Analysis of posttraumatic stress disorder in children with road traffic injury in Wenzhou,China

Objective: Road traffic accidents are the leading health threat to children and cause significant long-term mental health problems. This study aimed to characterize posttraumatic stress disorder (PTSD) in children suffering from road traffic injuries (RTIs) in Wenzhou, China.

Methods: We conducted a retrospective study of 537 children (aged 1 to 13 years old) with RTIs. The epidemiological features, PTSD incidence, clinical manifestation, and risk factors were analyzed based on a customized PTSD risk factor questionnaire. The outcome factors were also evaluated by means of the logistic regression method.

Results: The PTSD incidence was 24.77% in children with RTIs. The incidence of PTSD was related to the personality, family environment, and family care of the children. It was found that early psychological intervention and reasonable family care from the family might promote physical and mental welfare as well as contribute to the development of more effective treatments to prevent PTSD.

Conclusion: For susceptible children, in addition to dealing with the somatic injury, psychological intervention and family care should be carried out as early as possible.     

Etiology of fatal thoracic aortic injuries: Secondary data analysis

Objectives: Motor vehicle crashes remain a leading cause of death in the United States (US). Thoracic aortic dissection due to blunt trauma remains a major injury mechanism, and up to 90% of these injuries result in death on the scene. The objective of this study is to understand the modern risk factors and etiology of fatal thoracic aortic injuries in the current US fleet.

Methods: Using a unique, linked, Fatality Analysis Reporting System (FARS) and Multiple Cause of Death (MCOD) database from 2000–2010, 144,169 drivers over 16 years of age who suffered fatal injuries were identified. The merged database provides an unparalleled fidelity for identifying thoracic aortic injuries due to motor vehicle accidents. Thoracic aortic injuries were defined by ICD-10 codes S250. Univariate and multivariate logistic regression models for presence of any thoracic aortic injuries were fitted. Age, gender, BMI weight categories, vehicle class, model year, crash type/direction, severity of crash damage, airbag deployment location, and seatbelt use, fatal injury codes, and location of injury were considered. Odds ratios (OR) and corresponding 95% confidence intervals (95%CI) are calculated.

Results: There were 2953 deaths (2.10%) related to thoracic aortic injuries that met the inclusion criteria. Nearside crashes were associated with an increased odds (OR = 1.42, 1.1-1.83), while rollover crashes (OR =.44,.29-.66) were associated with a reduced odds of fatal thoracic aortic injury. Using backward selection on the full multivariate model, the only significant model effects that remained were vehicle type, crash type, body region, and injury type.

Conclusions: The increased prevalence of fatal thoracic aortic injury in nearside crashes, increasing age, and vehicle type provide some insight into the current US fleet. Important factors, including model year, had significantly lower levels of the injury in univariate analysis, demonstrating the effect of safety improvements in newer model vehicles. Further study of this fatal injury is warranted, including comparisons of those who survive the injury.     

Personal injury recovery cost of pedestrian–vehicle collisions in New South Wales,Australia

Background: There is a need for routine estimates of injury recovery costs from pedestrian collisions using hospital separation records for economic evaluations.

Objective: To estimate the cost of injury recovery following pedestrian–vehicle collisions using the personal injury recover cost (PIRC) equation using key demographic and injury characteristics.

Method: An estimation of the costs of on-road pedestrian–vehicle collisions involving individuals who were injured and hospitalized in New South Wales (NSW), Australia, from 2002 to 2011 using the PIRC equation. The PIRC estimates individual injury recovery costs and does not include costs associated with property damage, vehicle repair, or rescue services. Individual recovery costs associated with severe traumatic brain injury (TBI) were estimated. The injured individual's mean, median, and total injury recovery costs are described for key demographic, injury, and crash characteristics.

