亲细胞非均质分子脂质对人脑胶质瘤细胞的作用

目的:检测不同浓度亲细胞非均质分子脂质(ＣＨＭＬ)对人脑胶质瘤细胞的抑制效果。方法:将指数生长期的ＳＨＧ－４４胶质瘤细胞分７组,在１~５组分别加入浓度ＣＨＭＬ－６．０为５００μｇ·ｍｌ－１,２００μｇ·ｍｌ－１,１００μｇ·ｍｌ－１,５０μｇ·ｍｌ－１,２０μｇ·ｍｌ－１的ＣＨＭＬ复合液,第６组加ＶＭ２６,第７组加培养液作对照。于２４、４８、７２ｈ加入ＭＴＴ反应,测定ＯＤ值。结果:各药物组与对照组的ＯＤ值之间差别均有极显著的意义,其中两两比较检验表明５００μｇ·ｍｌ－１、２００μｇ·ｍｌ－１组的肿瘤抑制率优于ＶＭ２６组。结论:ＣＨＭＬ对人脑胶质瘤细胞有显著抑制作用,并有一定剂量－效应关系,尤其是５００μｇ·ｍｌ－１和２００μｇ·ｍｌ－１的药物组作用更为突出。     

甘丙肽在离体新生大鼠三叉神经主核神经元引发的两种不同膜电位和膜电流

运用细胞内记录和全细胞膜片钳技术 ,在 7～ 16d大鼠带三叉神经残根的 4 0 0 μm厚脑桥切片上进行研究。细胞内电流钳记录显示三叉神经主核灌流甘丙肽引发两种膜电位变化 :54.2 %细胞超极化 (3.2±1.2 )mV ;35.4 %细胞去极化 (2 .9± 1.3)mV ,两者均伴有兴奋性突触后电位抑制和膜电阻减小。电压钳实验显示甘丙肽也引致两种膜电流变化 :57.9%细胞出现外向性电流 (11.6± 6 .1)pA ,该电流可被四乙基胺所抑制 ,其反转电位为 (- 77.1± 5.3)mV ;2 7.3%细胞出现内向性电流 (10 .9± 5.9)pA ,该电流可被细胞外低钠所抑制而被细胞外高钾所增强 ,其反转电位为 (- 2 9.2± 4 .3)mV。两电流均可被甘丙肽激动剂M16所模拟 ,为甘丙肽阻断剂M35和M4 0所阻抑。上述结果提示 ,甘丙肽在突触后膜引发两种不同的膜电活动 :钾离子外流引发超极化和外向性电流 ;钠离子内流和钾离子外流引发去极化和内向性电流 ,两种反应均能抑制三叉神经主核神经元的突触传递。     

丁咯地尔抑制NE和GIu引起的单个脑细胞游离钙增高

目的：研究丁咯地尔对去甲肾上腺素（ＮＥ）和谷氨酸（Ｇｌｕ）引起大鼠单个脑细胞内游离钙增高的影响。方法：应用ＡＲ－ＣＭ－ＭＩＣ阳离子测定系统测量细胞内游离钙（［Ｃａ２＋］１）．结果：细胞外钙为 １．３ ｍｍｏｌ·Ｌ－１,丁咯地尔 ０．ｌ,ｌ．０,１０．０μｍｏｌ·Ｌ－１对细胞静息［Ｃａ２＋］．无明显影响,对ＮＥ诱导的［Ｃａ２＋］增高明显抑制,对Ｇｌｕ 诱导的［Ｃａ２＋］ 增高具有一定的抑制作用。结论：丁咯地尔能抑制ＮＥ和Ｇｌｕ 引起的单个脑细胞游离钙增高。     

类鸦片受体δ2介导的免疫细胞激活作用

将人粒细胞和Ｍｙｔｉｌｕｓｅｄｕｌｉｓ免疫细胞分别与不同浓度的类鸦片肽ＤＡＭＡ（１０（－１３）～１０（－１０）ｍｏｌ／Ｌ）或δ拮抗剂在３７和２３℃保温１０～２０ｍｉｎ，用计算机显微图像分析法分析两种细胞的活化情况。结果显示细胞免疫活性随ＤＡＭＡ浓度增加而提高，细胞发生阿米巴样变形或变长（形状因子小于０．５）。当加入δ拮抗剂ｎａｌｔｒｉｎｄｏｌｅ（１０（－１０）ｍｏｌ／Ｌ）时，ＤＡＭＡ对以上两种细胞的免疫激活作用均受到显著抑制（Ｐ＜０．０５），说明该类鸦片肽受体能被低浓度ｎａｌｔｒｉｎｄｏｌｅ封闭；然而，同样浓度的另一种δ拮抗剂钠洛酮却没有这种封闭作用，提示ＤＡＭＡ通过δ_２受体的介导发挥对免疫细胞的激活作用。     

精神分裂症Ⅰ 型和 Ⅱ 型患者血清铜、锌含量的测定比较

采用美国ＰＥ３１００原子吸收分光光度计测定精神分裂症７１例（Ⅰ型３６例，Ⅱ型３５例）和健康对照组３１人的血清铜、锌的含量。结果发现精神分裂症血清铜含量平均为１８．８６±４．２２μｍｏｌ／Ｌ，Ⅰ型略高于Ⅱ型；对照组平均１７．５７±３．１９μｍｏｌ／Ｌ，略低于病例组，三者均无显著性差异（Ｐ＞０．０５）。病例组血清锌平均２０．７８±４．８６μｍｏｌ／Ｌ，Ⅰ型略高于Ⅱ型，对照组平均２２．４１±２．９１μｍｏｌ／Ｌ略高于病例组，三者亦无显著性差异（Ｐ＞０．０５）。     

