苯并三氮唑与5—羟基苯并三氮唑在NaCl溶液中对铜缓蚀作用的SERS研究

采用表面增强拉曼光谱技术（SERS）研究了w＝0．03NaCl溶液中BTA（苯并三氨唑）及其衍生物5CBTA（5－羟基苯并三氮唑）对铜的缓蚀作用机理，发现5CBTA对铜的作用与BTA的作用机理相似，在较大正电位下两者都是通过三氮唑环与铜形成配合物覆盖在铜表面，随着电位负移在铜电极表面吸附的聚合物膜逐渐转化分为分子形式吸附，5CBTA中的－COOH基团只是起到空间位阻的作用，没有参与电极表面的吸附。两者配使用以BTA吸附为主，其缓蚀机理没有发生改变，也没有产生协同效应。     

带钩软体Cu140宫内节育器的研制和试用

带钩软体Ｃｕ１４０ＩＵＤ的设计构思为：１．带钩的ＩＵＤ可固定在宫底肌层内；２ＩＵＤ体部柔软，能适应不同大小形态的宫腔和收缩时变形；３．铜套面积１４０ｍｍ２在环的体部分布合理，铜面积减少可获得同样满意的避孕效果。放置３９４例经一年随访按生命表法统计一年净累计带器妊娠率１．０３％，因症取出率１．０４％，脱落率３．３６％，副反应小。脱落与ＩＵＤ的质量和放置技术有关。未掌握放置技术时脱落率达１０．６９％，正确放置到位者脱落率低。提高ＩＵＤ质量和放置技术，钩铜１４０将成为一种理想的新颖ＩＵＤ。     

Relationship between oxidative stress and extrinsic coagulation pathway in haemodialyzed patients

Enhanced oxidative stress (SOX), endothelial dysfunction and haemostatic abnormalities are common in end-stage renal failure patients undergoing maintenance haemodialysis (HD). We studied associations among circulating immunoreactive total lipid peroxides as a marker of short-time SOX, autoantibodies against oxidized LDL as a surrogate of prolonged SOX, copper/zinc superoxide dismutase (Cu/Zn SOD) as a major antioxidant enzyme, tissue factor (TF) as a principal initiator of extrinsic coagulation pathway counteracted by its inhibitor (TFPI), and prothrombin fragment 1+2 (F 1+2) as a surrogate of activated haemostasis.

Pre-dialysis blood levels of all the markers studied were higher in 24 clinically stable HD patients compared to 11 healthy controls. Spearman's correlations among the three SOX markers were positive but nonsignificant in both HD patients and controls. In HD subjects, increased Cu/Zn SOD levels directly correlated with those of TF (rho=0.551, p=0.005) and TFPI (rho=0.501, p=0.001); the coagulation markers were also positively associated with each other (rho=0.663, p=0.0004). In healthy subjects, the relations between Cu/Zn SOD, TF and TFPI levels were inverse but not significant, and the direct association between TF and TFPI was nonsignificant either.

In conclusion, increased plasma levels of Cu/Zn SOD, the antioxidant enzyme with emerging endothelial cell-protective and antithrombotic properties, may be a novel part of the system counteracting activated extrinsic coagulation system in maintenance HD patients.     

Familial amyotrophic lateral sclerosis with bulbar onset and a novel Asp101Tyr Cu/Zn superoxide dismutase gene mutation

We describe a patient with familial amyotrophic lateral sclerosis (FALS) in whom we identified a novel missense mutation in exon 4 (Asp101Tyr) of the Cu/Zn superoxide dismutase (SOD1) gene. The disease started with a bulbar symptom (rapidly progressive hoarseness) and at autopsy showed degenerative changes restricted to the upper and lower motor neuron systems (more strictly, with lower motor predominance, showing the most severe degeneration in the nucleus ambiguus). Occasional intracytoplasmic Lewy-body-like hyaline inclusions that were immunoreactive for ubiquitin and SOD1, but immunonegative for neurofilament protein, were found in the lower motor neurons. This is the first report of hoarseness as the initial manifestation of FALS. This SOD1 gene mutation may be associated with a particular clinicopathological phenotype.     

The roles of free radicals in amyotrophic lateral sclerosis

The mutations of the Cu,Zn superoxide dismutase (Cu,Zn-SOD) gene observed in amyotrophic lateral sclerosis (ALS) patients suggest that free radicals play a role in this fatal disease. Free radicals trigger oxidative damage to proteins, membrane lipids, and DNA, thereby destroying neurons. Mutations of the SOD gene may reduce its superoxide dismutase activity, thereby elevating free radical levels. In addition, the mutant SOD protein may function as a peroxidase to oxidize cellular components, and it may also react with peroxynitrite—a product of the reaction between superoxide and nitric oxide—to ultimately form nitrate proteins. The selective degeneration of motor neurons in ALS may be caused by the high level of Cu,Zn-SOD present in and the large number of glutamatergic synapses projecting to these neurons. Free radical-triggered and age-accumulated oxidation may modify the program controlling motor neuron death, thereby initiating apoptosis of motor neurons in young adults.     