Results: There were 9,781 pedestrians who were injured, costing an estimated total of $2.4 billion in personal injury recovery costs, an annual cost of $243 million. Males had a total injury recovery cost 1.7 times higher than females. The median injury recovery cost decreased with increasing age. TBI ($248,491) and spinal cord and vertebral column injuries ($264,103) had the highest median injury recovery costs for the body region of the most severe injury. TBI accounted for 22.6% of the total injury recovery costs for the most severe injury sustained. Just over one third of pedestrians sustained 4 or more injuries, with a median cost of $243,992, which was 1.6 times higher than the cost for a pedestrian who sustained a single injury ($153,682).

Conclusions: Personal injury recovery costs following pedestrian–vehicle collisions where a pedestrian is injured are substantial in NSW. The PIRC equation enables the economic cost burden of road traffic injury to be calculated using hospital separation data. The PIRC enables comprehensive personal injury recovery costs to be estimated and would aid in economic evaluations of preventive strategies in road safety.     

人工纳米材料富勒烯（C60）低剂量长期暴露对鲫鱼的氧化伤害

为更好地判断人工纳米材料(富勒烯,C60)对水生生物的潜在健康危害,以鲫鱼(Carassius auratus)幼鱼为受试生物,研究了低剂量C60(0.04～1.0 mg·L-1)长期(32 d)暴露对鲫鱼的氧化伤害.结果表明,各实验组中鲫鱼幼鱼脑、肝脏、鳃组织中的还原型谷胱甘肽(GSH)含量都发生显著降低(p＜0.05),其中1 mg·L-1 nC60,aq的暴露对鳃组织GSH含量的抑制率为14.3%,高于对鱼脑、肝脏组织中的抑制率;肝脏组织中过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性,以及鳃组织中Na -K -ATP酶活性均被显著激活,其最大活性分别是对照的121.34%(0.04 mg·L-1暴露组)、114.80%(0.04 mg·L-1暴露组)和348.59%(0.20mg·L-1暴露组).实验结果揭示,长期暴露引起机体组织的氧化应激可能是水环境中C60的致毒机制之一.     

贵州主要城市PM2.5的氧化性损伤评价

对贵州省主要城市(贵阳、安顺、遵义、都匀)按季节进行PM_2.5样品的采集,应用质粒DNA评价法研究了贵州省主要城市PM_2.5氧化性损伤能力,并与PM_2.5质量浓度、微量元素含量做相关性分析。结果表明,PM_2.5全样TD₂₀值均小于其相应的水溶样TD₂₀值;四个城市PM_2.5氧化性损伤能力均表现为冬季>秋季>春、夏季;城区PM_2.5氧化性损伤能力强于背景区;研究区内PM_2.5样品的氧化性损伤能力表现为都匀市最强,安顺市最弱;PM_2.5全样和水溶样的TD₂₀值与质量浓度之间无明显相关关系;PM_2.5水溶样的TD₂₀值与相应的12种微量元素的浓度总和呈负相关关系(P<0.05);全样Al、Mn、Cd、Pb的含量与PM_2.5全样TD₂₀值呈明显负相关关系,水溶样Cd、Pb、Cu的含量与PM_2.5水溶样TD₂₀值呈明显负相关关系,表明研究区PM_2.5氧化性损伤可能与样品中水溶性元素Cd、Pb、Cu等的含量有关。     

低剂量长波紫外胁迫下活性污泥硝化活性及氧化应激响应

选取具备良好硝化能力的活性污泥为试验对象,考察其在不同强度（0,0.15,0.39,0.62和1.16μE/（L·s））及不同时间（0,1,2,3和4h）的长波紫外（UVA）辐照下,氨氧化菌（AOB）及亚硝酸盐氧化菌（NOB）活性的响应情况.结果显示：UVA辐照强度的增加对NOB活性产生显著性影响（P<0.01）,而对AOB活性的影响则微乎其微（P>0.05）,且随UVA辐照时间的延长,AOB与NOB之间活性差异越大.动力学拟合结果表明UVA辐照下NOB的衰亡速率（b=0.6938h^-1）远大于AOB （b=0.1423h^-1）,NOB对于UVA辐照的耐受性低于AOB.UVA辐照下AOB与NOB活性差异可能与UVA诱导的氧化应激效应有关,即UVA辐照能够诱导微生物胞内活性氧（ROS）水平的激增,对细胞膜形成氧化性损伤,破坏细胞膜结构完整性,加速微生物走向衰亡.     

