乌鲁木齐地区慢性精神分裂症患者发中八种微量元素含量的测定与分析

作者对乌鲁木齐地区６５例汉族慢性精神分裂症患者和８０名汉族健康人，采用离子耦合等离子体发射光谱法，对头发中八种微量元素的含量进行了测定。结果表明、男性患者发中铜、钼、镉含量较正常人明显降低，而铁，锰含量较正常人为高；女性患者发中锌、铜、锰、锶、镉、镁含量较正常人为低。采用Ｂａｙｅｓ逐步判别分析方法得出的判别函数，提示男性发锌、铜、锰、钼、镉，女性铜、钼、镉、锰与慢性精神分裂症关系较密切。     

实验性脑缺血及再灌流期微量元素的研究

本文采用电感耦合氩等离子发射光谱法测定了大鼠全脑缺血、再灌流不同时间脑组织和全血微量元素铬、铜、锌、铁、锰、钼、铅、镉和硒的含量。脑组织铬含量在缺血30分钟后再灌流30分钟(I30′R30′)和再灌流60分钟(I30′R60′)较对照组升高(P<0.05);脑组织铜在I30′R60′较对照组升高(P<0.05)。全血铬含量在I30′R30′较对照组降低(P<0.01);全血铜在I30′R30′较缺血30分钟组和对照组均低(P<0.05)。其它元素脑及全血含量实验组与对照组无显著性差异。结果证明:再灌流时血铬、铜向脑内转移,铬、铜与缺血性脑血管病的急性损伤期有关。     

微量元素和脑动脉硬化症相互关系的初步探讨

本文采用粒子访发X线发射光谱法测定了44例脑动脉硬化症患者头发中铬、硒、锰、铜、锌、铁、镍和钒8种微量元素含量,并同时测定了上述患者的糖、脂代谢情况,以探索这些元素与脑动脉硬化症发病之间的关系。     

帕金森病人头发、血清、脑脊液中微量元素含量的研究

帕金森病人头发、血清、脑脊液中微量元素含量的研究潘宝英，陈清林，苏常春本研究从１９８８～１９９１年对７４例帕金森病（ＰＤ）患者的头发、血清以及３２例患者的脑脊液中铜、锌、铁、锰、铬的含量进行检测并与５４例健康者对比研究。资料和方法：（１）取本院ＰＤ专...     

缺血缺氧可促进新生鼠神经干细胞的增殖

目的观察缺血缺氧对新生鼠皮层及海马神经干细胞的影响。方法制作新生鼠缺血缺氧性脑病(hypoxla-ischemic encephalopathy,HIE)模型,实验动物每天两次腹腔注射Brdu,每次剂量50mg/kg,用于标记各组动物的神经干细胞增殖情况。分别于 模型建立后3d、7d、14d和28d取脑组织行抗Brdu的免疫组化染色,分别观察HIE模型组和对照组动物之间海马及皮层Brdu阳性细 胞数目及细胞形态、分布情况;并比较他们之间的差异。结果正常新生SD(Sprague-Dsawley)大鼠脑内Brdu阳性细胞弥散分布于 各脑区,在海马的齿状回、脑室下区等部位有干细胞密集分布。缺血缺氧后新生动物脑内细胞坏死明显的区域见Brdu阳性细胞呈灶 状增生。各个阶段缺血缺氧组动物皮层及海马的Brdu阳性细胞数目均比假手术组明显增多,差别有统计学意义。假手术组动物皮 层及海马的Brdu阳性细胞数目和正常组差别无统计学意义。结论缺血缺氧可促进新生SD大鼠皮层及海马的神经干细胞增殖。     

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。     

癫痫大鼠脑组织内IgG免疫反应阳性细胞分布及意义

目的研究中枢神经系统内ＩｇＧ在癫痫发病机理中的作用。方法用免疫细胞化学法观察ＩｇＧ免疫反应阳性（ＩｇＧ－ＩＲ）细胞在正常成年大鼠和癫痫大鼠脑组织内分布情况。结果对照组大鼠皮层和海马均有ＩｇＧ－ＩＲ细胞分布。癫痫大鼠相应部位内ＩｇＧ－ＩＲ细胞分布较对照组显著增多（Ｐ＜０．０１）。结论ＩｇＧ能够进入且存在于脑组织内并在癫痫发病免疫学机理中发挥一定作用     

血管性痴呆患者红细胞内微量元素的变化

目的:探讨血管性痴呆患者红细胞内微量元素锌、铜、铁、锰、硒、铅、铝、镉的变化。方法:测定40例血管性痴呆患者红细胞内上述8种微量元素的含量并与对照组进行比较。结果:痴呆组与对照组相比锌、锰、硒含量降低;铜、铁、铅、铝、镉含量升高,差异有显著性(均P<0.05)。结论:血管性痴呆的发病与多种微量元素有着直接和间接的关系,这些微量元素的改变可作为血管性痴呆的诊断及预后判断的参考指标。     

