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Pregnancy protects nervous tissues against the neurotoxicity of intrathecal bupivacaine in rabbits 妊娠保护兔神经组织免受鞘内布比卡因的神经毒性。
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-06-27 DOI: 10.1016/j.ntt.2025.107519
Ju-Feng Ma , Jing Zhang , Rui He , Ju-Hui Niu , Shen Yang

Background

Local anesthetics have been associated with spinal neurotoxicity, including the risk of persistent neurological injury. Pregnancy is known to increase the sensitivity of nervous tissue to local anesthetics, potentially elevating the risk of neurological deficits in obstetric patients following spinal block. This study aimed to investigate the effects of pregnancy on the neurotoxicity of intrathecal bupivacaine.

Methods

Pregnant and non-pregnant rabbits were administered three injections of either 0.375 % or 0.75 % bupivacaine, or normal saline, at 48-h intervals (average volume: 200 μl). Seven days after the first injection, electron microscopic scores (EMS), spinal neuronal apoptotic rates, intracellular Ca2+ concentrations, and mitochondrial membrane potential were evaluated.

Results

The EMS indicated more severe neurotoxicity in non-pregnant rabbits compared to pregnant rabbits in the bupivacaine-treated groups (median [Q1-Q3]: 23 [21–26] vs. 21 [18.5–24], P = 0.045). Pregnant rabbits exhibited significantly lower apoptosis rates and intracellular Ca2+ concentrations, along with a higher mitochondrial membrane potential compared to their non-pregnant counterparts (0.99 % ± 1.33 % vs. 2.03 % ± 2.09 %, P < 0.01; 240 ± 104 vs. 257 ± 112, P < 0.01; 84.1 % ± 6.1 % vs. 69.9 % ± 15.4 %, P < 0.01).

Conclusion

These findings indicated that pregnancy protects nervous tissue against the toxicity of intrathecal bupivacaine.
Conclusion: These findings suggest that pregnancy confers a protective effect on nervous tissue against the neurotoxicity induced by intrathecal bupivacaine.
背景:局麻药与脊髓神经毒性有关,包括持续性神经损伤的风险。已知妊娠会增加神经组织对局麻药的敏感性,可能会增加脊髓阻滞后产科患者神经功能缺损的风险。本研究旨在探讨妊娠对鞘内布比卡因神经毒性的影响。方法:给怀孕和未怀孕家兔注射0.375 %或0.75 %布比卡因或生理盐水,每隔48 h注射3次(平均体积:200 μl)。第一次注射后7天,观察电镜评分(EMS)、脊髓神经元凋亡率、细胞内Ca2+浓度和线粒体膜电位。结果:EMS显示,与布比卡因治疗组的妊娠兔相比,未妊娠兔的神经毒性更严重(中位数[Q1-Q3]: 23[21-26]比21 [18.5-24],P = 0.045)。怀孕的兔子表现出显著降低细胞凋亡率和细胞内钙离子浓度,以及更高的线粒体膜电位比没有怀孕同行(0.99 % ±1.33  % 2.03 vs % ±2.09  %,P 结论:这些研究结果表明,孕期保护神经组织对鞘内bupivacaine的毒性。结论:妊娠对神经组织对鞘内布比卡因引起的神经毒性有保护作用。
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引用次数: 0
Pregnancy outcomes following maternal exposure to favipiravir: A Terafar case series 孕妇接触法匹拉韦后的妊娠结局:特拉法病例系列
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-07-16 DOI: 10.1016/j.ntt.2025.107524
Nusret Uysal , Baris Karadas , Secil Karaca Kurtulmus , Merve Tor , Ismail Yilmaz , Nihal Olgac Dundar , Yusuf C. Kaplan

Objective

To assess pregnancy outcomes following maternal favipiravir exposure, with a particular focus on congenital malformations and neonatal development.

Methods

A case series, including data from pregnancies with favipiravir exposure between 2020 and 2021, was conducted at Izmir Katip Celebi University Teratology Information Center. Pregnant women and their infants were evaluated through structured interviews, ultrasonography, neonatal follow-ups, and developmental assessments. Congenital malformations were classified per EUROCAT criteria, and development was assessed using the Denver Developmental Screening Test-III.

