Evaluation of geometrically personalized THUMS pedestrian model response against sedan–pedestrian PMHS impact test data

Objective: Evaluating the biofidelity of pedestrian finite element models (PFEM) using postmortem human subjects (PMHS) is a challenge because differences in anthropometry between PMHS and PFEM could limit a model's capability to accurately capture cadaveric responses. Geometrical personalization via morphing can modify the PFEM geometry to match the specific PMHS anthropometry, which could alleviate this issue. In this study, the Total Human Model for Safety (THUMS) PFEM (Ver 4.01) was compared to the cadaveric response in vehicle–pedestrian impacts using geometrically personalized models.

Methods: The AM50 THUMS PFEM was used as the baseline model, and 2 morphed PFEM were created to the anthropometric specifications of 2 obese PMHS used in a previous pedestrian impact study with a mid-size sedan. The same measurements as those obtained during the PMHS tests were calculated from the simulations (kinematics, accelerations, strains), and biofidelity metrics based on signals correlation (correlation and analysis, CORA) were established to compare the response of the models to the experiments. Injury outcomes were predicted deterministically (through strain-based threshold) and probabilistically (with injury risk functions) and compared with the injuries reported in the necropsy.

Results: The baseline model could not accurately capture all aspects of the PMHS kinematics, strain, and injury risks, whereas the morphed models reproduced biofidelic response in terms of trajectory (CORA score = 0.927 ± 0.092), velocities (0.975 ± 0.027), accelerations (0.862 ± 0.072), and strains (0.707 ± 0.143). The personalized THUMS models also generally predicted injuries consistent with those identified during posttest autopsy.

Conclusions: The study highlights the need to control for pedestrian anthropometry when validating pedestrian human body models against PMHS data. The information provided in the current study could be useful for improving model biofidelity for vehicle–pedestrian impact scenarios.     

环境污染物导致氧化应激的关键信号通路及其检测方法

环境污染物能够以多种途径进入生物体内,在体内产生含氧自由基等活性氧物质,并通过多种信号通路及酶反应引起氧化应激,造成生物体内的脂质过氧化、蛋白质损伤、DNA表达改变、酶失活等,从而引发心血管疾病、风湿类疾病、感染及癌症等的发生。本文对环境污染物致氧化应激产生的原因、涉及的信号通路及酶反应、造成的危害,以及常见的基于细胞模型的氧化应激检测方法进行了综述,期望为评价环境污染物和检测氧化损伤提供参考。     

阿维菌素对中华绒螯蟹肝胰腺氧化胁迫效应和组织结构的影响

采用半静态染毒法,研究不同浓度(1.6、8.0、16.0μg·L-1)阿维菌素在胁迫中华绒螯蟹12、24、48、96 h时肝胰腺超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)积累量等氧化胁迫相关指标的变化;并在胁迫60 d时,记录各实验组和对照组中华绒螯蟹肝胰腺颜色的变化并进行组织病理观察。3个阿维菌素浓度组为实验组,空白组和溶剂组为对照组。结果表明在整个实验过程中空白组和溶剂组各个时间点各项指标之间无显著差异(P>0.05);低浓度(1.6μg·L-1)组SOD和CAT活力变化不显著(P>0.05);中浓度(8.0μg·L-1)组SOD和CAT活力变化趋势一致,持续被诱导,SOD活力在24 h以后显著高于空白组(P<0.01),CAT活力在48 h以后显著高于空白组(P<0.01);高浓度(16.0μg·L-1)组SOD和CAT活力在12 h~24 h之间变化趋势一致,表现为显著升高(P<0.05),但是在48 h之后,SOD活力显著下降(P<0.05);96 h时,高浓度组SOD活力显著低于空白组(P<0.01),而CAT活力显著高于空白组(P<0.01);在整个实验过程中各实验组MDA积累量逐渐增加,高浓度组氧化胁迫指标的变化幅度大于低浓度组。胁迫60 d时,取样观察可见对照组中华绒螯蟹肝胰腺正常,各实验组中华绒螯蟹肝胰腺发生了不同程度的病变,肝胰腺颜色由最开始的橘黄色变成了淡黄色、黄白色甚至白色,高、中、低各浓度组肝胰腺白化所占的比例分别是66.6%、57.1%和25.0%。组织病理分析显示,淡黄色肝胰腺的病理变化主要是B细胞数量减少,肝胰腺上皮细胞部分肿大并出现空泡;黄白肝病理观察可见肝胰腺上皮细胞中空泡数量增多,体积增大,且空泡内出现内容物,细胞核固缩;白肝的病理表现主要是基膜增厚,上皮细胞大量脱落,散落在管腔中,空泡数量进一步增多,肝胰腺的生理功能受损。由此得出,阿维菌素会对中华绒螯蟹肝胰腺造成氧化胁迫和组织损伤,且阿维菌素和对肝胰腺的氧化胁迫效应和组织结构损伤程度有一定的剂量-效应关系。     

