Postnatal management and outcome for fetal-diagnosed intra-cerebral cystic masses and tumours

The increasing availability and resolution of non-invasive prenatal imaging has increased our ability to diagnose accurately a wide variety of fetal anomalies. It has also resulted in the serendipitous discovery of ‘lesions’ that may have little clinical impact upon the child's subsequent development although their ability to raise parental anxiety can be great. The purpose of this review is to put the postnatal clinical relevance of some of these findings into their proper context. Copyright © 2009 John Wiley & Sons, Ltd.     

Sonography of fetal cerebrospinal anomalies

Congenital anomalies of the central nervous system (CNS) are among the most frequent malformations. Current ultrasound equipment can give a precise diagnosis of many of these lesions from early gestation. High-resolution transvaginal probes play a major role both in allowing an early diagnosis and for better defining subtle details of both normal and abnormal cerebral anatomy. The diagnostic accuracy of prenatal ultrasound is, however, heavily dependent upon the expertise of the sonologist, the type of equipment employed, and the time dedicated to the scan. Fetal sonography is effective in identifying neural tube defects, although alpha-fetoprotein screening seems to give a greater sensitivity. The accuracy of ultrasound in the identification of CNS malformations other than neural tube defects remains unclear because of the ascertainment biases of the few large prospective studies that have been conducted to date. Copyright © 2002 John Wiley & Sons, Ltd.     

Cardiotocographic and sonographic findings in two cases of antenatally diagnosed intrauterine fetal brain death

Intrauterine fetal brain death is a rare cause of a fixed fetal heart rate pattern. Seven cases have been previously reported in the literature, but only two of them were diagnosed prenatally and all the newborns died soon after delivery. Two additional cases of antepartum diagnosis of intrauterine fetal brain death, managed expectantly, are reported. We had the unique opportunity to document progressive sonographic cerebral changes during the follow-up period, following the neurological event, while the fetus continued life and growth in utero. The cardiographic and sonographic findings suggesting intrauterine fetal brain death were a prolonged fixed fetal heart rate, even following a vibroacoustic and contraction stress test; an atonic fetus without breathing and body movement; and the appearance of hydramnios and the development of ventriculomegaly.     

Toxicity of 4-methylimidazole on isolated brain mitochondria: using both in vivo and in vitro methods

4-methylimidazole (4MI) is a compound widely used in various industrial and consumer applications. The most important sources of exposure include chemical caramel coloring, ammoniated molasses, dyes and pigments, rube, cleaning and agricultural chemicals. Toxicity attributed to 4MI in foods has recently become a focus of research. Recent studies showed that 4MI induced adverse changes in various target tissues. Brain is known to be a target organ for 4MI-induced toxicity but its cytotoxic mechanisms have not yet been elucidated. In this study, experiments were divided into two parts: (1) using in vivo methodology, doses of 4MI at 100, 200, or 300 mg/kg were administered orally to mice daily for 14 to obtain brain mitochondria; and (2) utilizing in vitro methodology, brain mitochondria were incubated with 4MI at 400, 800, or 1600 μM concentrations. Subsequently, the neurotoxicity of 4MI was assessed using mitochondrial dysfunction tests, including reactive oxygen species (ROS) formation, mitochondrial membrane potential (MMP) collapse, mitochondrial swelling, and cytochrome c release. Our results from both in vivo and in vitro experiments on isolated brain mitochondria showed a significant decrease in complex II activity and also marked elevation in the ROS formation, MMP collapse, mitochondrial swelling, and enhanced release of cytochrome c. Data indicated that 4MI induced neurotoxicity through the impairment of electron transfer chain especially at complex II and elevated ROS formation leading to subsequent oxidative stress events including mitochondrial membrane depolarization, mitochondrial swelling, and release of cytochrome c, which is the starting point of mitochondrial-mediated apoptosis signaling and neurodegeneration.     

Organophosphate dichlorvos induced dose‐related differential alterations in lipid levels and lipid peroxidation in various regions of the fish brain and spinal cord

Abstract

The effect of dichlorvos (DDVP) (0–0, dimethyl 2: 2‐dichlorovinyl phosphate), on various lipid fractions and lipid peroxidation in the discrete areas of the brain and spinal cord were studied in the fresh water teleost (Heteropneustes fossilis). Fishes were exposed to three different doses (3.0, 6.0 and 9.0 ppm) of DDVP daily for 7 days. Dose‐related increase in the levels of total lipids, cholesterol and esterified fatty acids was detected in the fore brain, optic lobes, cerebellum, medulla oblongata and spinal cord. However, phospholipids were significantly decreased in the aforementioned regions of the central nervous system. The rate of lipid peroxidation was significantly increased in all the regions of the CNS.     