强电磁脉冲环境下计算机设备的防护

探讨了强电磁脉冲对计算机设备的损伤机理和破坏作用,介绍了国内外在强电磁脉冲防护领域的研究发展状况,对计算机脉冲防护技术和措施做了详尽的介绍.结合国内外研究现状和发展趋势,建议加强相关领域的研究,并指出今后的研究方向,以提高强电磁脉冲环境下计算机设备的生存能力.     

电化学-臭氧耦合氧化体系的氧化效能

利用电化学-臭氧耦合氧化体系降解了水中的对氯苯酚,从动力学角度探讨了耦合氧化体系降解有机物的协同作用机制.结果表明,电化学与臭氧耦合氧化体系降解4-CP具有明显的协同效果,900 s后,该耦合氧化体系对4-CP和COD的去除率分别为92.7%和64.9%;而单独电解与单独臭氧氧化对上述两者去除率的之和仅有69.7%和30.1%.氧还原产物H2O2浓度和光电流的测试结果表明,电化学-臭氧耦合氧化体系的协同机制包括两部分:即臭氧在阴极表面得到电子生成臭氧负离子;溶解氧在阴极表面发生还原反应生成H2O2.以上2个因素均能有效地促进体系.OH的形成.     

环境汞污染粮食暴露对大鼠脑自由基的诱导及共存硒的影响

采用电子顺磁自旋共振（ESR）技术,研究实地环境汞污染粮食暴露不同时间后在大鼠脑中引发的自由基及脂质过氧化损伤情况,探讨实地环境汞污染氧化损伤的微观致毒机理。并对粮食中共存的硒元素作用进行分析。结果表明,环境汞污染粮食暴露7d后,大鼠脑中自由基相对强度及脂质过氧化产物MDA含量均出现显著升高（p<0.05）。ESR图谱分析表明,环境汞污染粮食暴露诱发大鼠脑中产生烷基自由基（R?）及羟基自由基（?OH）。自由基及MDA水平在暴露前期（<90d）相对稳定,长暴露90d后,自由基及脂质过氧化产物MDA水平有大幅升高（83%,100%）。大鼠脑中汞、硒元素含量7d暴露后均出现显著上升,两元素间有较强相关性,暴露前期大鼠脑中自由基水平相对稳定应与硒的清除作用有关。     

内质网应激在PFOS致大鼠肝损伤中的作用

通过全氟辛烷磺酸(PFOS)28 d大鼠经口染毒评价PFOS肝损伤效应,探讨内质网应激在PFOS毒效应中的作用。Wistar大鼠随机分组,分别以0 mg·kg~(-1)、5 mg·kg~(-1)和10 mg·kg~(-1)PFOS灌胃染毒28 d。HE染色观察大鼠肝脏形态改变。ELISA法测定各组丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)和淀粉酶(AMY)含量变化。紫外分光光度法测定肝组织匀浆中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性变化。RT-PCR检测肝脏内质网应激标志蛋白表达水平。结果表明,PFOS造成大鼠体重降低、肝重增高(P0.05),组织切片显示肝细胞出现脂质沉积。PFOS不同剂量组大鼠ALT随暴露浓度增加,分别为(50.96±10.02)U·L~(-1)、(71.73±11.55)U·L~(-1),显著高于对照组(P0.05),AST、ALP含量与对照组相比显著上升(P0.05),高剂量组AMY水平为(833.46±63.05)U·L~(-1),与对照组相比显著降低(P0.05)。GSH-Px和SOD水平随PFOS浓度增加出现了显著降低(P0.05),而MDA水平显著升高(P0.05)。内质网应激标志蛋白表达均较对照组显著上升(P0.05)。以上结果说明PFOS可导致大鼠肝细胞损伤,其机制可能与内质网应激调控有关。