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本文引用的文献

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Validity and reliability of an occupational exposure questionnaire for parkinsonism in welders.焊工帕金森病职业暴露问卷的有效性和可靠性
J Occup Environ Hyg. 2009 Jun;6(6):324-31. doi: 10.1080/15459620902836856.
2
Impairment of nigrostriatal dopamine neurotransmission by manganese is mediated by pre-synaptic mechanism(s): implications to manganese-induced parkinsonism.锰对黑质纹状体多巴胺神经传递的损害是由突触前机制介导的:对锰诱导的帕金森症的启示。
J Neurochem. 2008 Dec;107(5):1236-47. doi: 10.1111/j.1471-4159.2008.05695.x. Epub 2008 Sep 20.
3
Age-dependent decline of steady state dopamine storage capacity of human brain: an FDOPA PET study.年龄依赖性人脑稳定状态多巴胺储存能力下降:一项 FDOPA PET 研究。
Neurobiol Aging. 2010 Mar;31(3):447-63. doi: 10.1016/j.neurobiolaging.2008.05.005. Epub 2008 Jun 9.
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Manganese and welding fume exposure and control in construction.建筑行业中锰及焊接烟尘的暴露与控制
J Occup Environ Hyg. 2007 Dec;4(12):943-51. doi: 10.1080/15459620701718867.
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Sequelae of fume exposure in confined space welding: a neurological and neuropsychological case series.受限空间焊接烟雾暴露的后遗症:一个神经学和神经心理学病例系列
Neurotoxicology. 2007 Mar;28(2):298-311. doi: 10.1016/j.neuro.2006.11.001. Epub 2006 Dec 12.
6
Nigrostriatal dopamine system dysfunction and subtle motor deficits in manganese-exposed non-human primates.锰暴露的非人灵长类动物黑质纹状体多巴胺系统功能障碍及细微运动缺陷
Exp Neurol. 2006 Dec;202(2):381-90. doi: 10.1016/j.expneurol.2006.06.015. Epub 2006 Aug 22.
7
[18F]FDOPA PET and clinical features in parkinsonism due to manganism.[18F]氟代多巴正电子发射断层扫描与锰中毒所致帕金森综合征的临床特征
Mov Disord. 2005 Apr;20(4):492-496. doi: 10.1002/mds.20381.
8
The sensitivity of 18-fluorodopa positron emission tomography and magnetic resonance imaging in Parkinson's disease.18-氟多巴正电子发射断层扫描和磁共振成像在帕金森病中的敏感性
Eur J Neurol. 2004 Jan;11(1):5-12. doi: 10.1046/j.1351-5101.2003.00709.x.
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Manganese poisoning in Moroccan miners.摩洛哥矿工中的锰中毒
Br J Ind Med. 1955 Jan;12(1):21-35. doi: 10.1136/oem.12.1.21.
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Health effects of welding.焊接对健康的影响。
Crit Rev Toxicol. 2003;33(1):61-103. doi: 10.1080/713611032.

职业性锰暴露无症状焊工[¹⁸F]FDOPA PET 摄取减少。

Reduced uptake of [¹⁸F]FDOPA PET in asymptomatic welders with occupational manganese exposure.

机构信息

Department of Neurology, Washington University School of Medicine, 660 South Euclid Ave., Box 8111, St. Louis, MO 63110, USA.

出版信息

Neurology. 2011 Apr 12;76(15):1296-301. doi: 10.1212/WNL.0b013e3182152830. Epub 2011 Apr 6.

DOI:10.1212/WNL.0b013e3182152830
PMID:21471467
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3090062/
Abstract

BACKGROUND

Welding exposes workers to manganese (Mn) fumes, but it is unclear if this exposure damages dopaminergic neurons in the basal ganglia and predisposes individuals to develop parkinsonism. PET imaging with 6-[(18)F]fluoro-l-dopa (FDOPA) is a noninvasive measure of nigrostriatal dopaminergic neuron integrity. The purpose of this study is to determine whether welding exposure is associated with damage to nigrostriatal neurons in asymptomatic workers.

METHODS

We imaged 20 asymptomatic welders exposed to Mn fumes, 20 subjects with idiopathic Parkinson disease (IPD), and 20 normal controls using FDOPA PET. All subjects were examined by a movement disorders specialist. Basal ganglia volumes of interest were identified for each subject. The specific uptake of FDOPA, K(i), was generated for each region using graphical analysis method.

RESULTS

Repeated measures general linear model (GLM) analysis demonstrated a strong interaction between diagnostic group and region (F(4,112) = 15.36, p < 0.001). Caudate K(i)s were lower in asymptomatic welders (0.0098 + 0.0013 minutes(-1)) compared to control subjects (0.0111 + 0.0012 minutes(-1), p = 0.002). The regional pattern of uptake in welders was most affected in the caudate > anterior putamen > posterior putamen. This uptake pattern was anatomically reversed from the pattern found in subjects with IPD.

CONCLUSIONS

Active, asymptomatic welders with Mn exposure demonstrate reduced FDOPA PET uptake indicating dysfunction in the nigrostriatal dopamine system. The caudate K(i) reduction in welders may represent an early (asymptomatic) marker of Mn neurotoxicity and appears to be distinct from the pattern of dysfunction found in symptomatic IPD.

摘要

背景

焊接使工人接触到锰 (Mn) 烟雾,但目前尚不清楚这种暴露是否会损害基底神经节中的多巴胺能神经元,并使个体易患帕金森病。使用 6-[(18)F]氟-L-多巴 (FDOPA) 的 PET 成像,是一种非侵入性测量黑质纹状体多巴胺能神经元完整性的方法。本研究的目的是确定焊接暴露是否与无症状工人的黑质纹状体神经元损伤有关。

方法

我们使用 FDOPA PET 对 20 名接触 Mn 烟雾的无症状焊工、20 名特发性帕金森病 (IPD) 患者和 20 名正常对照者进行了成像。所有患者均由运动障碍专家进行检查。为每位患者确定了基底神经节的感兴趣区。使用图形分析方法为每个区域生成 FDOPA 的特定摄取量 K(i)。

结果

重复测量一般线性模型 (GLM) 分析表明,诊断组和区域之间存在强烈的相互作用 (F(4,112) = 15.36, p < 0.001)。无症状焊工的尾状核 K(i)(0.0098 + 0.0013 分钟(-1))低于对照组(0.0111 + 0.0012 分钟(-1)),p = 0.002)。焊工的摄取模式主要受尾状核 > 前壳核 > 后壳核影响。这种摄取模式与 IPD 患者的模式在解剖学上相反。

结论

有 Mn 暴露的活跃、无症状焊工表现出 FDOPA PET 摄取减少,表明黑质纹状体多巴胺系统功能障碍。焊工尾状核 K(i) 的减少可能代表 Mn 神经毒性的早期(无症状)标志物,并且似乎与症状性 IPD 中发现的功能障碍模式不同。