ABC－ELISA法检测重症肌无力患者三种自身抗体的研究

本文利用ＡＢＣ－ＥＬＩＳＡ法检测了９７例ＭＧ病人血清内三种抗体：ＡｃｈＲａｂ、Ｐｒ－Ｍａｂ、ＣＡＥａｂ。结果发现：（１）全身型ＡｃｈＲａｂ、ｐｒ－Ｍａｂ阳性率明显高于眼肌型（Ｐ＜０．０１）；ＡｃｈＲａｂ与Ｐｒ－ＭａｂＰ／Ｎ值呈线性正相关（ｒ＝０．７９７Ｐ＜０．０１）。（２）合并胸腺异常者ＣＡＥａｂ阳性率为８４．２％，明显高于对照组（Ｐ＜０．０１）；此组病人ＡｃｈＲａｂ与ＣＡＥａｂＰ／Ｎ值呈显著正相关，Ｐｒ－Ｍａｂ与ＣＡＥａｂＰ／Ｎ值呈非常显著正相关。（ｒ＝０．５１２和ｒ＝０．５９８Ｐ＜０．０１）。（３）８例病人作了治疗前后抗体检测。激素治疗后或切除异常胸腺后，抗体滴度多数下降或有转阴趋势。     

老年人急性脑梗塞患者红细胞变形能力与红细胞 ATP 酶活性关系的研究

检测了６０例老年人急性脑梗塞患者的红细胞变形能力（ＥＤ），红细胞ＡＴＰ酶活性和红细胞内离子浓度的变化。结果显示：老年人急性脑梗塞患者红细胞滤过指数（ＥＦＩ）较对照组显著增高（Ｐ＜０．００１）；红细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶活性和Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性明显降低（Ｐ＜０．００１）；红细胞内Ｎａ＋、Ｃａ２＋浓度明显增高（Ｐ＜０．００１），而Ｍｇ２＋浓度明显降低（Ｐ＜０．０１）。脑梗塞患者红细胞ＥＦＩ与Ｎａ＋－Ｋ＋－ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性、Ｍｇ２＋浓度呈负相关（ｒ＝－０．５４２、－０．４１７、－０．４３６）（Ｐ＜０．００１）；与红细胞内Ｎａ＋、Ｃａ２＋浓度呈正相关（ｒ＝０．４７３、０．４６６，Ｐ＜０．００１）；提示脑梗塞病人ＥＤ降低与红细胞ＡＴＰ酶活性降低有关。     

阿尔茨海默病患者早老素-1基因内含子多态性分布的研究

目的 探讨早老素－１（ＰＳ－１）基因第８外显子３’端内含子等位基因多态性在散发性阿尔茨海默病（ＳＡＤ）发病机制中的作用。方法 应用聚合酶链反应－限制性片段长度多态性（ＰＣＲ－ＲＦＬＰ）方法检测７５例ＳＡＤ患者（ＳＡＤ组）和７３例正常老年人（对照组）的ＰＳ－１基因第８外显子３’端内含子等位基因多态性分布。结果 ＳＡＤ组１等位基因频率明显高于对照组（Ｐ〈０．０１,ＲＲ＝１．８３）,２等位基因频率明显低于对照组（Ｐ〈０．０１,ＲＲ＝０．５５）;ＳＡＤ组２／２基因型频率低于对照组（Ｐ〈０．０５,ＲＲ＝０．３２）。结论 ＰＳ－１基因多态性与ＳＡＤ发病有关,ＳＡＤ发病与ＰＳ－１基因２等位基因呈明显负关联,与１等位基因呈明显正关联。ＰＳ－１基因２等位基因对ＳＡＤ发病可能有保护作用,１等位基因可能是ＳＡＤ发病的危险因素之一。     

