急性脑梗死患者脊液中抑制性氨基酸递质的动态观察

目的：为研究脑梗死后脑内抑制性氨基酸（ＩＡＡｓ）递质的变化规律及其意义。方法：采用高效液相色谱（ＨＰＬＣ）法测定了起病７ｈ～１０ｄ的脑梗死病人及对照组的ＣＳＦ中ＩＡＡｓ的浓度。结果：脑梗死７ｈ后ＣＳＦ中ＩＡＡｓ已显著升高,并于２ｄ达到高峰,３～５ｄ后降至正常水平。ＧＡＢＡ浓度与梗死时间存在抛物线性回归关系而和梗死最大直径存在直线回归关系。结论：脑梗死患者脑内ＧＡＢＡ等ＩＡＡｓ的异常升高可能对脑组织     

大鼠全脑缺血再灌流后4个脑区的谷氨酸,门冬氨酸,甘氨酸…

应用高效液相色谱仪，紫外分光光度检测器监测，测定大鼠全脑缺血再灌流后６ｈ￣７ｄ的海马、纹状体、丘脑和新皮层组织匀浆中谷氨酸（Ｇｌｕ）、门冬氨酸（Ａｓｐ）、甘氨酸（Ｇｌｙ）和ｒ－氨基丁酸（ＧＡＢＡ）含量变化。结果显示在海马和丘脑Ｇｌｕ含量于再灌流后６ｈ￣３ｄ下降（Ｐ〈０．０５和０．０１），ＧＡＢＡ含量升高（Ｐ〈０．０５和０．０１），在纹状体和新皮层除ＧＡＢＡ外，分别于６ｈ￣５ｄ均有不同呈度的升高。比     

谷氨酸对急性脑缺血再灌注大鼠皮层乙酰胆碱活性影响的在体动态电化学研究

为了研究脑缺血时兴奋性氨基酸与胆碱能神经的关系，采用双侧颈总动脉夹闭（ＣＣＡＯ）的脑缺血动物模型，用乙酰胆碱离子选择性微电极（ＡＣｈ－ＩＳＭｓ）检测皮层ＡＣｈ释放量，观察脑缺血再灌注时谷氨酸对大鼠皮层ＡＣｈ释放量的影响。结果表明：１０－１ｍｏｌ／ＬＧｌｕ对ＡＣｈ－ＩＳＭｓ无干扰作用，在生理状态下不能显著地促进皮层ＡＣｈ的释放，但可使脑缺血３ｍｉｎ时皮层ＡＣｈ释放量较未加Ｇｌｕ组增加５８．１％（Ｐ＜０．０１），再灌注后皮层ＡＣｈ活性恢复减慢。结果提示：Ｇｌｕ协同ＡＣｈ释放的效应在脑缺血时明显放大，推测Ｇｌｕ和ＡＣｈ可能在缺血性脑损伤中有放大的协同作用。     

实验性犬SAH后CVS血浆、CSF中ET、CGRP含量动态变化及巴曲酶的保护作用研究

采用放免法动态观察了２５只实验性犬ＳＡＨ后ＣＶＳ动物模型的血浆、ＣＳＦ中ＥＴ及ＣＧＲＰ含量变化及巴曲酶的保护作用。结果：单纯注血组及巴曲酶治疗组的血浆、ＣＳＦ中ＥＴ含量较对照组明显增高（Ｐ＜０．０１），ＣＧＲＰ含量明显降低（Ｐ＜０．０１）。单纯注血组在注血后３０ｍｉｎ血浆、ＣＳＦ中ＥＴ含量开始升高，ＣＧＲＰ含量开始下降，至第７ｄＥＴ达最高值，ＣＧＲＰ达最低值。经蛛网膜下腔及静脉注入巴曲酶０．４ＢＵ／ｋｇ／ｄ组，血浆及ＣＳＦ中ＥＴ含量均较同期单纯注血组明显降低（Ｐ＜０．０１），而ＣＧＲＰ则明显升高（Ｐ＜０．０１）。提示血浆、ＣＳＦ中ＥＴ、ＣＧＲＰ失衡是ＳＡＨ后ＣＶＳ的原因之一。巴曲酶可防止ＥＴ升高和ＣＧＲＰ降低。     

