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.     

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.     

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。     

基于关键区海温的华南香蕉寒害长期预报模型探讨

根据华南地区10个代表站点1961-2005年的气候资料、海温资料、历史灾情记录对华南香蕉寒害长期预报模型进行了研究。结果表明,构造的华南香蕉寒害指数与前人研究和历史灾情记录吻合,可以代表华南香蕉寒害的强弱。通过相关分析,找出了影响华南冬季寒害的前期夏季海温关键区为（5°S~5°N,170°~120°W）、（50°~60°N,180°~140°W）、（20°~30°N,140°~110°W）、（30°~40°N,140°~150°E）、（40°~50°N,150°~170°E）,关键区海温对华南冬季寒害影响具有明确的物理意义。利用逐步回归分析,以关键区海温为自变量建立了华南香蕉寒害长期预报模型。其中1961-1990年的数据用于建模,1991-2004年数据用于模型检验。模型拟合准确率和预报准确率均高于88%,这表明此模型具有较高的精度。     

紫外辐射(UV-BC)对47种植物叶片的表观伤害效应

采用叶片实验法研究了模拟紫外辐射(UV-BC)胁迫对47种植物叶片伤斑面积、叶绿素含量的影响.实验结果表明,叶片伤害面积和叶绿素含量的变化与紫外辐射剂量[辐射强度(T_n)×辐射时间(d)]成正相关关系.实验确定了47种植物的紫外辐射伤害阈值,并根据叶片伤害值对植物抗紫外辐射能力进行了排序.     

工伤总估校正发生率及工伤发生时间分析

为完整地了解总的工伤发生率，探讨工伤发生的时间分布规律，在某厂调查了１９８８～９１年工伤发生情况。用俘获——再俘获（Ｃ－Ｍ）方法估计总的工伤发生率。结果表明，若按安环科登记的工伤记录，四年共发生工伤２００人次，粗发生率为１０．０‰；但是，若用安环科和卫生科两个来源收集到的工伤人次数，以Ｃ－Ｍ的方法估计，总的工伤发生人次数为５３３，总估校正发生率为２６．７‰。安环科工伤登记的工伤仅是全部工伤的５０．７％，漏记率为４９．３％。工伤发生率在年龄小于２０岁和工龄小于５年的最高．工伤多发生在一年中的第三季度和三月份；一星期中，周一工伤最多；一天中工伤发生在早班最多，占５８．２％，而发生在工作后１—２小时之间也最多，占２３．７％，上午９—１０点之间是工伤发生最多的时段（占１７．５％）。     

汞污染地区粮食对大鼠脑组织氧化损伤影响

应用典型汞矿和典型化工厂粮食对大鼠进行暴露,研究了大鼠脑组织中MAD、SOD、GSHPx以及脑汞含量的变化情况。结果表明,与对照组相比,经过7d暴露后,清镇组大鼠及万山组大鼠脑汞蓄积均出现显著性差异(清镇,p<0.05;万山,p<0.01)。生理生化指标结果表明,暴露3d后,清镇组脑组织GSHPx与对照组相比有显著差异(p<0.05);暴露7d后,万山组脑组织GSHPx及MDA与对照组相比有显著性差异(GSHPx,p<0.05;MDA,p<0.01),清镇组脑组织各指标与对照组相比均有显著性的差异(p<0.05),证明经7d暴露后,大鼠脑组织中已产生脂质过氧化损伤。进而表明上述两处典型汞污染地区汞污染极为严重,可能已经通过食物链严重影响到当地公众健康与安全。     

环境污染健康损害补偿办法探究——以中国现行人身损害赔偿法为借鉴

随着社会经济的迅猛发展,环境污染问题日益加重,由此造成的居民健康损害事件和案件逐年增多,但缺乏有效的解决途径和办法。环境污染健康损害作为一种新型的人身损害,有其自身的特点,因此需要针对其特殊性制定合理、有效的环境污染健康损害补偿办法,来保护和救济环境污染健康损害受害人,以维护社会安定团结和人民健康幸福。文章通过分析中国现行人身损害赔偿法律法规中赔偿项目、标准及计算方法,以求对制定环境污染健康损害补偿办法有所启示。