出血性卒中患者脑脊液微量元素和抗氧化酶含量的研究

本文测定３６例脑出血、３１例ＳＡＨ患者的脑脊液微量元素和抗氧化酶含量的变化，结果发现：脑出血和ＳＡＨ的脑脊液锌、硒、铬、铁、镁含量，ＧＳＨ－Ｐｘ活性和Ｇ／Ｍ比值明显低于对照组（Ｐ＜０．０５或Ｐ＜０．０１），铜、ＭＤＡ含量及ＳＯＤ活性明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）。提示：微量元素和抗氧化酶与出血性卒中有密切关系。     

急性脑血栓形成不同时期一氧化氮含量的变化

探讨急性脑血栓形成不同时期一氧化氮（ＮＯ）含量的变化。测定３０例急性脑血栓形成患者发病不同时期血清中ＮＯ、ＳＯＤ、ＭＤＡ的含量。另选２８例性别、年龄组成相似的健康人作为正常对照。结果表明，脑血栓形成期，ＮＯ、ＳＯＤ含量显著降低（Ｐ＜０．０５），ＭＤＡ含量显著增高（Ｐ＜０．０１）；脑水肿期，ＮＯ含量较前显著增高（Ｐ＜０．０１）达正常水平（Ｐ＞０．０５），ＳＯＤ含量进一步降低（Ｐ＜０．０５），ＭＤＡ含量进一步增高（Ｐ＜０．０５）；进入稳定期后，ＮＯ较前稍降低（Ｐ＞０．０５）仍在正常水平（Ｐ＞０．０５），ＳＯＤ含量增高（Ｐ＜０．０１）仍低于正常（Ｐ＜０．０５），ＭＤＡ含量较前下降（Ｐ＜０．００１）仍高于正常（Ｐ＜０．０１）。提示：急性脑血栓形成早期ＮＯ含量降低与脑缺血损伤有关，脑水肿期ＮＯ参与脑损伤。     

肝豆状核变性患者肌肉铜,锌,铁,镁含量及二巯基丁二酸钠疗效…

本文对２５例肝豆状核变性（ＨＬＤ）患者的腓肠肌铜、锌、铁、镁含量及二巯基于二酸钠（ＤＭＳ）疗效进行了研究。     

GMP—140与脑血栓形成的关系研究

目的探讨急性脑血栓形成不同时期ＧＭＰ－１４０含量的变化。方法测定３２例急性脑血栓患者病后３ｄ内血浆中ＧＭＰ－１４０、ＳＯＤ和ＭＤＡ的含量，其中２５例患者于病程第１０～１４ｄ再次抽血复查。另选２８例性别、年龄组成相似的动脉硬化患者作为对照。结果与动脉硬化组比较，脑血栓患者急性期血浆中ＧＭＰ－１４０和ＭＤＡ含量显著增高（Ｐ＜０．０５），ＳＯＤ含量显著降低（Ｐ＜０．０５）；至稳定期，脑血栓患者血浆中ＧＭＰ－１４０、ＭＤＡ和ＳＯＤ含量与脑动脉硬化组无显著差异（Ｐ＞０．０５）。结论急性脑血栓形成时ＧＭＰ－１４０含量增高与脑组织损伤有关     

二巯基丁二酸钠冲击治疗肝豆状核变性临床疗效及对体液微量元素的影响

２８例肝豆状核变性患者采用二巯基丁二酸钠（Ｎａ－ＤＭＳ）静脉冲击疗法，成人剂量１．０～２．０ｇ／次，儿童０．５～１．０ｇ／次，共８周。结果：２６例临床症状改善，２例无效，以假性硬化型和肝豆状核变性型疗效好。疗后平均２４小时尿铜比疗前明显增高（Ｐ＜０．０１），疗后各周的尿排铜量与时间呈负相关（ｒ＝－０．８０６，Ｐ＜０．０２）。该药对血、尿、脑脊液的锌、铁、钙含量无明显影响。１１例出现齿龈及鼻粘膜渗血，少数病例出现恶心及发热、皮疹等过敏反应。证实Ｎａ－ＤＭＳ是一种高效低毒的巯基类驱铜剂     