Results

Of 45 pregnancies, 37 resulted in live births (including 1 set of twins), seven were electively terminated, and one ended in intrauterine death. Among the 28 infants with first-trimester exposure, 7.1 % (n = 2) had major malformations (congenital ichthyosis and hydronephrosis) and an additional 7.1 % (n = 2) had minor malformations (pleural effusion, patent foramen ovale). A review of exposure windows relative to critical developmental periods did not indicate a consistent or conclusive temporal association with the observed anomalies. Preterm birth and low birth weight rates were 9.6 % and 6.4 %, respectively. Neonatal jaundice occurred in 32.2 % of neonates. Developmental screening was normal in most cases, with one infant—who did not have any congenital malformations—exhibiting mild language delay.

Conclusion

Our study does not indicate a major teratogenic signal regarding favipiravir exposure in pregnancy, though the higher elective termination rate suggests increased risk perception. While study limitations prevent definitive conclusions, our findings may be of value to clinicians in counseling pregnant women regarding favipiravir exposure.
目的评估孕妇法匹拉韦暴露后的妊娠结局,特别关注先天性畸形和新生儿发育。方法在Izmir Katip Celebi大学畸形学信息中心进行了一系列病例研究,包括2020年至2021年期间接触favipiravir的妊娠数据。通过结构化访谈、超声检查、新生儿随访和发育评估对孕妇及其婴儿进行评估。根据EUROCAT标准对先天性畸形进行分类,并使用丹佛发育筛查测试- iii评估发育。结果45例妊娠中,37例活产(包括1对双胞胎),7例选择性终止妊娠,1例宫内死亡。在28名妊娠早期暴露的婴儿中,7.1% (n = 2)有严重畸形(先天性鱼鳞病和肾积水),另外7.1% (n = 2)有轻微畸形(胸腔积液,卵圆孔未闭)。对与关键发育时期相关的暴露窗的回顾并没有表明与观察到的异常有一致或结论性的时间关联。早产和低出生体重率分别为9.6%和6.4%。新生儿黄疸发生率为32.2%。发育筛查在大多数情况下是正常的,有一个没有任何先天畸形的婴儿表现出轻微的语言迟缓。结论:我们的研究并未表明妊娠期接触法匹拉韦有主要的致畸信号,尽管较高的选择性终止率表明风险认知增加。虽然研究的局限性阻止了明确的结论,但我们的研究结果可能对临床医生就favipiravir暴露对孕妇进行咨询有价值。
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引用次数: 0
Corrigendum to: “Pregnancy outcomes following maternal exposure to Favipiravir: A Terafar case series” [Neurotoxicology and Teratology 110 (2025) 107524] “孕妇接触Favipiravir后的妊娠结局:Terafar病例系列”[神经毒理学和畸形学110(2025)107524]的更正。
IF 2.8 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-08-05 DOI: 10.1016/j.ntt.2025.107534
Nusret Uysal , Baris Karadas , Secil Karaca Kurtulmus , Merve Tor , Ismail Yilmaz , Nihal Olgac Dundar , Yusuf C. Kaplan
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引用次数: 0
Introduction to “Effects of stress exposure during development on neurobehavioral and neuroendocrine function” “发育过程中应激暴露对神经行为和神经内分泌功能的影响”的介绍。
IF 2.8 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 DOI: 10.1016/j.ntt.2025.107520
Jerrold S. Meyer , Sonya Sobrian , Gregg D. Stanwood
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引用次数: 0
Effects of N-acetylcysteine after repeated exposure to ethanol in memory and neurotransmission in zebrafish 反复暴露于乙醇后n -乙酰半胱氨酸对斑马鱼记忆和神经传递的影响。
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-06-12 DOI: 10.1016/j.ntt.2025.107508
Daiana Alves Spilere, Guilherme Lodetti, Ana Carolina Salvador de Farias, Amanda Gomes Teixeira, Eduardo Ronconi Dondossola, Eduardo Pacheco Rico

Introduction

In the brain, alcohol metabolites alter the functioning of several neurotransmission systems, such as glutamatergic and cholinergic, in addition to impairing memory and learning. Medications for Alcohol Use Disorders (AUD) cause adverse effects and contraindications. N-acetylcysteine (NAC) has been shown to protect memory and restore acetylcholinesterase (AChE) levels. Additionally, it functions as an antioxidant that works alongside glutathione, which is associated with the glutamatergic synapse. In this context, the current research aimed to examine the neuroprotective effects of NAC in animals that underwent repeated ethanol exposure (REE), along with the impacts on memory and the cholinergic and glutamatergic signaling pathways in zebrafish.

