青海藏族青年外周血淋巴细胞酸性a——醋酸萘酯酶反应类型及其正常值的探讨

本文用酸性α——醋酸萘酯酶(ANAE)反应标记淋巴细胞的化学方法,对青海105例正常藏族青年外周血淋巴细胞ANAE阳性率进行了观察,发现试验对象外周血淋巴细胞的ANAE总阳性率为77.8±6.61％,并按三种酶型进行统计分析,其中ANAE反应为1-3个“点状颗粒型”的淋巴细胞百分率为51.15±8.72,4-8个“点状颗粒型的”淋巴细胞百分率为18.5±6.94,“弥散型”的淋巴细胞百分率为8.26±5.18,同时比较了不同性别的正常值及酶型变化,并在方法上进行了探讨。     

T-cell subsets in the cerebrospinal fluid and peripheral blood of multiple sclerosis patients treated with high-dose intravenous methylprednisolne

To determine the effects of high-dose intravenous methylprednisolone (MP) on lymphocytes and lymphocyte subpopulations in the cerebrospinal fluid (CSF) and peripheral blood (PB) in multiple sclerosis (MS) patients, we studied 67 patients with definite MS treated with MP. They were classified according to the disease course: 32 chronic progressive (CP) patients, 25 relapsing-remitting (RR) patients, and 10 patients with a chronic progressive disease course accompanied by relapses and remissions (CP + RR). MS patients were treated with 1000 mgr intravenous MP daily for 10 consecutive days. Before and after MP treatment we simultaneously studied CSF and PB CD3 +, CD4 +, CD8 +, CD20 +, and Ial + cells subsets. Kurtzke's Expanded Disability Status Scale (EDSS) was used for clinical evaluation. Progression rate was defined as the ratio of EDSS to disease duration. Thirteen patients with lumbar disk herniation were investigated as controls. Before MP, we found in MS patients, especially in the CP group, significantly lower CD4 + T-cell percentages in the PB with respect to controls (P<0.05). The percentage of CD4 + T-cells in the CSF of MS patients was significantly higher compared with PB (p = 0.0001), and tended to be higher than in controls (p = 0.072). The CSF mononuclear cell counts were significantly correlated with higher percentages of CSF CD3 + (r = 0.40) and CD4 + (r = 0.47) T-cells and lower CSF CD8 + (r = -0.33) T-cell percentages. B-cell percentages in the CSF were significantly elevated compared with controls for all MS groups. No relation could be obtained between T- or B-cell subsets and EDSS or progression rate. After MP, a significant decrease in PB CD8 + T-cell percentage and simultaneously an increase of the percentage CD8 + T-cells in CSF was noted in the entire MS group and in the CP and RR MS patients. Except for the CP + RR MS patients, CD4 + T-cell percentages in the PB or CSF showed insignificant changes. Our findings support the view that in MS MP might affect the inflammatory process of demyelination by a selective and dissociative effect on T-suppressor/cytotoxic cells in the PB and CSF.     

学习困难儿童智力亚型的研究

以ＷＩＳＣ－ＣＲ１１个分测验量表分为变量对１０３名学习困难及与之配对的学业良好儿童进行聚类分析。结果显示，两组儿童均聚为３个智力亚型。学习困难儿童第１型ＦＩＱ中等偏上，与对照组第２型相当，但常识和译码分测验量表分低；第２型ＦＩＱ中等偏下，ＶＩＱ显著落后ＰＩＱ，该型ＰＩＱ与对照组第３型相等，但译码量表分显著低于对照组；第３型属边缘智能，算术分测验成绩更差。结果提示，学习困难儿童存在不同的智力亚型，表现为智力水平不等和智力结构方面的缺陷。     

冬虫夏草对慢性肾功能衰竭T细胞亚群的影响

对51例慢性肾功能衰竭(简称肾衰)同步做有关肾功能指标及T细胞亚群检测,其中28例为口服冬虫夏草动态观察组。结果:肾衰组T细胞亚群较正常对照组明显降低(P均<0.01),且白蛋白(ALb)、血红蛋白(Hb)均与OKT_4、OKT_4/OKT_3呈正相关(P均<0.05);动态组经配对t检验,OKT_4、OKT_4/OKT_8明显升高(P均<0.05),肾功能各指标均有明显改善(P<0.05～0.01),显示冬虫夏草可明显改善肾衰患者的肾功能状态和提高细胞免疫功能。     

ALTERATIONS OF mRNA LEVELS OF ai-ADRENOCEPTOR SUBTYPES WITH MATURATION AND AGEING IN DIFFERENT RAT BLOOD VESSELS

1. Alterations of mRNA levels of ai-adrenoceptor subtypes during maturation and ageing were determined by reverse trans-cription-polymerase chain reaction (RT-PCR) in aortae and renal, pulmonary and mesenteric arteries isolated from 3,12 and 24-month-old rats. 2. The steady state levels for α_1A-, α_1B- and α_1D-adrenoceptors in aorta declined with maturation and ageing. In renal artery there was a decrease in mRNA for the α_1B-adrenoceptor in aged rats. However, in mesenteric and pulmonary arteries there were no changes in mRNA levels for the three subtypes of α₁-adrenoceptors as a result of maturation and ageing. 3. The results suggest that expression of α₁-adrenoceptors is changed heterogeneously in different blood vessels during maturation and ageing in rats.     