缺血性脑卒中患者红细胞膜脂质、微粘度及血清脂质分析

对５３例缺血性脑卒中（ＩＳ）患者红细胞膜胆固醇（膜ＣＨ）、膜磷脂（膜ＰＬ）、膜微粘度（膜）及血清脂质进行测定，并与４１例对照组相比。结果显示：①ＩＳ患者膜ＣＨ、膜ＣＨ与膜ＰＬ比值（膜ＣＨ／膜Ｐｕ及膜显著增高（Ｐ＜０．０１），膜亏与膜ＣＨ及膜ＣＨ／膜ＰＬ呈显著正相关；②ＩＳ组血清胆固醇（ＣＨ）、载脂蛋白Ｂ（ＡＰＯ－Ｂ）均显著增高（Ｐ＜０．０１），高密度脂蛋白胆固醇（ＨＤＬ－ＣＨ）和载脂蛋白Ａ＿１（ＡＰＯ－Ａ＿１）显著降低（Ｐ＜０．０１），膜ＣＨ和膜与ＡＰＯ－Ｂ呈显著正相关，而与ＨＤＬ－ＣＨ、ＡＰＯＡ＿１呈显著负相关。     

脑血栓形成者血清胰岛素及与PAI-1关系的探讨

目的探讨脑血栓形成者是否存在胰岛素抵抗（ＩＲ）,并进一步探讨其与血浆纤溶酶原激活物-１（ＰＡＩ－１）活性的关系。方法选择６７例无糖尿病病史的ＣＴＢ患者,根据梗死面积分为大中病灶组（４３例）和小灶组（２４例）、另取２８例健康成人作对照组。分别用发色底物法和放免法测定血浆ＰＡＩ－１活性、ＩＳ、Ｃ肽水平。结果（１）ＣＴＢ组ＰＡＩ－１活性、ＩＳ、Ｃ肽水平明显高于对照组（Ｐ均＜０．０１）;但两不同梗死面积组间无显著差别：（２）ＣＴＢ组ＰＡＩ－１与ＩＳ、Ｃ肽及ＩＳ与Ｃ肽间呈显著正相关（Ｐ均＜０．００１）,有极显著性差异。结论（１）ＩＲ和／或ＨＩ可能参与了ＣＴＢ的发生;（２）血浆ＰＡＩ－１活性增高与ＩＳ及Ｃ肽有关．ＰＡＩ－１活性增高致血浆纤溶活性降低．可能是ＩＲ与ＣＴＢ的中间环节。     

急性缺血性脑血管病患者血ICAM—1,VCAM—1,CD62p的改变？…

目的 探讨急性缺血性脑血管病患者中性粒细胞表面细胞间粘附分子（ＩＣＡＭ－１）、血管粘附分子（ＶＣＡＭ－１）和血小板Ｐ选择素（ＣＤ６２ｐ）的改变及其临床意义。方法应用流式细胞术测定１２１例缺血患者发病４８小时内ＩＣＡＭ－１、ＶＣＡＭ－１、ＣＤ６２ｐ的改变。结果 （１）各种急性脑缺血患者ＩＣＡＭ－１均较对照组升高，Ｐ〈０．０１）；脑血全形成和腔隙性脑梗死ＣＤ６２ｐ升高，Ｐ〈０．０５；脑血栓形成ＶＣＡＭ     

癫痫病人脑脊液中苯妥因钠,卡马西平浓度测定及其临床价值

用高效液相色谱法测定９２例癫痫病人脑脊液（ＣＳＦ）中苯妥因钠、卡马西平浓度，并结合临床进行分析，结果发现：ＣＳＦ中苯妥因钠、卡马西平与临床疗效和中枢神经系统的毒副反应关系密切；与血总浓度呈正相关（ｒ＝０．３７，Ｐ＜０．０５；ｒ＝０．７３，Ｐ＜０．０５）；与血游离浓度无显著区别（Ｐ＞０．０５）；药物剂量与ＣＳＦ中苯妥因钠、卡马西平水平无线性关系（ｒ＝０．１３４，Ｐ＞０．０５；ｒ＝０．１４，Ｐ＞０．０５）；病程对血脑屏障通透性的影响可能改变ＣＳＦ中苯妥因钠、卡马西平浓度。     

