Assessment of the neurotoxicity of intramuscular artemether in mice

Artemether has been shown to be a very reliable antimalarial drug particularly because of its potency against multidrug resistant strain of malaria parasite; however, there is concern about its potential toxic effects. This study was designed to evaluate the neurotoxic effect of artemether using a mouse model. The photomicrographs of brains of the mice in the different artemether treated groups showed neurodegeneration. This observation is an indication that artemether may be neurotoxic in mice.     

Histopathological impact of industrial wastewater on the vital organs of Oreochromis mossambicus

The acute toxicity of paper mill wastewater to Oreochromis mossambicus was investigated with the lethal concentration (LC50) value 6.5% for 96?h exposure. This concentration was used as a baseline to study the effects of paper mill effluent on histopathological changes in gills, liver, kidney, and brain of fish. In the gills, filament cell proliferation, cellular infiltration, hemorrhage, and epithelial lifting were observed. In the liver, vacuolation of hepatocytes and necrosis were noted. In kidney, exfoliation and swollen with pyknotic nuclei were identified. Similarly, the brain also showed enlarged pyramidal cells, binucleated nuclei, vacoulation, and necrosis. These changes occurred predominantly in 21days following exposure of fish to the industrial waste water. Paper mill wastewater was found to be highly toxic to fish.     

Impact of environmental concentrations of beta-cypermethrin on the antioxidant system in the brain and liver of zebrafish (Danio rerio)

Beta-cypermethrin (beta-CYP) is a widely used pyrethroid pesticide, the extensive application of which may potentially cause damage to non-target organisms. To investigate the effect of beta-CYP on the antioxidant system of aquatic animals, adult zebrafish were exposed to environmentally relevant dosages (0.01, 0.1 and 1.0 μg/L) of beta-CYP. The activities of four antioxidant enzymes in zebrafish liver and brain tissue were tested after 7, 15 and 30 days of exposure. Our results showed that exposure of beta-CYP could induce different levels of increase in hepatic superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPx) activities at 7 and 15 days post exposure (dpe), but caused apparent inhibition of hepatic SOD, GR and GPx activities at 30 dpe. Unlike in liver tissue, SOD and CAT activities in zebrafish brain did not show any apparent response to beta-CYP during the whole treatment period. In addition, increased brain GPx activities were observed at 7 and 30 dpe.     

二氧化硫吸入对大鼠脑组织细胞的氧化损伤作用

研究了低浓度二氧化硫(SO₂ ) 对大鼠中枢神经系统毒理作用的机理,以及SO₂ (28mg/m³)吸入对大鼠脑组织细胞抗氧化酶活性和脂质过氧化水平的影响.结果表明,SO₂吸入可引起超氧化物歧化酶(Cu、Zn-SOD)活性降低、谷胱甘肽过氧化物酶(GSH-Px)活性升高、过氧化氢酶(CAT)活性无明显改变以及脑组织脂质过氧化水平显著升高.这些结果意味着SO2通过产生活性氧自由基引起脂质及其他生物大分子的氧化损伤,可能是低浓度SO₂毒理作用的机制之一.     

纳米硫硒化镉对小鼠肾脏和脑组织SOD活力和MDA含量的影响

为了探讨纳米硫硒化镉(CdSeS)对小鼠肾脏和脑组织的急性氧化损伤作用,将20只雄性昆明小鼠随机分成4组,采用尾部静脉注射进行一次性染毒,3个染毒组分别注入0.1、0.2、0.4mg·mL-1的纳米CdSeS粉末(20～30nm)悬液1mL,对照组注入等体积生理盐水.染毒3d后对肾脏和脑组织匀浆中超氧化物歧化酶(SOD)活力和丙二醛(MDA)含量分别进行测定,从而检测纳米CdSeS对肾脏和脑组织的急性氧化损伤作用.结果显示,随着纳米CdSeS染毒浓度的升高,小鼠肾脏和脑组织中SOD活力呈逐渐降低趋势,而MDA含量呈逐渐升高趋势,均显示出一定的剂量-效应关系;较高浓度组(肾:ρCdSeS≥0.2mg·mL-1;脑:ρCdSeS≥0.4mg·mL-1)SOD活力、MDA含量与对照具有显著性差异(p<0.05,p<0.01),而较低浓度组则没有显著性差异(p>0.05).以上结果提示纳米CdSeS能够对小鼠肾脏和脑组织造成氧化损伤,并且能穿过血脑屏障作用于脑部。     

