The Contribution of Pre-impact Posture on Restrained Occupant Finite Element Model Response in Frontal Impact

Objective: The objective of this study was to discuss the influence of the pre-impact posture to the response of a finite element human body model (HBM) in frontal impacts.

Methods: This study uses previously published cadaveric tests (PMHS), which measured six realistic pre-impact postures. Seven postured models were created from the THUMS occupant model (v4.0): one matching the standard UMTRI driving posture as it was the target posture in the experiments, and six matching the measured pre-impact postures. The same measurements as those obtained during the cadaveric tests were calculated from the simulations, and biofidelity metrics based on signals correlation (CORA) were established to compare the response of the seven models to the experiments.

Results: The HBM responses showed good agreement with the PMHS responses for the reaction forces (CORA = 0.80 ± 0.05) and the kinematics of the lower part of the torso but only fair correlation was found with the head, the upper spine, rib strains (CORA= 0.50 ± 0.05) and chest deflections (CORA = 0.67 ± 0.08). All models sustained rib fractures, sternal fracture and clavicle fracture. The average number of rib fractures for all the models was 5.3 ± 1.0, lower than in the experiments (10.8 ± 9.0).

Variation in pre-impact posture greatly altered the time histories of the reaction forces, deflections and the rib strains, mainly in terms of time delay, but no definite improvement in HBM response or injury prediction was observed. By modifying only the posture of the HBM, the variability in the impact response was found to be equivalent to that observed in the experiments. The postured HBM sustained from 4 to 8 rib fractures, confirming that the pre-impact posture influenced the injury outcome predicted by the simulation.

Conclusions: This study tries to answer an important question: what is the effect of occupant posture on kinematics and kinetics. Significant differences in kinematics observed between HBM and PMHS suggesting more coupling between the pelvis and the spine for the models which makes the model response very sensitive to any variation in the spine posture. Consequently, the findings observed for the HBM cannot be extended to PMHS. Besides, pre-impact posture should be carefully quantified during experiments and the evaluation of HBM should take into account the variation in the predicted impact response due to the variation in the model posture.     

土壤及铁锰结核中锰氧化菌的氧化特性分析

利用从土壤铁锰结核及其附近土壤中分离筛选得到的4株锰氧化菌,研究了不同pH、Mn(Ⅱ)初始浓度下菌株的锰氧化效率及生长情况,并用SEM-EDS及TEM对菌株WHS26、GY16形成的生物氧化锰及水羟锰矿进行了表征.结果表明,pH及Mn(Ⅱ)初始浓度对菌株的锰氧化效率均有影响,4株菌在pH 7~8、Mn(Ⅱ)初始浓度为10~20 mmol·L-1时,锰氧化效率最高;GY16、WHS26形成的生物氧化锰的形貌与化学合成的水羟锰矿存在明显差异,前者呈胶膜状附着在菌株表面,后者呈结晶态.该结果可为生物氧化锰应用于重金属污染修复提供技术支撑.     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.     

Influence of hypothyroidism on oxidative stress,c-Fos expression,cell cycle,and apoptosis in rats testes

The molecular basis of male reproduction for cross-regulation between androgen and thyroid hormone axes is still rudimentary. This study aims to define a possible mechanism of hypothyroidism-induced reproductive influence with respect to sex hormone, mineral, sperm motility, oxidative stress, c-Fos expression, cell cycle, and apoptosis in rat testes. The Wistar rats were randomly divided into control group (NS) and hypothyroidism group [1 ml/100g BW/day, 0.1% propylthiouracil (PTU)] by intragastric gavage for 60 days. Blood samples were collected to measure the serum levels. The epididymis was excised to measure sperm motility and testes were excised to measure mineral, oxidative stress, c-Fos expression, cell cycle, and apoptosis. After 60 days, body weight, relative testes weight, triiodothyronine, and total thyroxine were all significantly decreased, whereas thyroid stimulating hormone was increased in the hypothyroidism group. A significant increase in sex hormone level of estradiol (E2) and significant decreases in testosterone (T) and T/E2 ratio were observed following PTU treatment. And sperm quality was also significantly changed. There were significant decreases in the contents of calcium (Ca²⁺) and zinc (Zn²⁺). On the other hand, malondialdehyde and hydrogen peroxide contents significantly increased, whereas the activity of superoxide dismutase, catalase and nitric oxide synthase and nitric oxide content significantly decreased in hypothyroid rats. The mRNA and protein expressions of c-Fos decreased significantly. The cell percentage in G0/G1 phase increased significantly, whereas decreased significantly in S and G2/M phases. Also, a significant increase in testicular cell apoptosis was observed in hypothyroid-treated rats. These results suggested that hypothyroidism could affect reproductive function in the form of changed sex hormone levels, sperm motility and testicular Ca²⁺ and Zn²⁺, and enhanced oxidative stress leading to c-Fos abnormal expression and increased apoptosis.     