脂多糖诱导鼠脑中的白细胞介素—6基因表达

目的 分子水平研究正常鼠脑内的白细胞介素－６（ＩＬ－６）分布和诱导水平。方法 脂多糖（ＬＰＳ）１００ｕｇ／ｋｇ,ｉｐ,不同时间,用ＰＴ－ＲＣＲ对鼠脑的６个不同区域,进行ＩＬ－６信使核糖核酸（ｍＲＮＡ）半定量分析。结果 ＩＬ－６ｍＲＮＡ表达由高到低依次为海马,下丘脑,脑干,小鼠,丘脑和皮层。除皮层表达高峰在６小时外,其余在４小时。结论 ＬＰＳ诱导的ＩＬ－６ｍＲＮＡ在正常鼠脑的不同部位表达曲线不同。     

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。     

Mass spectrometric identification of Cu, Zn, Fe, Co, Mn, Mg, and Pb in mammalian brain.

Combining the techniques of thin-layer chromatography (TLC) and mass spectrometry, we unambiguously identified the trace metals Cu, Zn, Fe, Pb, Mn, Co, and Mg in the brain of a female human who had no evidence of any pathologic disease in the central nervous system, and in brains from mouse, rat, guinea pig, and rabbit. These trace metals were also found in anatomic regions of human brain: cortex (gray), cortex (white), caudate nucleus, putamen, hippocampus, and thalamus, and in anatomic regions of rat brain: hypothalamus, cerebellum, stem striatum, and "the rest." The metals were characterized from the color and Rf values of their tetraphenylporphyrin chelates on TLC and from the mass and pattern of molecule ion cluster of the mass spectrum. The unexpected presence of lead in the brain is discussed.     

Age-dependent and region-specific differences in the distribution of trace elements in 7 brain regions of Long-Evans Cinnamon (LEC) rats with hereditary abnormal copper metabolism

Cu, Mn, Mo, Rb and Zn concentrations of 7 brain regions in LEC rats were determined before (4 and 10 weeks old) and after (20 weeks old) the onset of jaundice. Cu in the LEC rat brain was less concentrated in all regions at 4 weeks of age and in synaptosomal fractions at 10 weeks but, conversely, more concentrated in 3 regions at 20 weeks than in control rats. Furthermore, Mo and Rb in 6 regions at 10 weeks of age and Mn at 20 weeks were more concentrated in the LEC rat brain than in control rats. These results showed that abnormal distributions of trace elements exist in the LEC rat brain before the onset of jaundice.     

Effects of long-term phenytoin treatment on brain weight and zinc and copper metabolism in rats

The effects of phenytoin (PHT) treatment on brain weights and the zinc (Zn) and copper (Cu) concentrations in liver, kidney, and five parts of the brain have been studied in rats. After 32 wk of treatment (daily doses 72–88 mg/kg body weight), significantly reduced brain weights were found in rats sacrificed during treatment, but not in those sacrificed after 14 d of abstinence. The weight reduction mainly seemed to affect cortex, but cerebellum was also influenced. The PHT treatment during 18 wk did not significantly reduce the brain weights. At the end of treatment, significantly increased serum Cu concentrations were found, as well as decreased Zn levels in the liver and low Cu levels in the kidney. No large alterations were found in the trace element concentrations of different brain regions. The PHT treatment for 32 wk induced physical dependence, recorded as convulsions. It is suggested that PHT through a chelate binding with Zn and Cu interferes with the metabolism of the trace elements and the drug may cause a Zn deficiency. The observed decrease of the brain weights may have some parallel to the mental side effects of the drug observed during chronic epilepsy therapy.     

血清微量元素含量与儿童智力发育低下的相关性研究

测定１０４例智力发育低下儿童及８８名正常儿童血清锌，铜，钴，镉，锰含量，结果发现智力发育低下组与正常组对照比较，锌显著低于正常组，镉显著高于正常组，根据智商（ＩＱ）的高低，将患儿分为严重，重度，中度，轻度进行比较，发现ＩＱ与血清锌值呈正相关趋势，与血清镉值有负相关趋势，根据脑电图异常程度分组比较也得出同样的结论。     

Manganese mineral interactions in brain.

Manganese (Mn) is an essential mineral but is toxic when taken in excess. However, whether its interactions with other minerals in organs and cells are involved in mechanisms underlying Mn toxicity is poorly understood. We designed a developmental rat model of chronic Mn treatment (Group A: 1 mg MnCl2.4H2O per ml of drinking water; Group B: 10 mg MnCl2.4H2O per ml of drinking water; Group C: 20 mg MnCl2.4H2O per ml of drinking water; Control Group given water without manganese addition). Employing the model and instrumental neutron activation analysis, we investigated two hypotheses: (i) chronic manganese treatment alters the brain regional distribution of manganese and this altered manganese distribution also leads to region-specific changes of other metals; (ii) chronic manganese treatment induces differential changes in subcellular distributions of metals and electrolytes. In the treated rats, brain Mn level showed dose-related increases, the most pronounced being noted in striatum, hypothalamus, and hippocampus: these increases also led to alterations in regional distribution pattern of Mn. In the treated rats, Fe level was increased in hypothalamus, cerebellum, hippocampus, pons and medulla, and striatum. Cu level was increased in pons and medulla, hippocampus, midbrain, and striatum. Se level was increased in cerebellum, striatum, midbrain, hypothalamus, and pons and medulla. Zn level was increased in hypothalamus and striatum. Ca level was increased in midbrain but decreased in cerebellum; however, Mg and Al levels were not markedly affected. In brains of Mn-treated rats, Mn levels in subcellular fractions were all increased, being especially marked in nuclei, mitochondria, and synaptosomes; the subcellular distributions of Fe, Cu, Zn, and Mg were differentially altered although those of Al and Ca were minimally affected. These results are consistent with our hypotheses and may have implications in manganese neurotoxicity. The cellular and molecular mechanisms underlying manganese-mineral interactions in brain are still poorly defined and merit further investigation.     