Methods

The animals were exposed to 1 % ethanol for 8 days for 20 min daily. They received treatment with NAC after the eighth exposure to ethanol for 10 or 60 min. Euthanasia occurred 24 h after the last exposure. Inhibitory avoidance and object recognition tests were performed. Also, the choline acetyltransferase (ChAT) enzyme activities, AChE activity, and glutamate uptake were evaluated.

Results

The results show a significant AChE activity increase in the REE group and a decrease in those exposed to alcohol and treated with NAC for 10 min. No significant differences were found regarding ChAT activity. REE significantly reduced glutamate uptake. All groups except the ethanol group acquired aversive memory in inhibitory avoidance tests. Only the NAC-treated group demonstrated longer new object exploration in the recognition test. The study indicates that REE affects AChE, glutamate uptake, and aversive memory and that a single NAC treatment can mitigate these effects. These findings enhance the understanding of REE mechanisms and NAC's protective properties against ethanol-induced damage in zebrafish.
简介:在大脑中,酒精代谢物除了损害记忆和学习能力外,还会改变几种神经传递系统的功能,如谷氨酸能和胆碱能。治疗酒精使用障碍(AUD)的药物会导致不良反应和禁忌症。n -乙酰半胱氨酸(NAC)已被证明具有保护记忆和恢复乙酰胆碱酯酶(AChE)水平的作用。此外,它作为一种抗氧化剂,与谷胱甘肽一起作用,谷胱甘肽与谷氨酸能突触有关。在此背景下,目前的研究旨在研究NAC对反复乙醇暴露(REE)的动物的神经保护作用,以及对斑马鱼记忆和胆碱能和谷氨酸能信号通路的影响。方法:1 %乙醇浸泡8 天,每天20 min。他们在第八次暴露于乙醇10或60 分钟后接受NAC治疗。安乐死发生在最后一次接触后24 小时。进行了抑制性回避和目标识别测试。测定了胆碱乙酰转移酶(ChAT)活性、乙酰胆碱酯交换酶(AChE)活性和谷氨酸摄取。结果:结果显示,REE组乙酰胆碱酯酶活性显著增加,暴露于酒精和NAC治疗10 min组乙酰胆碱酯酶活性降低。在ChAT活性方面没有发现显著差异。REE显著降低谷氨酸摄取。在抑制回避试验中,除乙醇组外,其余各组均获得了厌恶记忆。只有nac处理组在识别测试中表现出更长时间的新物体探索。研究表明REE影响乙酰胆碱酯酶、谷氨酸摄取和厌恶记忆,单一NAC治疗可以减轻这些影响。这些发现增强了对REE机制和NAC对斑马鱼乙醇损伤的保护作用的理解。
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引用次数: 0
Metal exposure in Brazilian children of waste pickers from the largest open garbage dump in Latin America: Use of deciduous teeth as biomarker 拉丁美洲最大露天垃圾场拾捡者对巴西儿童的金属暴露:使用乳牙作为生物标志物
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-06-25 DOI: 10.1016/j.ntt.2025.107516
Andrea M. Dantas , Eliude B. Gomes , Raquel F. Gerlach , Airton C. Martins , Tara R. Zolnikov , Aline M. Susuki , Ana C.B. Bezerra , Fernando Barbosa Jr , Michael Aschner , Mariana R. Urbano , Monica M.B. Paoliello , Vanessa R.N. Cruvinel
Environmental exposures to metals is a concern for public health, due to their association with various adverse health outcomes, especially in children. The aim of this study was to analyze 21 metals (V, Cr, Mn, Co, Ni, Cu, Zn, As, Se, Rb, Ag, Cd, Ba, Ti, Pb, U, Sn, Mo, Ce, La, and Th) in deciduous teeth of waste pickers' children from an open garbage dump region (Estrutural region- Group 1), and compare them with children living in two other regions in Brasilia (Ceilandia – Group 2, and Plano Piloto – Group 3). Three hundred and two children participated in the study, and a single deciduous whole tooth (dentine plus enamel) was analyzed from each child. Socio-demographic variables, breastfeeding time, visits to the dentist, drinking water consumption, among others, were obtained through a questionnaire provided to the parents or guardians of the children. Metal analyses were performed by Inductively Coupled Plasma Mass Spectrometry (ICP-MS). Significantly higher concentrations of V, Co, Cu, and As were found in children from G1, where most parents were waste pickers, compared to the other two regions (p < 