不同甾体激素对交感神经节突触传递快速作用的比较

以牛蛙离体椎旁神经节为标本，单个方波电刺激节前纤维，细胞内记录Ｂ细胞的动作电位，在正常情况下节前单个刺激，在Ｂ细胞发生一个动作单位，刺激与反应的关系是１∶１。灌流皮质醇（０．０１μｍｏｌ／Ｌ～１μｍｏｌ／Ｌ）、皮质酮（１μｍｏｌ／Ｌ）、孕酮（０．１μｍｏｌ／Ｌ）、１７β－雌二醇（０．００１μｍｏｌ／Ｌ）、醛固酮（０．００１μｍｏｌ／Ｌ）及胆固醇（０．１μｍｏｌ／Ｌ），比较它们对神经节Ｂ细胞突触传递的快速作用。结果显示，皮质醇可使１７０个Ｂ细胞中的５２个发生突触传递阻断，另外有４个细胞出现增强效应；皮质酮可使４８个Ｂ细胞中的１７个发生阻断；孕酮可使３７个Ｂ细胞中的１５个发生阻断；１７β－雌二醇可使２１个Ｂ细胞中的８个发生阻断；醛固酮对Ｂ细胞的突触传递无明显影响；胆固醇可使２１个Ｂ细胞中６个产生增强效应。实验结果表明，皮质醇、皮质酮、孕酮及１７β－雌二醇对牛蛙交感神经节部分Ｂ细胞突触传递具有快速阻断作用，尤以孕酮的作用最显著。盐皮质激素（醛固酮）对Ｂ细胞突触传递无明显影响，而胆固醇对Ｂ细胞突触传递有增强效应。     

TNF-α对血管内皮细胞VCAM-1诱导作用的研究

目的：探讨肿瘤坏死因子－α（ＴＮＦ－α）对血管内皮细胞ＶＣＡＭ－１表达的诱导作用。方法：通过血管内皮细胞培养,采用免疫组织化学方法分别观察不同浓度ＴＮＦ－α（０．２５０Ｕ．ｍＬ＾－１）２４小时内以及相同浓度（１００Ｕｍｌ＾－１）ＴＮＦ－μ０－α０－７２ｈ对内皮细胞ＶＣＡＭ－１表达的影响。结果：与对照组比较,ＴＮＦ－α对内皮细胞ＶＣＡＭ－１的诱导作用具有明显浓度与时间依赖性。结论：ＴＮＦ－α可诱导血     

PACAP对谷氨酸引起海马神经元损伤的保护作用

目的研究垂体腺苷酸环化酶激活肽（ＰＡＣＡＰ）对谷氨酸引起的海马神经元损伤的保护作用及其受体机制。方法海马神经元体外培养７ｄ，给予谷氨酸。结果当谷氨酸是０．１～１．０ｍｍｏｌ／Ｌ时，随着剂量的增加，神经元的存活率逐渐降低；１０－９ｍｏｌ／Ｌ～１０－１３ｍｏｌ／Ｌ的ＰＡＣＡＰ，能减轻谷氨酸引起的海马神经元损伤；ＰＡＣＡＰⅠ型受体特异性拮抗剂ＰＡＣＡＰ６－３８能抑制ＰＡＣＡＰ减轻谷氨酸对海马神经元损伤作用。结论ＰＡＣＡＰ具有减轻谷氨酸引起的海马神经元损伤的作用，该作用是由ＰＡＣＡＰⅠ型受体介导的。     

培养大鼠颈上神经节神经元γ—氨基丁酸电流的全细胞记录

在培养的大鼠颈上神经节神经元上，用全细胞膜片钳技术记录γ－氨基丁酸（ＧＡＢＡ）所激活的通道电流。当膜电位钳制在－６０ｍＶ时，压力喷射ＧＡＢＡ２０μｍｏｌ／Ｌ引起的峰电流为７３６±４８４ｐＡ（ｎ＝３１）。对ＧＡＢＡ电流与膜电位的关系的分析表明，当膜电位钳制在正负水平时，ＧＡＢＡ分别引起外向及内向电流，但外向电流的斜率稍大于内向电流，即存在轻度外向整流。电流的反转电位接近０ｍＶ。为了确定ＧＡＢＡ受体通道对Ｃｌ－的通透性，观察了改变细胞内Ｃｌ－浓度对ＧＡＢＡ电流的反转电位的影响。结果发现，所测的反转电位与用Ｇｏｏｄｍａｎ—Ｈｏｄｇｋｉｎ—Ｋａｔｚ方程预测的结果相符，提示ＧＡＢＡ受体对Ｃｌ－具有选择通透性，可能属ＧＡＢＡＡ受体。     

氧化修饰低密度脂蛋白刺激血管内皮细胞表达VCAM-1的实验研究

目的：探讨氧化修饰低密度脂蛋白（ＯＸ－ＬＤＬ）对血管内皮细胞表达血管细胞粘附分子－１（ＶＣＡＭ—１）的影响,以阐明其在动脉粥样硬化发生中的作用。方法：在血管内皮细胞的培养基中分别加入２５μｇ／ｍｌ的低密度脂蛋白（ＬＤＬ）和ＯＸ－ＬＤＬ,３7℃下温育 ２４小时,应用定量免疫细胞化学分析技术检测内皮细胞 ＶＣＡＭ－１蛋白的表达。结果：与对照组和ＬＤＬ组比较,ＯＸ－ＬＤＬ组内皮细胞ＶＣＡＭ－１蛋白的表达显著增加。结抡：ＯＸ－ＬＤＬ能够明显刺激内皮细胞ＶＣＡＭ－１的表达。     

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 -