锌、铜、镁含量在ICP及FGR母体血清中含量的变化

目的探讨妊娠期肝内胆汁淤积症(ICP)及胎儿生长受限(FGR)患者血清中锌、铜、镁含量的变化。方法以原子吸收分光光度法分别测定35名ICP患者、11例FGR患者及20例正常妊娠女性血清锌、铜、镁浓度。结果ICP患者血清锌含量为0.40±0.16μg/mL,较对照组明显降低(P0.05),铜含量1.88±0.43μg/mL,镁含量0.66±0.73μg/mL,均与对照组无显著性差异(P0.05);FGR组铜含量2.31±0.53μg/mL,较对照组明显升高,锌含量为0.46±0.13μg/mL,镁含量为0.47±0.44μg/mL,均较对照组明显降低,有显著性差异(P0.05);ICP组铜含量较FGR组低,有显著性差异(P0.05),而锌、镁含量两组相比较无显著性差异(P0.05)。结论针对孕妇血清锌、铜、镁含量变化进行饮食调整对孕期健康有重要意义。     

ICP-MS测定片仔癀肝宝中6种重金属的含量

目的：建立电感耦合等离子体质谱法（ICP-MS）测定片仔癀肝宝中铬（Cr）、铅（Pb）、镉（Cd）、砷（As）、汞（Hg）、铜（Cu）6种重金属的含量。方法：样品微波消解处理后,采用电感耦合等离子体质谱法测定。结果：Cr、Cu、As、Cd、Hg、Pb标液的工作曲线线性良好,相关系数大于0.999 3。其中Cr的平均回收率101.2%,相对标准偏差（RSD）7.6%;Cu的平均回收率96.4%,RSD3.5%;As的平均回收率101.3%,RSD1.8%;Cd的平均回收率100.2%,RSD0.3%;Hg的平均回收率100.5%,RSD4.2%;Pb的平均回收率104.2%,RSD5.6%。结论：该方法稳定可靠,灵敏度高,重现性好,可用于测定片仔癀肝宝中Cr、Cu、As、Cd、Hg、Pb 6种重金属的含量。     

The effects of CaEDTA injection on lead,zinc, copper and ALAD in erythrocyte,plasma and urine in lead-exposed workers: a 24-h observation

Summary To evaluate the effects of calcium disodium ethylenediamine tetraacetate (CaEDTA) on the concentrations of lead, zinc and copper in plasma, erythrocyte and urine, and the delta-aminolevulinic acid dehydratase (ALAD) activity in erytrocyte, we administered CaEDTA in 1-h intravenous infusion to ten male gun metal founders with blood-lead concentration of 39 to 64 g/dl (mean 49 g/dl). We found that the plasma concentration of lead, following a rapid rise within the first 3 h, fell temporarily to the level significantly lower than the initial level 19 h after start of the infusion. The plasma concentration of zinc fell to the minimal level 5 h after the infusion; and the erythrocyte concentration of zinc and the ALAD activity concurrently rose to the maximal level 5 h after the infusion. By contrast, no significant alteration was observed in the concentrations of copper in plasma and erythrocyte. The maximal level of urinary metal excretion was attained during the period between 1 and 2 h after start of CaEDTA infusion for lead; within 2 h for zinc; and between 2 and 4 h for copper. The urinary metal excretion returned to the initial level 14 to 24 h after infusion for zinc and copper; but lead excretion was still higher than the initial level during this period. The difference in the kinetics of the three metals following CaEDTA injection is discussed in the light of these findings.     

罗氏促排卵汤加减对肾虚型无排卵性不孕症卵巢动脉血流动力学的影响

目的 观察“罗氏促排卵汤加减”对肾虚型无排卵性不孕症卵巢动脉血流动力学的影响，从“妇人以血为本”的角度探讨肾虚型无排卵性不孕症的发病机理和“罗氏促排卵汤加减”的作用机制。方法 用经阴道彩色多普勒超声测量30例正常妇女、30例肾虚偏肾阳虚型无排卵性不孕症患者治疗前后月经周期四时期最大卵泡平均直径(MFD)，卵巢动脉血流阻力指数(RI)和搏动指数(PI)。结果 健康组月经周期卵巢RI、PI有显著周期性变化。治疗组肾虚症状消失或缓解，卵泡增大，MFD与治疗前相比有显著差异，与健康组相比仍较低，仍有显著差异；RI值下降，与治疗前相比有非常显著差异，与健康组相比无显著差异，且有显著周期性改变；PI值下降，与治疗前相比有非常显著性差异，但与健康组相比仍有非常显著性差异，且无自身周期性变化。结论 “罗氏促排卵汤加减”作用机制是调整下丘脑-垂体-性腺轴，整体调节机体功能；对观察对象的影响是卵巢血管阻力降低，血供增加，血循环改善。     

Mitochondrial metals as a potential therapeutic target in neurodegeneration

Transition metals are critical for enzyme function and protein folding, but in excess can mediate neurotoxic oxidative processes. As mitochondria are particularly vulnerable to oxidative damage due to radicals generated during ATP production, mitochondrial biometal homeostasis must therefore be tightly controlled to safely harness the redox potential of metal enzyme cofactors. Dysregulation of metal functions is evident in numerous neurological disorders including Alzheimer''s disease, stroke, Parkinson''s disease, Huntington''s disease, amyotrophic lateral sclerosis and Friedrich''s ataxia. This review describes the mitochondrial metal defects in these disorders and highlights novel metal-based therapeutic approaches that target mitochondrial metal homeostasis in neurological disorders.

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This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue-8