0.01). Pb and Cd concentrations were significantly higher in children from G2 and G3 compared with G1 (p < 0.01). Significantly higher levels of Cr, Mn, Zn and Se were found in children from G2 (p < 0.01), where residents also have very low income, analogous to G1. We found a trend towards an increase in metal concentrations in incisor compared to canine and molar teeth of children in all three groups. This study provides novel data and reinforces the use of deciduous teeth as potential matrix for biomonitoring children's metal exposures.
环境暴露于金属与各种不利的健康后果,特别是儿童的健康后果有关,因此是一个令人关切的公共健康问题。本研究的目的是分析一个露天垃圾场(e结构性区- 1组)拾捡者儿童乳牙中的21种金属(V、Cr、Mn、Co、Ni、Cu、Zn、As、Se、Rb、Ag、Cd、Ba、Ti、Pb、U、Sn、Mo、Ce、La和Th),并与生活在巴西ilia其他两个地区(Ceilandia - 2组和Plano Piloto - 3组)的儿童进行比较。312名儿童参加了这项研究,并对每个儿童的一颗乳牙(牙本质加牙釉质)进行了分析。社会人口变量、母乳喂养时间、看牙医次数、饮水消耗等都是通过向儿童的父母或监护人提供的调查表获得的。金属分析采用电感耦合等离子体质谱法(ICP-MS)。与其他两个地区相比,G1儿童中发现的V、Co、Cu和As浓度明显较高,因为该地区大多数父母都是拾捡垃圾的人(p <;0.01)。G2和G3患儿的铅和镉浓度明显高于G1 (p <;0.01)。G2组儿童的Cr、Mn、Zn和Se水平显著升高(p <;0.01),那里的居民收入也很低,类似于G1。我们发现,与所有三组儿童的犬齿和磨牙相比,门牙中的金属浓度有增加的趋势。本研究提供了新的数据,并加强了乳牙作为儿童金属暴露生物监测的潜在基质的使用。
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引用次数: 0
Effects of bisphenol-a on vasopressin regulating synaptic plasticity of hippocampus 双酚a对加压素调节海马突触可塑性的影响。
IF 2.8 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-07-24 DOI: 10.1016/j.ntt.2025.107531
Xiaohong Xu, Jinshan Wang, Yani Yang
The neuropeptide arginine vasopressin (AVP) plays an important role in the hippocampus by regulating neuronal excitability, synaptic plasticity, and other processes. Activity of AVP is regulated by sex hormones. The present study investigated the effects of bisphenol-A (BPA), a environmental endocrine disruptor, on AVP regulating synaptic plasticity of hippocamus. AVP at 10–100 nM significantly increased the dendrite complexity and dendrite spine density of hippocampal neurons in vitro, which was partially eliminated by AVP receptor 1a (V1aR) antagonist (RG7713) or oxytocin receptor (OTR) antagonist (L368–899). BPA at 10 nM increased neuronal dendritic complexity and spine density, which was partially eliminated by estrogen receptor (ERs) antagonist (ICI182,780) but completely abolished by antagonist of both ERs and ERRγ (Tamoxifen). BPA at 10 nM did not affect the effect of AVP (100 nM) on the dendrite complexity and spine density, but eliminated the promoting effects of DHT + AVP on the dendritic complexity. BPA at 1000 nM not only inhibited the dendritic complexity but also eliminated the promoting effects of AVP, 17β-estradiol (17β-E2) + AVP, and 11-ketodihydrotestosterone (DHT) + AVP on the dendritic complexity. In addition, BPA at 1000 nM down-regulated the levels of V1aR and OTR protein expressions. Meanwhile, BPA at 10 nM promoted the maintenance of LTP of CA2 in the hippocampal slices, but co-treatment of BPA eliminated the effect of 17β-E2 or DHT on LTP. BPA (10 nM) did not affect the promotion of long-term potentiation (LTP) by AVP, but eliminated the promotion of LTP by DHT + AVP. These results suggest that BPA at nanomoles levels affected AVP regulating modification of dendrite morphology and synaptic plasticity of hippocampus mainly by disrupting the effects of 17β-E2 and/or DHT on AVP activity.