Differential protective effects of motorcycle helmets against head injury

Background: Although numerous observational studies have demonstrated a protective effect of motorcycle helmets against head injury, the degree of protection against specific head injury types remains unclear. Experimental biomechanics studies involving cadavers, animals, and computer models have established that head injuries have varying etiologies. This retrospective cross-sectional study compared helmet protection against skull fracture, cerebral contusion, intracranial hemorrhage, and cerebral concussion in a consecutive series of motorcycle operators involved in recent traffic crashes in Kentucky.

Methods: Police collision reports linked to hospital inpatient and emergency department (ED) claims were analyzed for the period 2008 to 2012. Motorcycle operators with known helmet use who were not killed at the crash scene were included in the study. Helmet use was ascertained from the police report. Skull fracture, cerebral contusion, intracranial hemorrhage, and cerebral concussion were identified from International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes on the claims records. The relative risks of each type of head injury for helmeted versus unprotected operators were estimated using generalized estimating equations.

Results: Helmets offer substantial protection against skull fracture (relative risk [RR] = 0.31, 95% confidence interval [CI], 0.23, 0.34), cerebral contusion (RR = 0.29, 95% CI, 0.16, 0.53), and intracranial hemorrhage (RR = 0.47, 95% CI, 0.35, 0.63). The findings pertaining to uncomplicated concussion (RR = 0.80, 95% CI, 0.64, 1.01) were inconclusive. A modest protective effect (20% risk reduction) was suggested by the relative risk estimate, but the 95% confidence interval included the null value.

Conclusions: Motorcycle helmets were associated with a 69% reduction in skull fractures, 71% reduction in cerebral contusion, and 53% reduction in intracranial hemorrhage. This study finds that current motorcycle helmets do not protect equally against all types of head injury. Efforts to improve rotational acceleration management in motorcycle helmets should be considered.     

邻苯二甲酸二丁酯对KM小鼠神经行为学的影响及芒果苷的拮抗作用

探究邻苯二甲酸二丁酯(DBP)对小鼠神经行为学影响的剂量-反应关系,以及芒果苷(MAG)的拮抗作用。36只性成熟雄性KM小鼠随机分为4组:(1)生理盐水组,(2) 5 mg·kg~(-1)DBP组,(3) 25 mg·kg~(-1)DBP组,(4)125 mg·kg~(-1)DBP组,实验周期28d。应用国际通用的高架十字迷宫(EPM)和旷场实验(OFT)检测DBP暴露后KM小鼠的神经行为学变化;通过脑组织病理学切片,检测KM小鼠的靶组织脑海马CA1区病理变化;通过测定活性氧(ROS)、谷胱甘肽(GSH)、丙二醛(MDA)、DNA-蛋白质交联系数(DPC),检测KM小鼠的脑海马组织氧化损伤水平。以MAG作为抗氧化剂,36只KM小鼠随机分为4组:(1)生理盐水组,(2) 50 mg·kg~(-1)MAG组;(3) 125 mg·kg~(-1)DBP组;(4) MAG+DBP组,进行神经行为测试,同时评估各组KM小鼠脑海马组织氧化损伤。与对照组比较,随着DBP暴露剂量的升高,125 mg·kg~(-1)DBP组KM小鼠进入开放臂次数减少,停留时间偏短,运动距离较短,运动轨迹偏离中央区域;脑海马CA1区锥体神经细胞排列紊乱,细胞形态肿胀变形,树突缩短甚至消失;且脑系数下降,ROS、MDA含量及DPC系数逐渐上升,GSH含量逐渐降低,且差异均有统计学意义(P0.05, P0.01);加入拮抗剂MAG处理后,与125 mg·kg~(-1)DBP组比较,MAG+DBP组小鼠神经行为学出现一定程度的缓解,脑海马CA1区病理程度减轻,脑系数上升,ROS、MDA含量及DPC系数出现一定程度的下降,GSH含量出现一定程度的上升,且差异均有统计学意义(P0.05, P0.01)。DBP所致小鼠的神经行为学变化可能与脑海马组织的氧化损伤有关; MAG可通过降低小鼠脑组织氧化应激水平,对DBP暴露所致的小鼠神经行为学影响起到一定的保护作用。     

稀土元素的脑部蓄积性、毒性及其对人群健康的潜在危害

论述了稀土元素在动物脑部的蓄积性、对脑的毒性以及稀土区人群的脑部毒性效应，分析了稀土农业应用和稀土厂“三废”对生态环境和人群健康的潜在危害。     

充分利用"外脑"资源促进高等职业教育的改革与发展

面对诸多机遇和挑战,高等职业教育院校的竞争将愈加激烈;高等职业教育院校的主办者和管理者也将面临越来越严峻的考验.因此,若想跟上时代的步伐,适应社会的需求,仅靠自身的力量是远远不够的.联系我校发展实际,我们体会到,充分利用"外脑"资源可以促进信息交流与观念更新;促进产学研合作;促进学习型组织的形成;促进内部沟通状况的改善;促进客观公正地诊断与处理问题;促进管理决策的科学化和有效性.     

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。