围生期毒死蜱暴露致子代8周雄鼠睾丸组织的氧化损伤

毒死蜱是目前全世界使用和销售量最大的有机磷杀虫剂之一。为探讨围生期毒死蜱暴露致8周雄性子鼠睾丸组织的氧化损伤,选择健康Wistar妊娠母鼠于妊娠期(gestation days,GD)第6天至子鼠出生后(postnatal days,PND)21天通过灌胃染毒0、0.75、1.35和2.70 mg·kg~(-1)剂量的毒死蜱,待雄性子鼠8周龄取左侧睾丸实施组织病理学检查,右侧睾丸用以检测丙二醛(maleic dialdehyde,MDA)的含量和谷胱甘肽S转移酶(glutathione S transferases,GST)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、总超氧化物歧化酶(total superoxide dismutase,T-SOD)的活力。结果表明,与对照组比较,随着染毒剂量的增加子鼠体重和睾丸、附睾脏器系数有下降的趋势(P0.05);而MDA呈升高趋势(P0.05)。各组T-SOD和1.35、2.70 mg·kg~(-1)剂量组GSH-Px活力的下降及2.70 mg·kg~(-1)剂量组GST活力的升高均有统计学意义(P0.05)。睾丸组织病理学检查结果可见2.70mg·kg~(-1)剂量组睾丸组织有明显的损伤,管腔中精液量减少,生精细胞脱落增多。上述研究结果提示母鼠于围生期暴露于毒死蜱,可通过氧化损伤诱导子代雄性大鼠睾丸的毒性作用。     

不同粒径微塑料对三氯生在热带爪蛙蝌蚪体内积累分布及其生态毒性的影响

三氯生（TCS）作为药物和个人护理品（PPCPs）中常见的抗菌剂,在水环境中存在与聚苯乙烯微塑料（PS-MPs）复合污染的生态健康风险.本研究旨在探究0.1、5、20 μm PS-MPs吸附TCS在蝌蚪体内累积情况,以及对蝌蚪毒性的作用.结果表明,PS-MPs吸附TCS在蝌蚪体内的积累能力依次为：TCS+5 μm PS组>TCS+20 μm PS组>TCS+0.1 μm PS组,累积量分别为3.27、1.8 mg·g^-1、无累积效应.值得注意的是,蝌蚪经不同粒径PS-MPs（2 mg·L^-1）、TCS（1 μg·L^-1）单独及复合暴露7 d后,各实验组脂质代谢水平均表现出丙酮酸含量增加（p<0.05）、甘油三酯含量降低（p<0.05）的趋势.复合组中TCS+0.1 μm PS组蝌蚪体内丙酮酸（Pyruvate）含量上升水平最显著（p<0.05）;TCS+20 μm PS组蝌蚪体内甘油三酯（TG）含量下降水平最显著（p<0.05）,这可能与脂代谢调控基因ppar-α、cpt1-β表达水平显著提升有关（p<0.05）.此外,PS-MPs、TCS单一和复合暴露 还会增加蝌蚪体内CAT、SOD酶活性.与脂质代谢结果不同的是,复合组中TCS+5 μm PS组蝌蚪体内CAT、SOD酶活性上升最显著（p<0.05）,这可能与调控基因cat、sod表达水平显著提升有关（p<0.05）.研究表明,复合暴露组对蝌蚪生理水平的影响高于单一暴露组,而不同复合处理组对蝌蚪脂质代谢水平和抗氧化水平影响具有差异,该结果可为评估微塑料（MPs）吸附亲脂性污染物对水生动物的毒性效应和生态风险提供 信息和参考.     

