Traumatic brain injury-related hospitalizations and deaths among American Indians and Alaska natives — United States, 2008–2014

IntroductionDespite progress, injury remains the leading cause of preventable death for American Indian and Alaska Natives (AI/AN), aged 1 to 44. There are few publications on injuries among the AI/AN population, especially those on traumatic brain injury (TBI). A TBI can cause short- or long-term changes in cognition, communication, and/or emotion. Methods: To describe changes over time in TBI incidence by mechanism of injury, injury intent, and age group among AI/ANs, the CDC analyzed hospitalization and death data from the 2008–2014 Healthcare Cost and Utilization Project (HCUP) National Inpatient Sample (NIS) and the National Vital Statistics System (NVSS), respectively. Results: From 2008-2014, the incidence of TBI-related hospitalizations increased by 32% (1,477 in 2008 to 1,945 in 2014) and resulted in a 21% increase in age-adjusted rates of people hospitalized with TBI. TBI-related deaths increased in number (569 in 2008 to 644 in 2014) and age-adjusted rate (22.7 in 2008 to 25.4 in 2014) by approximately 13% and 12%, respectively. Motor-vehicle crashes were the leading cause of TBI-related deaths among AI/ANs aged 0–54 years. Practical application: Prevention efforts should focus on increasing motor-vehicle safety and advancing prevention strategies for other leading causes of TBI, including: falls, intentional self-harm, and assaults.     

The Structure of Energy Supply for Tissue Adaptation in Small Mammals Differing in Ecological Specialization

Multivariate factor analysis of the data on liver bioenergetics of mountain and forest voles has been performed. The specific features of tissue energy metabolism are best differentiated in the space of characters pertaining to the succinic acid oxidation system. The role of the dominant oxidation substrate in the structure of energy supply for the adaptation of tissue to a set of environmental factors in specialized and widespread species is discussed.     

妊娠小鼠子宫对2,3,7,8-四氯苯二噁英毒性的敏感性研究

对妊娠早期小鼠用不同剂量的TCDD进行处理，妊娠第9天采集血清、肝、肾、脑、脂肪、子宫和胎儿等样品，利用酵母报道基因系统进行组织中TCDD含量检测，结果发现脂肪中TCDD含量最高，其次是肝脏、子宫和胎儿．由于TCDD的毒性需通过体内包括细胞色素P4501A2在内的代谢酶的活化，采用免疫组化的方法对TCDD诱导的该酶的表达水平进行了检测，发现肝脏和子宫的阳性反应最强，并且所需剂量很低，肾脏和脂肪组织在较高剂量出现阳性反应，而脑组织则仅在更大剂量时出现微弱的阳性信号．此现象说明子宫和肝脏一样，可以通过芳香烃类受体诱导细胞色素P4501A2酶的产生，活化TCDD，引起对细胞的毒性并产生对胚胎的毒性．在低剂量时观察到的强烈的生殖毒性应该和TCDD在子宫的蓄积和子宫内敏感的细胞色素P4501A诱导能力有关．     

HPLC荧光检测法测定SO2吸入后小鼠脑、心和肺亚硫酸盐水平

为了探讨二氧化硫(SO2)吸入后是否可进入小鼠不同组织器官,运用高效液相色谱(HPLC)荧光检测(FD)法测定了SO2动式吸入后雄性小鼠脑、心和肺组织中SO2在体内的衍生物--亚硫酸盐含量组织匀浆液经还原、衍生和沉淀蛋白,取上清液进入色谱仪检测.亚硫酸盐测定标准曲线在0.126 μg·mL-1～126 μg·mL-1有良好的线性关系,检测限为0.04μg·mL-1(S/N=3),测定方法的回收率在97%～101%之间,日内和日间的精密度RSD低于9%.分析结果表明,SO2吸入后小鼠3种器官组织中亚硫酸盐含量比对照组显著增加(P＜0.05),且与SO2浓度呈明确的剂量效应关系(r＞0.92).这说明SO2被小鼠吸入后转化为亚硫酸盐并可分布到肺和其它器官如脑和心等,从而为SO2是一种全身性毒物的观点提供支持.此外,本文对HPLC荧光检测亚硫酸盐的方法作了改进,为研究SO2及其衍生物的毒作用提供了更为有效的方法.     

菊花组培快繁技术研究

以菊花嫩茎段为材料,进行无菌系建立、芽分化、生根等试验,探讨菊花组培快繁技术.结果表明:(1)以MS BA2.0 mg.L-1 NAA0.1 mg.L-1(单位下同)为培养基,分别置于普通培养室(不开灯,200~500 lux)与人工气候箱中培养,在前者条件下基本上不诱导芽的形成,25天后有部分黄白色愈伤组织形成;而在人工气候箱中培养则产生丛生芽,每茎段在30 d后可形成8~10个丛生芽.(2)分别以①MS BA1.0 NAA0.1,②MS BA2.0 NAA0.1,③MS BA3.0 NAA0.1为增殖培养基,培养25 d后芽增殖3.65~5.90倍.(3)在a.1/2MS NAA0.2;b.1/2MS IAA0.2;c.1/2MS IBA0.2共三个培养基中进行生根培养,生根率均达100%,但前两个培养基中长出的根系细长、数量少,而后一个培养基则根系粗短、数量多.     