THE ASTROGLIAL RESPONSE TO STABBING. IMMUNOFLUORESCENCE STUDIES WITH ANTIBODIES TO ASTROCYTE-SPECIFIC PROTEIN (GFA) IN MAMMALIAN AND SUBMAMMALIAN VERTEBRATES

The astroglial response t o stabbing. Immunofluorescence studies with antibodies to astrocyte-specific protein (GFA) in mammalian and sub-mammalian vertebrates
The astroglial response to stabbing was studied by immunofluorescence with GFA protein antisera in adult and newborn rats, chickens and goldfish. In the adult normal rat most astrocytes of the isocortex and corpus striatum are protoplasmic and do not stain by immunofluorescence. Two days after injury many astrocytes became brightly fluorescent in the stabbed hemisphere and were still fluorescent 2 months later. In the newborn rat the astroglial response was more limited. Reactive glial cells in the medial frontal cortex and pyramidal layer of the hippocampus had a radial appearance with thin immunofluorescent processes crossing at right angles to the surface of the cortex. In rats stabbed at birth and killed 1 month later many immunofluorescent astrocytes were present in the frontal cortex of both cerebral hemispheres. Radial glia were no longer observed. In the normal adult rat radial glial processes were seen by immunofluorescence extending at right angles from the lateral wall of the third ventricle into the hypothalamus. In the chicken cerebellum the astroglial response to stabbing was limited, with few immunofluorescent fibers in the vicinity of the wound. No changes were observed in the goldfish optic tectum by immunofluorescence.     

高原地区MS血清某些微量元素的含量变化及其意义探讨

目的　探讨高原环境下多发性硬化 (MS)血清某些微量元素含量的变化与发病的相关性。方法　以电感耦合等离子体发射光谱法测定 19例 MS患者血清 Zn、Cu、Fe、Mn、Al等 5种微量元素水平。结果　 MS患者血清 Mn、Al水平显著高于正常对照组 ,而 Cu含量则较低。 Zn和 Fe无明显变化。结论　微量元素的改变可能与 MS的发病机制有一定联系。     

Regional metal concentrations in Parkinson's disease, other chronic neurological diseases, and control brains

Metal deficiency or toxicity states have been recognized as a cause of several neurological disorders and are suspected in others. We analyzed four brain regions (frontal cortex, caudate nucleus, substantia nigra, and cerebellum) in 36 human brains for concentrations of 24 metals (Ag, Al, As, B, Be, Ca, Cd, Co, Cr, Cu, Fe, K, Pb, Mg, Mn, Mo, Na, Ni, P, Se, Ti, V, W, Zn). Regional metal concentrations, measured using atomic absorption and atomic emission spectroscopy, were compared between 9 Parkinson's disease (PD) brains, 15 brains from patients with other chronic neurological diseases, and 12 control brains. No significant metal concentration differences were noted between brains from PD and other chronic neurologic disease. However, parkinsonian brains (PD and parkinsonism secondary to neurofibrillary tangle disease) showed lower concentrations of magnesium in the caudate nucleus and copper in the substantia nigra than control brains. These findings may represent an etiologically important clue to parkinsonism.     

Glucocorticoids may alter antioxidant enzyme capacity in the brain: baseline studies

Glucocorticoids (GCs), the adrenal steroids secreted during stress, have been shown to increase the vulnerability of hippocampal neurons to metabolic insults, potentially by altering the neuronal defense capacity against oxidative damage. These experiments assessed the effect of long term in vivo GC supplementation on basal activity of the antioxidant enzymes copper/zinc superoxide dismutase (Cu/Zn SOD), manganese superoxide dismutase (Mn SOD), catalase, and glutathione peroxidase (GSPx). Kinetic enzyme studies were done using brain tissue from the hippocampus, cortex, cerebellum, and also from liver as a peripheral control. Cu/Zn SOD activity was significantly lower in all brain regions of GC-treated rats, but higher in the liver. Mn SOD activity was unaffected by treatment. Catalase in the brain appeared largely unaffected by GC treatment, although liver catalase was significantly decreased. GSPx activity was significantly decreased by GCs at high peroxide levels in all tissues. These results indicate that the presence of GCs may lower the antioxidant capacity of tissues in a region-specific manner, and that the deficit may not appear until the tissue is challenged with supranormal levels of oxidative products (as seen with GSPx).