神经肽精氨酸加压素(AVP)在海马中通过调节神经元兴奋性、突触可塑性等过程发挥重要作用。AVP的活性受性激素的调节。本研究探讨了环境内分泌干扰物双酚a (BPA)对AVP调节海马突触可塑性的影响。AVP 10-100 nM显著增加体外海马神经元树突复杂性和树突棘密度,AVP受体1a (V1aR)拮抗剂(RG7713)或催产素受体(OTR)拮抗剂(L368-899)可部分消除AVP复杂性和树突棘密度。10 nM BPA增加了神经元树突复杂性和脊柱密度,雌激素受体(er)拮抗剂(ici182780)部分消除了这一作用,但雌激素受体和ERRγ拮抗剂(他莫昔芬)完全消除了这一作用。10 nM BPA不影响AVP(100 nM)对树突复杂性和脊柱密度的影响,但消除了DHT + AVP对树突复杂性的促进作用。1000 nM BPA不仅能抑制树突复杂性,还能消除AVP、17β-雌二醇(17β-E2) + AVP和11-酮二氢睾酮(DHT) + AVP对树突复杂性的促进作用。此外,BPA在1000 nM时下调了V1aR和OTR蛋白的表达水平。同时,BPA在10 nM时促进了海马片CA2对LTP的维持,但BPA联合处理消除了17β-E2或DHT对LTP的影响。BPA(10 nM)不影响AVP对长期增强(LTP)的促进作用,但消除了DHT + AVP对LTP的促进作用。这些结果表明,纳米摩尔水平的BPA主要通过破坏17β-E2和DHT对AVP活性的影响来影响AVP,从而调节海马树突形态的改变和突触的可塑性。
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引用次数: 0
Micro(nano)plastics in the brain: Epigenetic perturbations in progression to neurodegenerative diseases 大脑中的微(纳米)塑料:神经退行性疾病进展中的表观遗传扰动
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-07-08 DOI: 10.1016/j.ntt.2025.107521
Mou Mondal , Apoorva Chouksey , Vikas Gurjar , Rajnarayan Tiwari , Rupesh K. Srivasatava , Pradyumna Kumar Mishra
As global plastic production escalates, micro(nano)plastics (MNPs) have become pressing ecological and biomedical concerns. These pollutants are increasingly implicated in the pathogenesis of neurodegenerative diseases. Due to their nanoscale size and surface reactivity, MNPs can cross the blood-brain barrier, accumulating in neural tissues. Once internalized, they disrupt neuronal homeostasis by inducing oxidative stress, mitochondrial dysfunction, and chronic neuroinflammation, key processes in neurodegenerative progression. Mitochondria, central to neuronal energy and redox regulation, are particularly vulnerable, leading to impaired ATP production, elevated ROS, and pro-apoptotic signaling. Recent studies reveal that MNPs also induce epigenetic changes, including aberrant DNA methylation, histone modifications, and dysregulation of non-coding RNAs. These alterations can result in synaptic instability, persistent transcriptional reprogramming, and heightened susceptibility to diseases like Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis. The mitochondrial epigenome is a vital target of MNP-induced disruption, offering potential biomarkers like methylated mtDNA and microRNAs for early diagnosis and prognosis. Understanding the molecular mechanisms behind these epigenetic alterations is essential for developing practical diagnostic tools and therapies. This review provides a comprehensive overview of MNP-induced neurodegeneration, focusing on mitochondrial and epigenetic disruptions. Moreover, it explores emerging biosensing technologies for detecting MNP-induced epigenetic alterations, highlighting the urgent need for further investigation to fully understand the neurotoxic potential of MNPs and develop preventive and therapeutic strategies for mitigating their effects on brain health.
随着全球塑料生产的升级,微(纳米)塑料(MNPs)已成为迫切的生态和生物医学问题。这些污染物越来越多地与神经退行性疾病的发病机制有关。由于它们的纳米级尺寸和表面反应性,MNPs可以穿过血脑屏障,在神经组织中积累。一旦内化,它们会通过诱导氧化应激、线粒体功能障碍和慢性神经炎症(神经退行性进展的关键过程)破坏神经元稳态。线粒体是神经元能量和氧化还原调节的核心,特别脆弱,导致ATP生成受损,ROS升高和促凋亡信号传导。最近的研究表明,MNPs还会诱导表观遗传变化,包括异常的DNA甲基化、组蛋白修饰和非编码rna的失调。这些改变会导致突触不稳定,持续的转录重编程,以及对阿尔茨海默病、帕金森病和肌萎缩性侧索硬化症等疾病的易感性增加。线粒体表观基因组是mnp诱导破坏的重要靶点,为早期诊断和预后提供了潜在的生物标志物,如甲基化的mtDNA和microrna。了解这些表观遗传改变背后的分子机制对于开发实用的诊断工具和治疗方法至关重要。这篇综述提供了mnp诱导的神经变性的全面概述,重点是线粒体和表观遗传破坏。此外,它还探讨了用于检测mnp诱导的表观遗传改变的新兴生物传感技术,强调迫切需要进一步研究以充分了解mnp的神经毒性潜力,并制定预防和治疗策略以减轻其对大脑健康的影响。
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引用次数: 0
The East Palestine train derailment: A complex environmental disaster 东巴勒斯坦火车出轨:一场复杂的环境灾难。