急性脑血栓形成不同时期——氧化氮含量的变化

探讨急性脑血栓形成不同时期一氧化氮（ＮＯ）含量的变化。测定３０例急性脑血栓形成患者发病不同时期血清中ＮＯ、ＳＯＤ、ＭＤＡ的含量。另选２８例性别、年龄组成相似的健康人作为正常对照。结果表明，脑血栓形成期，ＮＯ、ＳＯＤ含量显著降低（Ｐ〈０．０５），ＭＤＡ含量显著增高（Ｐ〈０．０１）；脑水肿期，ＮＯ含量较前显著增高（Ｐ〈０．０１）达正常水平（Ｐ〉０．０５），ＳＯＤ含量进一步降低（Ｐ〈０．０５），ＭＤＡ是     

帕金森氏病人头发,血清中微量元素含量的研究（附74例分析）

从１９８８年以来我们对７４例帕金森氏病人的头发和血清中微量元素含量研究并与５４例正常对照组对比，检测的结果发现ＰＤ病人头发铜、锌、铁、锰低于对照组（Ｐ＜０．０１）。病人血清铜、锌、锰也低于对照组。血清铜、锰含量随病情加重而递减，且有剂量效应关系。血清与头发相关性分析无相关关系（Ｐ＞０．０５）。其结果说明ＰＤ的发病原因与体内微量元素代谢缺陷可能有关系。     

精神分裂症患者细细胞微量元素的测定

为了解精神分裂症患者红细胞微量元素的变化，及其与抗精神病药治疗等因素的关系，对５０例精神病患者进行氯氮平、氯丙嗪治疗前后红细胞钙、镁、铜、锌、铁微量元素测定，并与５２名健康志愿者进行对照。结果显示，与对照组比较，治疗前患者组红细胞铜、钙显著增高（Ｐ〈０．０５－０．０１），而镁则显著降低（Ｐ〈０．０１）。服氯氮平４０天后，患者的红细胞铁显著降低，镁显著增高（Ｐ〈０．０５）。服氯丙嗪的患者治疗前后无变     

精神分裂症患者红细胞微量元素的测定

为了解精神分裂症患者红细胞微量元素的变化，及其与抗精神病药治疗等因素的关系，对５０例精神病患者进行氯氮平、氯丙嗪治疗前后红细胞钙、镁、铜、锌、铁微量元素测定，并与５２名健康志愿者进行对照。结果显示，与对照组比较，治疗前患者组红细胞铜、铁、钙显著增高（Ｐ＜０．０５～０．０１），而镁则显著降低（Ｐ＜０．０１）。服氯氮平４０天后，患者的红细胞铁显著降低，镁显著增高（Ｐ＜０．０５）。服氯丙嗪的患者治疗前后无变化。上述红细胞微量元素与药物剂量、病程、治疗前后的简明精神病评定分值无显著相关性（Ｐ＞０．０５）。提示红细胞某些微量元素在精神分裂症与正常对照者间存在着一定的差异，为进一步研究精神分裂症与微量元素代谢间的关系提供了一定的客观依据。     

多发梗塞性痴呆患者血浆和脑脊液中若干神经肽含量的变化

用放射免疫法测定了３０例多发梗塞性痴呆（ＭＩＤ）、３５例无痴呆多发脑梗塞患者（ＭＣＩ）及３０名健康人的血浆生长抑素（ＳＳ）、精氨酸加压素（ＡＶＰ）及β－内啡肽（β－ＥＰ）含量，同时测定了部分ＭＩＤ和ＭＣＩ患者脑脊液（ＣＳＦ）中ＳＳ、ＡＶＰ、β－ＥＰ含量。发现ＭＩＤ患者血浆ＳＳ、ＡＶＰ含量比ＭＣＩ组和健康对照组均降低（Ｐ＜０．０５），且随痴呆程度的加重，其含量有递减趋势。而血浆中β－ＥＰ在这三组间差异无显著性意义（Ｐ＞０．０５）。ＭＩＤ组ＣＳＦ中ＳＳ、β－ＥＰ含量低于ＭＣＩ组（Ｐ＜０．０５），而ＣＳＦ中ＡＶＰ含量在两组间无差异（Ｐ＞０．０５），ＣＳＦ中ＡＶＰ含量与痴呆的关系有待进一步研究。     

