阳性细胞表达情况及Western blot法检测Caspase3蛋白表达情况。结果安脑丸组NF-kBp65阳性细胞数明显少于模型组(P<0.05);安脑丸组GAP-43阳性细胞数明显多于模型组(P<0.05);同时安脑丸组caspase3阳性细胞数及蛋白表达与模型组比较均明显降低(P<0.05)。结论安脑丸可能通过下调NF-kBp65、Caspase3表达,上调GAP43表达,从而发挥对脑出血的保护作用。     

中药对大脑中动脉闭塞模型大鼠脑血管发生的作用

目的研究中药复方复健片对大脑中动脉闭塞（MCAO）模型大鼠脑血管发生的影响，并探讨其治疗缺血性脑卒中的作用机制。方法采用Tamura等方法制造大鼠MCAO模型。将30只大鼠随机分为药物组、MCAO模型组、假手术组。药物组于造模成功后6d按体重10g／kg灌胃给予复健片水溶液。余二组分别灌胃给予同等量NS，1次／d，共2周。观察模型大鼠脑内血管内皮细胞生长因子（VEGF）、碱性成纤维细胞生长因子（bFGF）、血小板源性生长因子（PDGF）的表达以及微血管密度的变化。结果药物组大鼠脑内VEGF、bFGF、PDGF表达明显增强．微血管密度增高。结论复健片可显著增加MCAO模型大鼠脑内VEGF、bFGF、PDGF的表达．提示其促进血管发生是治疗缺血性脑卒中的作用机制之一。     

安脑丸对脑出血大鼠学习记忆功能及血肿周围BDNF、NGB表达的影响

目的研究安脑丸对脑出血大鼠血肿周围脑源性神经营养因子(BDNF)、脑红蛋白(NGB)及学习记忆功能的影响。方法将40只SD雄性大鼠随机分为正常组、假手术组、模型组及安脑丸组,每组各10只大鼠,模型组及安脑丸组采用Rosenberg法制备脑出血模型,安脑丸组于制模后2 h开始给予安脑丸灌胃,连续治疗7 d后采用RT-PCR法检测血肿周围BDNF mRNA的表达水平,免疫组化法检测血肿周围NGB阳性细胞的表达水平,Morris水迷宫法检测大鼠空间学习记忆能力。结果与模型组比较,安脑丸组大鼠血肿周围BDNF mRNA表达明显增强,NGB阳性细胞表达明显增加,而逃避潜伏期明显缩短,差异均明显(P均<0...     

亚低温对局灶性脑缺血-再灌注大鼠脑皮质脑源性神经营养因子表达及神经元凋亡的影响

目的 观察局灶性脑缺血-再灌注后亚低温干预对大鼠脑源性神经营养因子表达及神经元凋亡的影响，并探讨脑源性神经营养因子在亚低温脑保护机制中的作用。方法 采用线栓法制备成年雄性SD大鼠左侧大脑中动脉闭塞局灶性脑缺血-再灌注改良模型，缺血时间2h。随机分为常温缺血组和亚低温缺血组。常温时大鼠脑温控制于36．5℃～37．5℃，肛温为35．9℃～36．9℃；亚低温时脑温维持于32．5℃～33．5℃，肛温为32．2℃～33．1℃。两组大鼠分别于脑缺血一再灌注及亚低温干预后2、6、24和72h进行神经功能缺损评分，并同时行三苯基氯化四唑（1TC）染色、HE染色、TUNEL染色、免疫组化染色及免疫组化与TUNEL双重染色，从而评估大鼠神经功能缺损状况；检测脑梗死体积及脑源性神经营养因子表达水平；观察组织病理学变化和神经元凋亡数量。结果 与常温缺血组相比，亚低温缺血组大鼠神经功能缺损评分低（P〈0．01），脑梗死体积小（P〈0．01），缺血灶周围脑皮质中的脑源性神经营养因子表达水平增高（P〈0．01），而且神经元凋亡数量少（P〈0．01）。在脑源性神经营养因子免疫组化染色呈阳性反应的神经元细胞核中，未发现TUNEL染色阳性者。结论 亚低温干预治疗可促进缺血灶周围的脑皮质对脑源性神经营养因子的表达，从而抑制神经元凋亡，减少大鼠脑梗死体积，改善神经功能缺损体征。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.