3种镉超富集植物毛状根体系对镉胁迫响应的比较

近年来,转基因毛状根组织被越来越多地应用于重金属和有机污染物的植物修复技术研究中,已成为进行污染物毒性响应机制研究的便捷的实验室工具。为了探究龙葵、油菜、芥菜3种镉(cadmium,Cd)超富集植物对Cd毒性胁迫响应的差异,以诱导出的3种植物毛状根为研究材料,从毛状根的生长状态、富集Cd的能力、根组织细胞的凋亡程度和抗氧化酶活性等方面进行了探讨。结果表明:Cd浓度为0~50μmol·L-1时,龙葵、油菜、芥菜毛状根受Cd毒害的影响都不明显;Cd浓度为75~100μmol·L-1时,龙葵、油菜、芥菜毛状根均表现出对Cd胁迫的防御响应。在较高的Cd浓度(100μmol·L-1)下,龙葵毛状根的生物量受Cd毒害的影响最小,芥菜次之,油菜受影响最大;同时龙葵毛状根富集的Cd含量最高(745.0μg·g-1),芥菜次之(681.4μg·g-1),油菜最差(505.2μg·g-1)。龙葵、油菜、芥菜毛状根在Cd胁迫下的细胞凋亡水平均随Cd浓度的升高而升高,当Cd浓度为100μmol·L-1时,龙葵毛状根比油菜和芥菜毛状根的细胞凋亡程度均低。同时3种植物毛状根在不同浓度Cd处理下抗氧化酶活性的变化有一定差异。从上述结果综合来看,龙葵毛状根受Cd毒害的影响最小、富集Cd的能力最好,是进一步开展Cd超富集植物转基因改造研究的较好的实验室载体。     

农药致慢性细胞毒性及基因毒性机制研究进展

大量流行病学研究和体内、体外检测分析表明,长期低剂量接触农药可以导致人体细胞和分子损伤,诱导细胞凋亡。农药致细胞及DNA损伤的机制主要与DNA加合物的形成、DNA单链和/或双链的断裂有关。此外,氧化应激参与农药致细胞及DNA损伤的过程,可能成为农药致细胞及DNA损伤的促发因素。从总体上看,其具体分子机制还不十分清楚,有待进一步研究。     

The impact of pesticides on oxidative stress level in human organism and their activity as an endocrine disruptor

Pesticides cause serious environmental and health problems both to humans and animals. The aim of this review is to discuss selected herbicides and fungicides regarding their mode of action and their influence on basic oxidative stress parameters and endocrine disruption properties tested in selected cell cultures in vitro. Because of numerous difficulties which animal studies are subject to, cell cultures are an excellent experimental model reflecting human exposure to different pesticides through all relevant routes. This experimental model can be used to monitor aggregate and cumulative pesticide exposures.     

Urinary 8-oxo-7, 8-dihydro-2′-deoxyguanosine concentrations after frying of bacon,a pilot study

Cooking fumes contain compounds that may give rise to oxidative stress and mutations when inhaled. The aim of this study was to evaluate if cooking fumes from frying of bacon induce oxidative stress by measurement of urinary 8-oxo-7,8-dihydro-2 deoxyguanosine, a marker of oxidatively damaged DNA. Three non-smoking women fried bacon for 3 h. Urine samples were taken as early morning void at the same time on four days; the morning before frying, the morning after first frying, the morning after three days of frying and one week after first urine sample. 8-Oxo-7,8-dihydro-2 deoxyguanosine, 1-hydroxypyrene and 2-hydroxyphenanthrene, metabolites of polycyclic aromatic hydrocarbons, were measured by liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS). 8-Oxo-7,8-dihydro-2 deoxyguanosine correlated weakly with concentrations of 1-hydroxypyrene (r = 0.31, p = 0.042), but it did not correlate with 2-hydroxyphenanthrene (r = ?0.074; p = 0.64). Average urinary 8-oxo-7,8-dihydro-2 deoxyguanosine concentrations increased from the day before frying (16.3 ± 4.2 nmol/L) to the third day of frying (26.2 ± 10.2 nmol/L), although not statistically significantly. Our pilot study shows that frying of bacon may result in increased oxidative stress which further emphasises the possible carcinogenic potential of cooking fumes.     

Effect of prochloraz fungicide on biotransformation enzymes and oxidative stress parameters in three-spined stickleback (Gasterosteus aculeatus L.)

The aim of this study was to characterize biomarker responses in three-spined sticklebacks exposed to prochloraz (Pcz). For this purpose, adult sticklebacks were exposed for 2 weeks to prochloraz at 0, 10, 50, 100 and 500 μg/L prior to one week of depuration in clean water. At days 7, 14 and 21, several hepatic biomarkers were measured including 7-ethoxyresorufin-O-deethylase (EROD), glutathione-S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT), total glutathione (GSH) content and thiobarbituric acid reactive substances (TBARS). Pcz induced a transient increase of antioxidant enzymes and a depletion of glutathione content during the first 7 days of exposure. This study showed that EROD activity and antioxidants were disrupted in a transient manner. GST was rapidly induced in a dose-dependent manner and this induction was persistent and observed also after depuration. GST appeared as a valuable biomarker to assess the exposure to Pcz.     

Cytotoxicity and DNA damage of five organophosphorus pesticides mediated by oxidative stress in PC12 cells and protection by vitamin E

Previous studies have demonstrated that pesticides could induce cytotoxicity and genotoxicity in vivo and in vitro, and that oxidative stress may be an important factor involved. However, investigations comparing the capability of different organophosphorous (OP) compounds to induce cytotoxicity, genotoxicity and oxidative stress are limited. Hence, the aim of this paper was to access the cytotoxic and genotoxic effects of five OPs or metabolites, Acephate (ACE), Methamidophos (MET), Chloramidophos (CHL), Malathion (MAT) and Malaoxon (MAO), and to clarify the role of oxidative stress, using PC12 cells. The results demonstrated that MET, MAT and MAO caused significant inhibition of cell viability and increased DNA damage in PC12 cells at 40 mg L^?1. MAO was more toxic than the other OPs. ACE, MET, MAT and MAO increased the levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA), and decreased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) at 20 mg L^?1 and 40 mg L^?1 to different degrees. Pre-treatment with vitamin E(600 μM)caused a significant attenuation in the cytotoxic and genotoxic effect; pre-treatment reversed subsequent OP-induced elevation of peroxidation products and the decline of anti-oxidant enzyme activities. These results indicate that oxidative damage is likely to be an initiating event that contributes to the OP-induced cytotoxicity.