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-07-01 Epub Date: 2025-07-17 DOI: 10.1016/j.ntt.2025.107522
Lynn T. Singer , Fredrick Schumacher , James Fabisiak , Laura J. Dietz , Timothy Ciesielski
This symposium, The East Palestine Train Derailment: A Complex Environmental Disaster, brought together scientists whose research represented initial scientific responses to the community health impacts of the chemical exposures incurred from a disastrous train derailment and subsequent combustion in East Palestine, Ohio in February, 2023. This derailment and burn led to multiple complex toxic exposures to air, soil and water, including vinyl chloride and butyl acrylate. Presenters described the multi-university consortium formed to assist with developing and communicating data-informed summaries to the affected community. Presenters also reported on the immediate health sequelae experienced by the community and the stress and uncertainty regarding long term effects. Plans were reported for several pilot studies funded by the National Institute on Environmental Health Sciences in immediate response to the disaster. Fredrick Schumacher, PhD outlined the aims of The Healthy Futures Research Study: Linking Somatic Mutation Rate with Baseline Exposure in East Palestine that plans to use somatic mutation rate (SMR) to measure the biological impact of environmental exposures based on proximity to the train derailment and residents’ clinical symptomatology. James Fabisiak, PhD shared plans for their study, East Palestine Community-Engaged Environmental Exposure, Health Data, and Biospecimen Bank that will measure chemical contaminants in indoor air and water in homes, monitor liver damage in residents and identify parents’ concerns about children’s health and development. As part of that study, Laura Dietz, PhD noted the major psychosocial stressors experienced by the community, particularly the psychological effects on children which the study will try to identify through parental report. Timothy Ciesielski, MD, PhD summarized the difficulties of drawing conclusions related to health and safety risk from the toxicants released through currently available government databases and his experience trying to provide the community with reliable and valid information in the context of working across state lines and multiple state and federal agencies.
本次研讨会题为“东巴勒斯坦火车脱轨:一场复杂的环境灾难”,汇集了科学家,他们的研究代表了对2023年2月俄亥俄州东巴勒斯坦灾难性火车脱轨和随后燃烧造成的化学品暴露对社区健康影响的初步科学反应。这种脱轨和燃烧导致多种复杂的有毒物质暴露于空气、土壤和水中,包括氯乙烯和丙烯酸丁酯。发言者介绍了为协助制定和向受影响社区传播数据知情摘要而组成的多所大学联盟。发言者还报告了社区所经历的直接健康后遗症以及长期影响的压力和不确定性。据报告,由国家环境健康科学研究所资助的几项试点研究计划是为了立即对灾难作出反应。Fredrick Schumacher博士概述了健康未来研究的目标:将东巴勒斯坦的体细胞突变率与基线暴露联系起来,该研究计划使用体细胞突变率(SMR)来测量基于火车脱轨和居民临床症状的环境暴露的生物学影响。James Fabisiak博士分享了他们的研究计划,东巴勒斯坦社区参与的环境暴露,健康数据和生物标本库,将测量室内空气和家庭水中的化学污染物,监测居民的肝损伤,并确定父母对儿童健康和发展的担忧。作为该研究的一部分,劳拉·迪茨博士指出了社区所经历的主要社会心理压力源,特别是对儿童的心理影响,该研究将试图通过父母报告来确定。Timothy Ciesielski,医学博士,总结了通过目前可用的政府数据库从释放的有毒物质中得出与健康和安全风险相关的结论的困难,以及他在跨州界和多个州和联邦机构工作的背景下试图为社区提供可靠和有效信息的经验。
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引用次数: 0
Identifying teratogens: Challenges and opportunities 识别致畸物:挑战与机遇
IF 2.6 3区 医学 Q3 NEUROSCIENCES Pub Date : 2025-05-01 Epub Date: 2025-06-17 DOI: 10.1016/j.ntt.2025.107453
Sonja A. Rasmussen
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Neurotoxicology and teratology
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