代森锰及其代谢物的神经毒性影响与机制研究

以SH-SY5Y和PC12细胞为实验模型,深入探讨了代森锰(Maneb)及其代谢产物对多巴胺能神经细胞的毒性影响与机制.结果表明,Maneb的有机部分和金属离子成分单独暴露不具有明显的毒性作用,联合暴露具有协同效应,且对细胞活性的抑制程度与同一浓度水平的Maneb相当,其原因与诱导活性氧自由基生成、细胞凋亡相关.此外,蛋白免疫印迹法发现,Maneb下调Bcl-2的表达、上调Bax、细胞色素C的水平,同时激活Caspase-3,提示线粒体凋亡途径在Maneb诱导多巴胺能神经细胞凋亡过程中的重要作用.     

Formation of Two Xylem Frost Injuries in One Annual Ring in Siberian Spruce under Conditions of Western Siberian Forest-Tundra

The phenomenon of the formation of two damaged xylem layers in one frost ring is described in Siberian spruce grown in western Siberian forest-tundra. Temperature conditions providing for the formation of pathological cell and tissue structures are determined. The relationship between the formation of double frost injuries and cold periods is demonstrated.     

Biomechanics of Brain and Spinal-Cord Injury: Analysis of Neuropathologic and Neurophysiology Experiments

This study analyzes 46 brain and 48 spinal-cord impact experiments. The velocity of brain impact was 2.0-10.0 m/s and displacement, 0.75-5.0 mm (5.3-33% compression) using a controlled pneumatic impact. The velocity of spinal-cord impact was 1.5-6.0 m/s and displacement, 1.25-3.25 mm (25-65% compression). Brain injury varied from cortical contusion, diffuse axonal injury (DAI), to fatalities, and spinal-cord injury from temporary to complete loss of somatosensory-evoked potentials. Logist functions were determined for each injury severity and various biomechanical parameters, VC, C, V, and combinations. Brain and spinal-cord injury is most strongly correlated to VC, the viscous response. The goodness-of-fit was x² = 22.1, R-0.84 and p< 0.0000 for fatal brain injury, x² = 27.5, R = 0.96 and p< 0.0000 for cortical contusion, and x² = 17.7, R = 0.49 and p < 0.0001 for partial recovery of spinal-cord conduction. Neural tissue is viscoelastic, with a rate-dependent tolerance related to energy absorption. VC is a measure of energy absorption by impact deformation and is predictive of neural contusion, DAI, long-duration coma, spinal-cord dysfunction, and death. Tolerances for various severities of neural injury are presented. At the tissue level, VC is the product of strain and strain-rate, ε dε/dt. The research shows that strain is not a sufficient parameter of neural injury risk, and that the product of strain and strain-rate is a key biomechanical parameter for brain and spinal-cord injury.     

邻苯二甲酸二丁酯诱导小鼠神经行为学改变及相关生理生化指标分析

探究邻苯二甲酸二丁酯诱导小鼠神经行为学改变及与细胞外调节蛋白激酶(ERK1/2)通路相关蛋白的关联.雄性KM小鼠36只,随机分成4组:生理盐水组、50 mg·kg~(-1)·d~(-1) DBP组、50 mg·kg~(-1)·d~(-1)维生素E(VE)组、DBP+VE组,连续灌胃处理28 d,观察Morris水迷宫结果,检测小鼠脑海马组织的氧化应激(活性氧(ROS)荧光强度、还原型谷胱甘肽(GSH)与丙二醛(MDA)含量)、脑源性神经营养因子(BDNF)、磷酸化cAMP反应元件结合蛋白(p-CREB)、caspase-3水平,Western blot分析ERK1/2及其磷酸化(p-ERK1/2)水平;HE、Nissl染色及Hoechst 33258荧光染色分析脑组织CA1区病理学变化.结果表明,与对照组比较,50 mg·kg~(-1)·d~(-1) DBP组小鼠的学习记忆下降,氧化应激、p-ERK1/2、caspase-3水平上升,BDNF、p-CREB表达下降,差异均有统计学意义(p0.05,p0.01);海马组织CA1病理学损伤及凋亡程度增加.给予抗氧化剂VE处理后,DBP+VE组小鼠的学习记忆上升,氧化应激、p-ERK1/2、caspase-3水平降低,BDNF、p-CREB表达上升,差异均有统计学意义(p0.05);海马组织CA1病理学损伤及凋亡程度降低.由此推测,DBP暴露导致小鼠海马组织CA1病理学损伤、神经元凋亡程度增加、学习记忆下降、其神经行为学改变可以通过添加VE得到缓解,相关生理生化指标测试表明ERK系统应激氧化性损伤机制参与介导了毒理学过程.