谷氨酸对急性脑缺血再灌注大鼠皮层乙酰胆碱活性影响的在体 …

为了研究脑缺血时兴奋性氨基酸与胆碱能神经的关系，采用双侧颈总动脉夹闭（ＣＣＡＯ）的脑缺血动物模型，用乙酰胆碱离子选择性微电极（ＡＣｈ－ＩＳＭｓ）检测皮层ＡＣｈ释放量，观察脑缺血再灌注时谷氨酸对六鼠皮层ＡＣｈ释放量的影响。结果表明：１０＾－１ｍｏｌｏ／Ｌ Ｇｌｕ对ＡＣｈ－ＩＳＭｓ无干扰作用，在生理状态下不能显著地促进皮层ＡＣｈ的释放，但可使脑缺血３ｍｉｎ时皮层ＡＣｈ释放量较示加Ｇｌｕ组增加５８．１％     

体外培养大鼠星形胶质细胞受损后的激活与反应性胶质化

用鼠脑星形胶质细胞（ＡＳ）原代培养技术建立体外ＡＳ机械性损伤模型。以ｃ—Ｆｏｘｓ、ｂＦＧＦ、ＰＣＮＡ、ＧＦＡＰ—ｍＲＮＡ、ＧＦＡＰ和Ｍｙｏｓｉｎ作为观察指标研究反应性星形胶质化的形成机制。结果显示：１．ｃ—Ｆｏｓ蛋白于损伤后４５ｍｉｎ即有阳性表达，伤后２ｈ消失；２．损伤后２ｈ，损伤边缘的ＡＳ开始表达ｂＦＧＦ，１２ｈ达高峰，２ｄ后表达强度开始回落；３．损伤边缘的部分ＡＳ于损伤后２ｈ开始表达ＰＣＮＡ，伤后１ｄ，ＰＣＮＡ阳性的ＡＳ沿损伤边缘呈列兵式整齐排列，２ｄ后ＰＣＮＡ阳性的ＡＳ分布于损伤周围区域；４．损伤后４ｈ，损伤边缘的ＡＳ开始表达Ｍｙｏｓｉｎ，并逐渐增加，而且朝向损伤区胞浆突起的阳性表达强于背向损伤区的突起；５．损伤边缘的ＡＳ于损伤后６ｈ开始表达ＧＦＡＰ—ｍＲＮＡ，１ｄ达高峰，２ｄ开始回落，３ｄ则只在少数ＡＳ中可检出ＧＦＡＰ—ｍＲＮＡ；６．损伤后１ｄ，ＧＦＡＰ表达明显增强，胞体肥大并向损伤区伸出粗大突起，２ｄＧＦＡＰ达高峰，３ｄ肥大ＡＳ的胞体和突起覆盖损伤区；７．在体外ＡＳ机械性损伤模型上，在没有神经元和其它复杂因素影响的条件下，ＡＳ对损伤的主要反应是胞体的肥大、突起的粗大，并能独立形成反应性星形胶质化。     

实验性犬SAH后CVS血浆,CSF中ET,CGRP含量动态变化及巴曲…

采用放免法动态观察了２５只实验性犬ＳＡＨ后ＣＶＳ动物模型的血浆，ＣＳＦ有ＥＴ及ＣＧＲＰ含量变化及巴曲酶的保护作用，结果；单纯性血组及巴曲酶治疗组的血浆，ＣＳＦ中ＥＴ含量较对照组明显增高（Ｐ〈０．０１），ＣＧＲＰ含量明显降低（Ｐ〈０．０１）。单纯注血组在注血后３０ｍｉｎ血浆，ＣＳＦ中ＥＴ含量开始升高，ＣＧＲＰ含量开始下降，至第７ｄＥＴ达最高值，ＣＧＲＰ达最代值。经蛛网膜下腔及静脉注入巴曲酶０．４ＢＵ     