Neonatal Rat Cerebellar Granule and Purkinje Neurons in Culture Express Different GABAA Receptors

We have established a culture system for microexplants of rat cerebellar cortical tissue in which cells develop morphologically, express type-A receptors for the inhibitory neurotransmitter γ-aminobutyric acid (GABA) and form GABAergic synaptic connections. Criteria of cell size and shape allow reliable identification of granule and Purkinje neurons, criteria confirmed by studies of the binding of antibodies to calbindin D28K and GABA. Both granule and Purkinje neurons express GABA_A receptors, but granule neurons fall into two classes in terms of their sensitivity. Granule neurons which do not show spontaneous synaptic currents are relatively insensitive to GABA, while granule neurons with synaptic currents are much more sensitive. The responses of Purkinje neurons to applications of 1 μM GABA are relatively insensitive to Zn²⁺ ions (10 μM), and are potentiated by chlordiazepoxide (100 μM) and La³⁺ ions (100 μM). Responses of innervated granule neurons, on the other hand, are blocked more strongly by Zn²⁺ ions, are less affected by chlordiazepoxide and are equally potentiated by La³⁺ ions. Hence these cultures provide a source of identifiable, functionally innervated cells which express distinct types of GABA_A receptors.     

重症肺炎患者T淋巴细胞亚群的研究

目的　研究重症肺炎患者T淋巴细胞亚群的变化。方法　用荧光单抗CD3 、CD4 、CD2 5 、CD95 、CD3 /CD2 5 、CD8 /CD2 8-对淋巴细胞进行标记和计数。结果　重症肺炎患者体内CD3 、CD95 、CD3 /CD2 5 减少 (P <0 .0 1,P<0 .0 5 ) ,CD4 、CD2 5 无明显变化 (P >0 .0 5 ) ,而CD8 /CD2 8-增加 (P<0 .0 1)。结论　重症肺炎患者T淋巴细胞因大量凋亡而总数减少 ,亚群的变化又造成免疫功能紊乱 ,因此在临床治疗过程中需调整患者免疫功能。     

Multiple Types of Ca2+ Channels in Mouse Motor Nerve Terminals

We measured neurotransmitter release and motor nerve terminal currents in mouse phrenic nerve-diaphragm and triangularis sterni preparations, to evaluate the role of Ca²⁺-channel subtypes in regulating transmitter release. Saturated concentrations of either ωagatoxin IVA [ω-Aga-IVA (0.3 μM), a blocker of P-type Ca²⁺channels] or ω-conotoxin MVIIC [ω-CTx-MVIIC (2 μM), a P-and Q-type Ca²⁺-channel blocker], inhibited nerve-evoked muscle contractions and the amplitude of endplate potentials respectively. In contrast, combined treatment with nifedipine (50 μM, a blocker of L-type Ca²⁺ channels) plus ω-conotoxin GVIA [ω-CTx-GVIA (2 μM), a blocker of N-type Ca²⁺ channels] did not elicit inhibitory effects on nerve-evoked muscle contractions, endplate potentials or nerve terminal waveforms. Because of the non-linear relationship between endplate potentials and Ca²⁺ signals, a small decrease in presynaptic Ca²⁺ entry can significantly reduce the amplitude of the endplate potential. Thus, we applied 3, 4-diaminopyridine (3, 4-DAP, a k⁺-channel blocker) or high Ca²⁺(10 mM) to accelerate and amplify the endplate potentials and Ca²⁺ currents. The endplate potentials amplified by 3, 4-DAP or by high Ca²⁺ correspondingly proved to be quite resistant to both ω-Aga-IVA and ω-CTx-MVIIC; ωAga-IVA exerted only a partial inhibitory effect on endplate potentials, and the ω-Aga-IVA-resistant component was further inhibited by ω-CTx-MVIIC. The component that was resistant to the two toxins could be completely blocked by the non-selective Ca²⁺ channel blocker Cd²⁺ (300 μM). A combination of the two toxins had no significant effects on either spontaneous transmitter release or postsynaptic resting membrane potentials of the diaphragm preparation and the Na⁺ and K⁺ waveforms of the triangularis sterni preparations. This finding suggests a preferential inhibitory effect at a presynaptic site. Measuring the Ca²⁺ currents in the triangularis sterni also revealed partial inhibition by ω-CTx-MVIIC with further incomplete inhibition by ω-Aga-IVA. Cd²⁺ (300 μM) abolished the toxin-resistant component of the Ca²⁺ current. In contrast, a combination of nifedipine (50 μM) with ω-CTx-GVIA (2 μM) was without inhibitory effect. We conclude that multiple types of Ca²⁺channels, i.e. ω-Aga-IVA-sensitive, ω-CTx-MVIIC-sensitive and toxin-resistant Ca²⁺ channels, coexist in mouse motor nerve terminals.     

Immune surveillance and autoantigen recognition in the central nervous system

The central nervous system (CNS) is considered to be a severely disadvantaged site for the elicitation of immune responses. First, there is no specialised lymphatic drainage. Second, both glia and neuronal cells normally do not express appreciable levels of major histocompatibility complex molecules. Third, the vasculature of the CNS is, at least in most places, lined by endothelial cells that have tight junctions and form a barrier (the blood-brain barrier) against most molecules and cells present in the circulation. Fourth, the cells most important in the initiation of immune responses, the leucocyte dendritic cell, are not present. Nevertheless, the existence of inflammatory diseases of this tissue, occurring naturally as in multiple sclerosis or in animals after peripheral immunisation with CNS autoantigens, indicates that the immune system can access and recognise antigens in this site. How this is achieved has become clearer in recent years and primarily seems to involve extravasation of activated but not resting T cells across the blood-brain barrier, and recognition of antigen on macrophage-like perivascular cells, rather than cells within the CNS parenchyme such as astrocytes or microglia. The processes involved in immunological patrolling of the CNS and development of autoimmune inflammatory disease are reviewed.