邻苯二甲酸二乙基己酯（DEHP）对金鲫鱼脑细胞DNA的损伤

为了研究邻苯二甲酸二乙基己酯(DEHP)对金鲫鱼(Carassius auratu)脑细胞DNA的损伤作用,采用不同浓度的DEHP溶液(0、25、50、100、200mg·L-1)对体外培养脑细胞进行染毒,应用单细胞凝胶电泳(彗星实验)检测脑细胞DNA的损伤效应.结果表明,染毒1.5h后,与对照组相比,DEHP各染毒组细胞尾部DNA百分率(Tail DNA%)和尾矩(Tail Moment)均显著升高(p<0.01),即DEHP染毒引起了脑细胞DNA的严重断裂;随着DEHP浓度的增加,DNA损伤程度加剧,细胞尾部DNA百分率及尾距与DEHP染毒浓度呈明显的剂量-效应关系.以上结果表明,DEHP可导致金鲫鱼脑细胞DNA损伤。     

噪声对脑、心脏、肝脏元素影响的研究

采用原子吸收法,试图从元素方面探讨强噪声暴露对机体重要器官的元素代谢的影响。结果发现与对照组相比经强噪声暴露后,脑、心脏、肝脏的元素锌、脑的元素钙及心肌的元素镁均呈极显著减少;而脑、心脏、肝脏的元素铜及心、肝脏的元素钙则呈极显著增加。在停止强噪声暴露后第5d,上述4种元素代谢仍没有恢复正常。结果表明：强噪声使机体重要器官的元素代谢严重障碍。提示强噪声环境是引起心脏病的原因之一,可能与强噪声使心肌元素代谢严重失调有关。     

考虑道路状况的应急配发站启用以及配送优化问题*

为了研究应急物资配发站启用及配送方案优化问题，综合考虑灾难事件下的道路损毁状况、道路复杂程度、需求不确定以及物资拆分配送等特点，以应急物资配发站启用成本、车辆启动成本、运输成本之和最小化为目标，建立应急物资配发站启用及配送模型，设计头脑风暴优化算法，结合算例，对该问题进行仿真，并将结果与遗传算法进行对比，验证模型的可行性和算法的有效性。结果表明，在决策时考虑道路状况能够有效降低系统成本，提高救援效率。     

Prediction of probability of fatality due to brain injury in traffic accidents

Abstract

Objective: Fatal brain injuries result from physiological changes in brain tissues, subsequent to primary damage caused by head impact. Although efforts have been made in past studies to estimate the probability of brain injury, none of them involved prediction of such physiological changes. The goal of this study was to evaluate the fatality prediction capability of a novel approach that predicts an increase in intracranial pressure (ICP) due to primary head injury to estimate the fatality rate using clinical data that correlate ICP with fatality rate.

Methods: A total of 12 sets of head acceleration time histories were used to represent no, severe, and fatal brain injury. They were obtained from the literature presenting head kinematics data in noninjurious volunteer sled tests or from accident reconstruction for severe and fatal injury cases. These were first applied to a Global Human Body Models Consortium (GHBMC) head–brain model to predict nodal displacement time histories of the brain, which were then fed into FEBio to predict ICP. A Weibull distribution was applied to the data for the relationship between fatality rate and ICP obtained from a clinical paper to estimate fatality rate from ICP (procedure A). Fatality rate was also estimated by applying the temporal and spatial maximum value of maximum principal strain (MPS_max) obtained from the GHBMC simulation to an injury probability function for MPS_max (procedure B). Estimated fatality rates were compared between the 2 procedures.

Results: Both procedures estimated higher average fatality rate for higher injury severity. The average fatality rate for procedure A without ischemia representation and procedure B was 72.4 and 51.0% for the fatal injury group and 8.2 and 21.7% for the severe injury group, respectively, showing that procedure A provides more distinct classification between fatal and nonfatal brain injury. It was also found that representation of ischemia in procedure A provides results sensitive to injury severity and impact conditions, requiring further validation of the initial estimate for the relationship between brain compression and ischemic cell death.

Conclusions: Prediction of the probability of fatality by means of a combination of simulations of the primary brain deformation and subsequent ICP increase was found to be more distinct compared to the prediction of primary injury alone combined with the injury probability function from a past study in the select 12 head impact cases.     

Proteomics analysis of zebrafish brain following chronically exposed to bisphenol A

Bisphenol A, a plastic monomer and plasticizer, is a well-known endocrine disrupter, widely present in the aquatic environment, but little is known regarding its neurotoxicity in fish. Herein, we investigated its effects on male zebrafish brain. Zebrafish were exposed to 10 µg/L BPA for 45 days. An isobaric tags for relative and absolute quantitation approach coupled with nano high-performance liquid chromatography-tandem mass spectrometry analysis was employed to detect and identify differentially expressed proteins. A total of 46 proteins was identified and categorized into functional classes that mostly included metabolism and transport, cytoplasm and organelle, ion and nucleotide binding, indicating that bisphenol A toxicity in fish brain is complex. The biological pathways of starch and sucrose metabolism, calcium signaling, and aminoacyl-tRNA biosynthesis were also induced. Proteomic analyses add new perspectives to bisphenol A neurotoxicity in aquatic organisms.