Diphenylhydantoin, Phenobarbital, and Primidone in Saliva, Plasma, and Cerebrospinal Fluid

Diphenylhydantoin, primidone, and phenobarbital were determined in saliva and plasma of 164 patients by gas-liquid chromatography. The saliva ratio was about one-tenth in patients on diphenylhydantoin, 0.32-0.38 on phenobarbital alone and with other drugs, 0.97 and 0.96 on primidone alone and with other drugs. The S/P ratio of phenobarbital was similar in patients treated with primidone alone or with co-medication. For diphenylhydantoin and primidone, the S/P and CSF/plasma ratio were similar; for phenobarbital the S/P ratio was lower due to the difference in pH of saliva and CSF. Thus the concentration in saliva serves as a measure of the nonprotein-bound or free concentration in plasma with the advantage that saliva is easy to obtain. Co-medication does not change the S/P ratio for the three drugs studied. The high correlation between levels in plasma and in saliva allows the plasma levels to be predicted from the concentration in saliva.     

Fasciitis, perimyositis, myositis, polymyositis, and eosinophilia

Several groups of cases of fasciitis and myositis with eosinophilia are reported. The common features are inflammation into fascia and/or perimysium, and/or muscle fibers; eosinophilia in blood and/or in muscle biopsy. The following classification of 24 cases is suggested: at one end of the spectrum are fasciitis with eosinophilia: diffuse fasciitis (Shulman syndrome): 10 cases (3 with hematological complications); 2 cases of diffuse fasciitis with muscle atrophy; 3 cases of restricted fasciitis. Relapsing perimyositis with eosinophilia belong to the same spectrum, either diffuse (5 cases) with myalgias, or localized (2 cases). Other cases are focal myositis or multiple myositis, polymyositis with eosinophilia. The relationship among these cases is discussed. There is a continuum among the different groups. The pathophysiology remains unknown.     

Caspases, apoptosis, and Alzheimer disease: causation, correlation, and confusion

Extensive neuron loss occurs in Alzheimer disease (AD) brain and some authors have speculated that dysregulation of apoptotic death pathways is etiologically responsible for the disease. Apoptosis is regulated in mammalian cells by a family of cysteine proteases called caspases. At least 7 different caspases (caspases 1, 2, 3, 6, 8, 9, and 12) have been implicated in regulating neuronal cell death in response to amyloid beta (A beta) exposure in vitro, in animal models of neurodegenerative diseases, and in AD brain itself. Despite this seemingly impressive array of data implicating caspases and apoptosis as etiologic factors in AD, the direct involvement of caspase-dependent neuronal apoptosis in AD pathogenesis remains uncertain. Alternative explanations for some findings, contradictory experimental observations, and lack of morphologically convincing apoptotic neurons in the vast majority of AD brains has led to the revised hypothesis that apoptosis-associated molecular events cause neuronal dysfunction in the absence of, or prior to, neuronal death. Unfortunately, this new view renders the term "apoptosis-associated" functionally meaningless since it bears no relationship with apoptotic death and fails to focus scientific investigation on the molecular insults that trigger the "apoptosis-associated" response in AD neurons. On balance, an etiologic role for caspases in AD is far from proven. It remains possible, however, that caspase-dependent neuronal death contributes to AD neuron loss and thus, caspase inhibition offers some hope for extending AD neuron survival so that other agents, targeting upstream events, may delay or reverse primary AD pathology.