不同抗生素种类及浓度对麻疯树培养的影响

以麻疯树(jatropha ctrcas)的子叶、真叶、根及其对应的愈伤组织作为实验材料,研究各种抗生素对其生长的影响;在MS培养基中添加不同浓度和不同种类的抗生素,比较其对麻疯树不同外植体及对应愈伤组织生长的影响.方差分析和总体观察的结果表明,用于筛选转化植株的最佳抗生素是卡那霉素,其最佳抗性筛选浓度范围为10～25mg/L.表9参10     

邻苯二甲酸二异壬酯单独暴露及与褪黑素联合作用对小鼠脑组织损伤研究

人类神经系统成熟的海马神经元细胞不能进行复制与自我修复,导致了神经系统易受到环境污染物损伤的风险.邻苯二甲酸二异壬酯(Diisonyl phthalate,DINP)是一种增塑剂替代产品,类雌激素作用较弱,正受到欧盟的推广使用.虽然目前已有一些研究表明了DINP的毒性,但有关其神经毒性的体内研究国内还较少.因此,本研究探讨了DINP单独暴露及与褪黑素联合作用对小鼠脑组织的影响.行为学分析显示,经灌胃200 mg·kg~(-1)·d~(-1)的DINP会导致小鼠行为学出现明显变化;脑组织病理学观察、免疫组化分析(半胱氨酸蛋白酶3(Caspase-3)、胶质纤维酸性蛋白(GFAP))、氧化应激水平检测(活性氧簇(ROS)、还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)活性、8-羟基脱氧鸟苷(8-OH-d G)、DNA-蛋白质交联(DPC))、炎症水平检测(肿瘤坏死因子ɑ(TNF-ɑ)、白介素1β(IL-1β))结果显示,小鼠脑组织海马区出现了病理学损伤,氧化应激和炎症水平上升(p0.01).DINP处理后予以50 mg·kg-1·d-1的褪黑素可以降低氧化应激水平,对小鼠脑组织海马区起到保护作用.以上数据表明,实验剂量(200 mg·kg~(-1)·d~(-1))DINP处理后可以导致小鼠脑组织损伤,同时予以褪黑素可以在一定程度上缓解这种损伤.     

A 6-year survey of road traffic accidents in Southwest China: Emphasis on traumatic brain injury

Background: The objective of this study is to provide an up-to-date overview of the patterns of injuries, especially traumatic brain injury (TBI) caused by RTAs and to discuss some of the public health consequences. Methods: A scientific team was established to collect road traffic accidents occurring between 2013 and 2018 in Chongqing, Southwest China. For each accident, the environment-, vehicle-, and person- variables were analyzed and determined. The overall injury distribution and TBI patterns of four types of road users (driver, passenger, motorcyclist and pedestrian) were compared. The environmental and time distribution of accidents with TBI were shown by bar and pie chart. The risks of severe brain injury whether motorcyclist wearing helmets or not were compared and the risk factors of severe TBI in pedestrian were determined by odds ratio analysis. Results: This study enrolled 2131 accidents with 2741 persons of all kind of traffic participants, 1149 of them suffered AIS1+ head injury and 1598(58%) died in 7 days. The most common cause of deaths is due to head injury with 714(85%) and 1266(79%) persons died within 2 hours. Among 423 persons suffered both skull fracture and intracranial injury, 102 (24.1%) have an intracranial injury but no skull fractures, while none of the skull fractures without intracranial injury was found. Besides, motorcyclists without a helmet were at higher risks for all the brain injury categories. The risk of pedestrian suffering severe TBI at an impact speed of more than 70 km/h is 100 times higher than that with an impact speed of less than 40 km/h. Conclusion: It is urgently needed to develop a more reliable brain injury evaluation criterion for better protection of the road users. We believe that strengthening the emergency care to head injury at the scene is the most effective way to reduce traffic fatality.     

Aluminum interaction with human brain tau protein phosphorylation by various Kinases

Abstract

Phosphorylation is an indispensable process for energy and signal transduction in biological systems. AlCl₃ at 10 nM to 10 uM range activated in‐vitro [γ‐³²P)ATP phosphorylation of the brain (tau) T protein in both normal human or E.coli expressed T forms; in the presence of the kinases P34, PKP, and PKC. However, higher concentrations of ALCl₃ inhibited the T phosphorylation with P34, PKP, and PKC to a maximum at 1 mM level. AlCl₃ at 100 uM to 500 uM range induced non‐enzymatic phosphorylation of T with γ‐ATP, γ‐GTP, and α‐GTP. AlCl₃ activated histone phosphorylation by P34 in a similar pattern. The hyperphosphorylation of T by Al³⁺ was accompanied by molecular shift and mobility retardation in SDS‐PAGE. This may demonstrate the mechanism of the longterm neurological effect of Al³⁺ in human brain leading to the formation of the neurofibrillary tangles related to Alzeheimer's disease.