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。     

脑缺血病人血小板肌球蛋白轻链激酶和Ca2+、Mg2+-ATP酶活性及其与[Ca2+]i关系的研究

目的探讨急性缺血性脑血管病血小板肌球蛋白轻链激酶（ＭＬＣＫ）和Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶活性的变化及与血小板胞浆游离钙浓度［Ｃａ２＋］ｉ的关系。方法用３２Ｐ同位素掺入法和比色法分别测定５８例脑缺血病人，及３５名健康对照者血小板ＭＬＣＫ和Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶活性。用荧光钙指示剂Ｆｕｒａ－２负载血小板扫描的方法，测定脑缺血病人血小板［Ｃａ２＋］ｉ浓度。结果ＴＩＡ组和脑梗死组ＭＬＣＫ活性与对照组相比均有明显增加（Ｐ＜０．０１），而Ｃａ２＋Ｍｇ２＋－ＡＴＰ酶活性均低于对照组（Ｐ＜０．０５，Ｐ＜０．０１）。ＴＩＡ组和脑梗死组血小板静息［Ｃａ２＋］ｉ；均高于对照组；血小板静息［Ｃａ２＋］ｉ与血小板ＭＬＣＫ活性呈显著正相关（Ｐ＜０．０１），而与血小板Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶活性呈负相关（Ｐ＜０．０５）。结论血小板ＭＬＣＫ和Ｃａ２＋、Ｍｇ２＋－ＡＴＰ酶活性与急性缺血性脑血管病的发生有密切关系，ＭＬＣＫ活性的变化可能是脑缺血病人血小板活化的分子基础。     

p53,CerbB—2和PCNA在脑胶质瘤中表达的意义及其 …

目的 研究７６例脑质瘤的ｐ５３ＣｅｒｂＢ－２和ＰＣＮＡ表达意义及其相关性。方法 应用ＳＰ微波免疫组化技术和统计学分析。结果 （１）在７６例脑胶质瘤组织中；ｐ５３，ＣｅｒｂＢ－２和ＰＣＮＡ的阳性表达率分别是４４．７４％（３４／７６），３４．２１％（２６／７６）和８０．２６％（６１／７６）。（２）ｐ５３的表达强度与胶质瘤的组织学类型和恶性程度呈显著正相关（Ｐ〈０．０１）。（３）ｐ５３ＣｅｒｂＢ－２和Ｐ     

Comparison of the effect of acetylsalicylic acid on platelet function in male and female patients with ischemic stroke

The aim of this study was to observe whether acetylsalicylic acid (ASA) had different effects in both sexes. Out of the ischemic stroke patients who were admitted to the National Taiwan University Hospital (NTUH), those who had not taken ASA or ASA-like drugs for more than 2 weeks were selected for this study. For the diagnosis of ischemic stroke, computed tomography (CT) of the brain was performed in all cases, and for differential diagnosis, other necessary procedures were employed in a few cases. The serum salicylate (SA) level was measured by Trinder's method, thromboxane B2 (TXB2) and 6-keto-PGF1 alpha by radioimmunoassay, threshold concentration of adenosine diphosphate (ADP) by Born's method, and circulating platelet aggregates (CPA) by Wu and Hoak's method. The present study showed that the means of serum SA levels after administration of the same dose of ASA were not significantly different between the two sexes. After ingestion of ASA, a single dose of 75 mg, 300 mg or 600 mg, or 300 mg 4 times a day, mean plasma TXB2 levels were significantly suppressed and mean threshold concentrations of ADP were significantly elevated in the two sexes. After administration of above-mentioned various doses of ASA, the abnormally high plasma TXB2 levels and abnormally low threshold concentrations of ADP and CPA ratios were significantly normalized in both male and female patients. Plasma 6-keto-PGF1 alpha levels were not influenced by ingestion of ASA 75 mg, but significantly depressed by administration of ASA 300 mg in both sexes. There were no sex differences in the antiplatelet effect of ASA in this experiment.     

The effect of aspirin on the size of the hemostatic plug

The prolongation of the bleeding time by aspirin is presumably due to interfering with platelet function. Direct quantitative studies evaluating the effects of aspirin on the platelet component of the hemostatic plug have not been described. We measured blood loss from a standard ear injury in rabbits after treatment with either 5 mg or 200 mg/kg of aspirin (ASA) or sodium salicylate (SA), and related this observation to the number of platelets incorporated into the hemostatic plug. The high dose of aspirin was chosen since this dose inhibits PGI2 biosynthesis. Both doses of aspirin but not salicylate caused a significant increase on blood loss from the treated ear compared to the control (ASA 5 mg/kg, 0.012 +/- 0.009 ml, (m +/- SE), n = 44, p = 0.03; ASA 200 mg/kg, 0.02 +/- 0.007 ml, n = 17, p less than 0.05). Both doses of aspirin also caused a significant increase in the number of platelets incorporated into the hemostatic plug when compared to the SA treated animals (ASA 5 mg/kg, 3.52 +/- 0.34 X 10(6) platelets per incision, (m +/- SE), n = 59; SA 5 mg/kg, 1.9 +/- 0.15 X 10(6) platelets per incision, n = 54, p less than 0.001; ASA 200 mg/kg, 3.19 +/- 0.54 X 10(6) platelets per incision, n = 22; SA 200 mg/kg, 1.5 +/- 0.26 X 10(6) platelets per incision, n = 23, p less than 0.001). This study suggests that following aspirin administration hemostasis is achieved by the incorporation of a greater number of platelets into the platelet plug.(ABSTRACT TRUNCATED AT 250 WORDS)     

The antithrombotic effect of aspirin and dipyridamole in relation to prostaglandin synthesis

The antithrombotic effect of aspirin (ASA) and dipyridamole (DIP) was evaluated in rabbits in which platelet thromboxane A2 (TXA2) and arterial prostacyclin (PGI2) were measured. An intracarotid cannula thrombosis model previously shown to be sensitive to antiplatelet agents was used. Prostaglandins were determined by radioimmunoassays for thromboxane B2 (TXB2) and 6-keto-prostaglandin PGF1 alpha, the stable metabolites of TXA2 and PGI2. In the aspirin-treated animals, reduction in thrombosis was seen only in rabbits which received a low-dose (1-2 mg/kg), and was related to a selective suppression of platelet TXA2. In contrast, higher doses of ASA (10 or 100 mg/kg), which suppressed both TXA2 and PGI2, were not associated with thrombus inhibition. DIP alone had a lesser antithrombotic effect which was augmented by low-dose ASA but not by high-dose ASA. It is concluded that 1) the antithrombotic effect of ASA in this animal model is dependent on selective TXA2 suppression; 2) ASA has no antithrombotic properties beyond its inhibition of prostaglandin synthesis by platelets; 3) selective suppression of TXA2 in vivo can be achieved in rabbits by a single dose of ASA but only over a narrow dose-range; 4) DIP may have an antithrombotic effect additive to that of low-dose ASA; 5) measurement of serum TXB2 may be used to determine the minimal ASA dose necessary to suppress TXA2 and therefore be most likely to spare PGI2.     

The effect of a thromboxane synthetase inhibitor, dazoxiben, and acetylsalicylic acid on platelet function and prostaglandin metabolism

Twenty-four men received either placebo, 0.1 g of the thromboxane synthetase inhibitor dazoxiben, 0.25 or 1.0 g of acetylsalicylic acid (ASA). Dazoxiben reduced the maximal rate of collagen-induced platelet aggregation, but less than did ASA. ASA abolished secondary, ADP-induced aggregation, dazoxiben not. Both drugs prolonged the bleeding-time. Plasma thromboxane B2 (TxB2) levels did not change significantly after dazoxiben, whereas the prostacyclin metabolite 6-keto-PGF1 alpha rose. The larger dose of ASA reduced both TxB2 and 6-keto-PGF1 alpha in plasma. Whole blood was allowed to clot in order to estimate prostaglandin metabolism. Both drugs prevented thromboxane production effectively. Formation of 6-keto-PGF1 alpha decreased by 95 per cent after ASA but was more than doubled after dazoxiben. Dazoxiben is a selective and effective thromboxane synthetase inhibitor, but has a weaker effect on platelet reactivity than ASA, possibly because endoperoxide formation is not prevented.     

急性期脑梗死患者血清MMP-9水平动态变化意义及与预后的关系

目的 通过对急性脑梗死患者不同时间点血清基质金属蛋白酶-9(Matrix Metalloproteinase,MMP-9)的测定和比较,探讨MMP-9水平与脑梗死TOAST分型及预后的关系.方法 收集急性脑梗死患者60例,对照组20例,分别测定急性脑梗死患者发病24h内、第5天和第10天的血清MMP-9含量,记录患者入院时的美国国立卫生研究所中风量表(NIHSS)评分;随访6个月,记录发病1个月时和发病6个月时的BI(Baahal Index)来评价预后.结果 (1)发病后24h内,脑梗死组TOAST各亚型血清MMP-9含量均升高,与对照组比较差异具有显著性(P<0.05),其中,CE组和LAA组MMP-9含量持续至第5天仍未下降,而SA组已逐渐降至正常水平;第10天各组MMP-9含量均降至正常水平.(2)发病后24h内血清MMP-9含量与相应时段NIHSS评分具有直线相关关系(r=0.883,P<0.01).(3)预后较好组其发病24h内血清MMP-9含量明显低于预后较差组(P<0.05).结论 (1)脑梗死后各组血清MMP-9的含量升高,但它们的变化趋势不尽相同.(2)发病后24h内MMP-9含量与与病情的严重程度有关.(3)脑梗死后24h内的血清MMP-9含量是预后的独立预测因素.

Abstract：

Objective To determine and compare the level of serum MMP-9 at acute stage of cerebral infarction and to approach the relationship among the level of serum MMP-9 and the classification of TOAST and the significance in prognosis. Methods 60 patients with cerebral infarction were included in our study,while 20 healthy people served as the control group. The serum specimens were gathered for MMP-9 determination with ELISA on admission, at the 5th and 10th day of onset. All patients were scored according to the American National Institutes of Health stroke scale ( NIHSS) on admission and recorded Barthal Index(BI) in the 1st and 6 month of onset. Results (1)The serum level of MMP-9 increased after cerebral infarction,and was significantly higher than those in the control group(P <0. 05). There was no significant difference between CE and LAA group ( P>0. 05). MMP-9 in CE and LAA group was significantly higher than those in SA group (P <0. 05) . MMP-9 in SA group decreased to normal level while was still higher in CE and LAA group on the 5th day of onset. On the 10th day MMP-9 in all groups decreased to normal. (2) There was a positive correlation between MMP-9 within 24 hours of onset and NIHSS( r = 0. 883 ,P < 0. 01) . (3) The serum level of MMP-9 in the cases with better prognosis was significantly lower than those with worse prognosis. Conclusions (1) The serum levels of MMP-9 in all groups increased, but the tendency of their variation was not similar;( 2 ) Serum level of MMP-9 was related to NIHSS, can reflect the severity of the state of cerebral the severity of the state of cerebral infarction;( 3 ) The level of serum MMP-9 within 24 hours of onset can predict prognosis of cerebral infarction independently.     

One milligramme of acetylsalicylic acid daily inhibits platelet thromboxane A2 production

To seek the lowest dose of acetylsalicylic acid (ASA) capable of inhibiting platelet thromboxane A₂ (TxA₂) production, 18 healthy volunteers ingested 9 mg, 3 mg or 1 mg of ASA/day for twenty days and the release of TxB₂ (a metabolite of TxA₂) during the spontaneous clotting of blood was measured by radioimmunoassay. In addition, the production of prostacyclin (epoprostenol, PGI₂) was investigated by measuring the urinary excretion of its break-down product, 6-ketoprostaglandin F_1α (6-keto-PGF_1α) by radioimmunoassay. Significant inhibition of platelet TxA production was seen from the 15th day of treatment onwards with 1² mg of ASA (maximally 15 %), from the 4th day of treatment onwards with 3 mg of ASA (maximally 40 %), from the 1st day of treatment onwards with 9 mg of ASA (maximally 67 %). No ASA dose changed platelet counts or urinary 6-keto-PGF_1α excretion. One mg of ASA daily, is the lowest dose ever shown to inhibit platelet TxA₂ production.     

Antioxidant effect of acetylsalicylic and salicylic acid in rat brain slices subjected to hypoxia

Acetylsalicylic acid (ASA) reduces the incidence of ischemic stroke mainly through its antithrombotic action; however, it also has a direct neuroprotective effect. The present study was designed to evaluate the effect of ASA on oxidative stress and the activity of nitric oxide synthase (NOS) in an in vitro model of hypoxia in rat brain slices. Rat brain slices were perfused with nitrogen (hypoxia) for a maximum of 120 min, after which we measured lipid peroxidation, glutathione levels, glutathione-related enzyme activities, and constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) activities. In brain tissue subjected to hypoxia, ASA reduced oxidative stress and iNOS activity (all increased by hypoxia), but only when used at higher concentrations. The effects of salicylic acid (SA) were similar but more intense than were those of ASA. After oral administration, the effect of SA was much greater than that of ASA, and the decrease in cell death with SA was seen much more clearly. In view of the greater effect of SA compared to ASA on changes in oxidative stress parameters in a model of hypoxia, and higher brain concentrations of SA when it is administered alone than when ASA is given (undetectable levels), we conclude that SA plays an important role in the cytoprotective effect in brain tissue after ASA administration.     

The recovery of platelet malondialdehyde production after a single intake of aspirin--the effect of dosage

We studied the recovery pattern of platelet malondialdehyde (MDA) formation after a single intake of various doses of aspirin (ASA). In normal subjects, there were striking differences in the recovery pattern between large doses (1,000 or 500 mg) and small doses (100 or 50 mg) of oral ASA. The 2 day lag phase was present in the large dose group which showed the complete inhibition of the circulating platelets 2 hr after oral ASA but not in the small dose group which showed the incomplete inhibition. The difference of recovery time between these two groups was about 2 days. These data suggest that ASA's effect on megakaryocytes might affect the recovery pattern of MDA formation by the circulating platelets. In 2 patients with chronic idiopathic thrombocytopenic purpura, the 2 day lag phase was not observed in the recovery even after a large ASA dose.     

The effect of active serum albumin on PC12 cells: I. Neurite retraction and activation of the phosphoinositide second messenger system.

Vertebrate blood sera contain a factor that triggers oscillatory chloride currents in Xenopus oocytes through activation of the phosphoinositide/Ca2+ second system. The active serum component consists of lipids bound to an isoform of serum albumin that we have named active serum albumin (ASA). In undifferentiated PC12 cells, micromolar concentrations of ASA inhibit the early morphological changes induced by NGF, whereas in differentiated PC12 cells ASA caused a rapid withdrawal of neurites, which was reversible and dependent upon culture age. In contrast to normal serum, plasma and thrombin did not cause neurite retraction. Preincubation of ASA with monospecific antibodies to serum albumin suppressed its ability to induce neurite retraction in a dose dependent fashion. As in the oocyte, ASA activated the phosphatidylinositol second messenger system of PC12 cells, causing a several fold increase in Ins1,4,5P3 levels within minutes of application. The Ins1,4,5P3 increase was also blocked, in a titratable fashion, when ASA was preincubated with monospecific antibodies to serum albumin. This suggests that ASA-induced neurite retraction in PC12 cells may depend, at least in part, on activation of the phosphatidylinositol second messenger system. Results involving albumin-depleted sera show that ASA is the main factor responsible for serum vulnerability of neurites in PC12 cells. These findings point to some limitations in the use of serum in culture media, and raise the possibility that the serum factor may impair neuronal plasticity in disorders that are accompanied by the activation of blood coagulation together with a breakdown of the blood-brain barrier.     

Immunoglobulins and complement components in 37 patients infected by HIV-1 virus: comparison of general (systemic) and intrathecal immunity

Intrathecal (IT) immunity was assessed by simultaneous analysis of paired cerebrospinal fluid (CSF) and sera of 37 patients infected by human immunodeficiency virus-1 (HIV-1). Only 8 of these 37 patients had no neurological or neuropsychiatric symptoms. There were 3 prominent abnormalities observed: (1) IT IgA production occurred in 15 patients, IT IgM production in 14 patients, and IT IgG production in 34 patients. (2) IT Anti-HIV-1 antibody specific activity (ASA) was higher than in serum in 33 of the 37 patients indicating that IT synthesis of antibody specific for HIV-1 occurs even in asymptomatic patients; IT anti-HIV-1 antibody synthesis was not correlated with clinical severity or neurological involvement. IT anti-herpes simplex ASA was also higher than serum ASA in 6 patients indicating a possible associated herpes simplex virus infection. (3) IT production of the complement component C4 was found frequently and was highly correlated with increased serum C4. IT C3 levels were decreased in 21 of 37 patients indicating that complement activation is a frequent accompaniment of the IT immune response in HIV-1-positive patients. These results indicate a unique and localized IT immune response which is different from the pattern observed in the systemic immune compartment in HIV-1-seropositive individuals and from the pattern common to the other CNS infectious diseases.