蛛网膜下腔出血后大鼠脑组织游离氨基酸的变化

本文利用大鼠的蛛网膜下腔出血（ＳＡＨ）模型研究了ＳＡＨ后脑组织１８种氨基酸的变化。结果表明，ＳＡＨ后一周内Ｇｌｕ、Ｇｌｙ、Ｔａｕ、Ｐｈｅ、Ａｌａ、Ｌｅｕ、γ—ＧＡＢＡ、Ｌｙｓ、Ａｓｐ、Ｔｈｒ、Ｓｅｒ都有不同程度的升高，以Ｇｌｕ升高最明显，约为对照组的３３．４～２００％，提示这些氨基酸尤其是兴奋性氨基酸在ＳＡＨ后脑损害机制中起一定作用。Ｖａｌ、Ｍｅｔ、Ｉｌｅ、Ｈｉｓ、Ａｒｇ、Ｐｒｏ、Ｃｙｓ，在ＳＡＨ一周内无明显变化，提示这些氨基酸在ＳＡＨ后的脑损害机制中不起作用或很少起作用。     

实验性犬SAH后CVS血浆、CSF中NPY、ANP含量动态变化及巴曲酶的保护作用研究

目的探讨蛛网膜下腔出血（ＳＡＨ）后脑血管痉挛（ＣＶＳ）的发病机理和防治方法。方法采用放免法动态观察了犬ＳＡＨ后血浆、ＣＳＦ中神经肽Ｙ（ＮＰＹ）、心钠素（ＡＮＰ）含量动态变化及巴曲酶的保护作用。结果单纯注血组及巴曲酶治疗组血浆、ＣＳＦ中ＮＰＹ、ＡＮＰ含量较注血前及同期正常对照组明显增高（Ｐ＜０．０１）；单纯注血组在注血后３０ｍｉｎ血浆、ＣＳＦ中ＮＰＹ含量开始升高，ＣＳＦ中ＡＮＰ含量亦在注血后３０ｍｉｎ升高，血浆ＡＮＰ含量则在第２ｄ开始升高，至第７ｄ最高。蛛网膜下腔给药组和静脉注入巴曲酶０．４ＢＵｋｇ－１ｄ－１组血浆、ＣＳＦ中ＮＰＹ、ＡＮＰ含量均明显低于同期单纯注血组（Ｐ＜０．０１）。结论血浆、ＣＳＦ中ＮＰＹ、ＡＮＰ的异常增高是ＳＡＨ后ＣＶＳ的原因之一，巴曲酶可以防止ＮＰＹ和ＡＮＰ的异常增高。     

脊髓损伤及其继发损伤时的兴奋性氨基酸含量变化

采用Ａｌｌｅｎ’ｓ打击法以５０ｇ／ｃｍ和１００ｇ／ｃｍ致伤大鼠脊髓，于伤后１０分钟、１小时、２小时、４小时、８小时、２４小时取伤段脊髓，用氨基酸微量检测技术测定天冬氨酸（ＡＳＰ）和谷氨酸（Ｇｌｕ）含量。结果显示：脊髓损伤（ＳＣＩ）后１０分钟两个致伤组ＡＳＰ、Ｇｌｕ均较对照组（单纯椎板切除无损伤）明显升高；但伤后１～２４小时两组ＡＳＰ较对照组明显降低，其中２小时和２４小时降低最显著，ＡＳＰ在８小时虽也降低，但较２小时略回升；５０ｇ／ｃｍ组伤后１小时、４小时、８小时Ｇｌｕ含量较１０分钟时降低，但仍高于对照组。１００ｇ／ｃｍ组伤后２小时、２４小时Ｇｌｕ降低最明显。结果表明ＳＣＩ后兴奋性氨基酸ＥＡＡ存在两个高低不同的反应峰，提示ＥＡＡ参与了ＳＣＩ后的继发性损伤。     

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.     

Summary of Legislation of 1933 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -