Spinal canal narrowing during simulated frontal impact

Between 23 and 70% of occupants involved in frontal impacts sustain cervical spine injuries, many with neurological involvement. It has been hypothesized that cervical spinal cord compression and injury may explain the variable neurological profile described by frontal impact victims. The goals of the present study, using a biofidelic whole cervical spine model with muscle force replication, were to quantify canal pinch diameter (CPD) narrowing during frontal impact and to evaluate the potential for cord compression. The biofidelic model and a sled apparatus were used to simulate frontal impacts at 4, 6, 8, and 10 g horizontal accelerations of the T1 vertebra. The CPD was measured in the intact specimen in the neutral posture (neutral posture CPD), under static sagittal pure moments of 1.5 Nm (pre-impact CPD), during dynamic frontal impact (dynamic impact CPD), and again under static pure moments following each impact (post-impact CPD). Frontal impact caused significant (P<0.05) dynamic CPD narrowing at C0-dens, C2-C3, and C6-C7. The narrowest dynamic CPD was observed at C0-dens during the 10 g impact and was 25.9% narrower than the corresponding neutral posture CPD. Interpretation of the present results indicate that the neurological symptomatology reported by frontal impact victims is most likely not due to cervical spinal cord compression. Cord compression due to residual spinal instability is also not likely.     

Effect of the free radical scavenger MCI-186 on spinal cord reperfusion after transient ischemia in the rabbit

Objective: Paraplegia remains a serious complication of aortic operations. The production of free radicals during reperfusion after transient ischemia is believed to induce secondary spinal neuronal injury, resulting in paraplegia. The aim of the present study was to clarify the protective effect and method of administration of antioxidants on the neurological and histological outcome in the animal model for reperfusion injury after transient spinal cord ischemia. Methods: New Zealand white rabbits underwent surgical exposure of the abdominal aorta that was clamped for 15 minutes to achieve spinal cord ischemia. Group A animals received two 10 mg/kg doses of 3-methyl-l-phenyl-2-pyrazolin-5-one (MCI-186) at the time of release of the aortic clamp and 30 minutes later. In group B, MCI-186, 5 mg/kg, was given three times, at the time of aorta clamp release, 30 minutes and 12 hours later. In group C (control group), one dose of vehicle was administered. Neurological status was assessed using modified Tarlov’s score until 168 hours after operation. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. Results: Groups A and B animals had better neurological function than group C (p(0.001). In contrast, group C animals exhibited paraplegia or paraparesis with marked neuronal necrosis. The number of surviving neurons within examined sections of the spinal cord was significantly greater in group B than in group C (p(0.001). Conclusion: In a 15-minute ischemia-reperfusion model using rabbits, systemic repetitious administration of MCI-186, a free radical scavenger, was found to have a protective effect on the spinal cord neurons both neurologically and histologically. We postulate that the drug minimizes the delayed neuronal cell death for reperfusion injury after transient ischemia by reducing the free radical molecules. Moreover, it was thought that we could protect delayed neuronal cell death more effectively by administering MCI-18612 hours later.     

Mechanisms mediating the brain stem control of somatosensory transmission in the dorsal horn of the cat's spinal cord: an intracellular analysis

Summary The effect of brainstem stimulation was studied on neurones recorded intracellularly in the superficial and deeper laminae of the lumbosacral dorsal horn of the spinal cord in anaesthetised cats. Stimulation in the nucleus locus coeruleus (LC) produced a hyperpolarisation in 4/13 multireceptive neurones and produced a biphasic action consisting of a hyperpolarisation which was followed by a depolarisation in 3/13 neurones. These actions were produced irrespective of whether the multireceptive neurone was located in the superficial or deeper laminae of the dorsal horn. Stimulation failed to produce postsynaptic potentials in the remaining 6/13 multireceptive neurones. The amplitude of hyperpolarisation was increased by the passage of depolarising pulses through the recording microelectrode and decreased by hyperpolarising pulses. Stimulation in other brainstem areas such as, the lateral (FTL), paralemniscal (FTP) and central (FTC) divisions of the tegmental field and the nuclei raphe magnus (NRM) and reticularis magnocellularis (RMc) also hyperpolarised neurones in the dorsal horn. The polarity of hyperpolarisation evoked from some brainstem areas (FTP, FTC, RMc) could be reversed to depolarisation by the passive diffusion of ions from the recording microelectrode containing 3M-KCl. Brainstem (LC, NRM, FTP, FTL) stimulation generated long lasting (700 ms) hyperpolarisation on 4/4 selectively nocireceptive neurones of lamina I. There was, however, no effect on the activity of 5/5 neurones recorded in laminae I/II which in addition to receiving excitatory cutaneous inputs were inhibited by heat stimuli. Stimulation in LC also produced dorsal root potentials (DRPs) and reduced the amplitude of simultaneously recorded excitatory postsynaptic potentials (EPSPs) generated by the activation of primary afferent fibres in 3 multireceptive neurones. It is concluded that inhibition of nociceptive transmission in the spinal cord from LC and other brainstem areas may involve both pre- and postsynaptic mechanisms.     

hTERT启动子调控hNIS基因介导肺癌细胞碘摄取和131I治疗的实验研究

目的 构建含人端粒酶反转录酶(hTERT)核心启动子调控的人钠/碘同向转运体(hNIS)基因重组腺病毒,并靶向转染至肺癌A549细胞中特异性表达.探讨hTERT启动子调控的hNIS基因介导放射性碘治疗肿瘤的可能性.方法 应用AdEasy系统构建重组腺病毒Ad-hTERT-hNIS,同时构建巨细胞病毒(CMV)启动子调控的hNIS重组腺病毒Ad-CMV.hNIS作为阳性对照,不含hNIS的重组腺病毒Ad-CMV作为阴性对照.应用反转录.聚合酶链反应(RT-PCR)方法验证hTERT在转染肿瘤细胞中的转录活性,摄碘实验检测表达的hNIS蛋白功能,细胞克隆形成实验评价131I对转染肿瘤细胞的毒性作用.结果 成功构建重组腺病毒Ad-hTERT-hNIS、Ad-CMV-hNIS及Ad-CMV,并经PCR验证正确.RT-PCR证实hNIS cDNA能从Ad-hTERT-hNIS转染的细胞中扩增出来.Ad-hTERT-hNIS和Ad-CMV-hNIS转染的肺癌A549细胞摄碘能力比阴性对照组Ad-CMV转染的细胞分别提高了23和31倍,且摄碘能力可以被NaClO4抑制.Ad-hTERT-hNIS和Ad-CMV-hNIS转染的肺癌A549细胞均可被131I杀死,2组细胞成活率分别为(31.2±1.45)%和(23.6±4.08)%,而阴性对照组和未转染病毒组分别为(89.0 ±2.99)%和(91.2 ±4.63)%.结论 hTERT启动子调控的hNIS重组腺病毒转染肿瘤细胞后,应用131I治疗有望成为一种新的基因靶向治疗手段.     

Genetic variation in serotonin transporter alters resting brain function in healthy individuals.

BACKGROUND: Perfusion functional magnetic resonance imaging (fMRI) was used to investigate the effect of genetic variation of the human serotonin transporter (5-HTT) gene (5-HTTLPR, SLC6A4) on resting brain function of healthy individuals. METHODS: Twenty-six healthy subjects, half homozygous for the 5-HTTLPR short allele (s/s group) and half homozygous for the long allele (l/l group), underwent perfusion functional and structural magnetic resonance imaging during a resting state. The two genotype groups had no psychiatric illness and were similar in age, gender, and personality scores. RESULTS: Compared with the l/l group, the s/s group showed significantly increased resting cerebral blood flow (CBF) in the amygdala and decreased CBF in the ventromedial prefrontal cortex. The effect of functional modulation in these regions by 5-HTTLPR genotype cannot be accounted for by variations in brain anatomy, personality, or self-reported mood. CONCLUSIONS: The 5-HTTLPR genotype alters resting brain function in emotion-related regions in healthy individuals, including the amygdala and ventromedial prefrontal cortex. Such alterations suggest a broad role of the 5-HTT gene in brain function that may be associated with the genetic susceptibility for mood disorders such as depression.     

血管内皮生长因子在高原脑水肿形成中作用的实验研究

目的:探讨血管内皮生长因子(VEGF)在高原脑水肿形成中的作用。方法:建立大鼠模拟高原模型,应用脑干湿重比率法定量脑水肿情况、应用荧光素钠透过率测定BBB通透性、应用实时荧光定量RT-PCR法检测脑组织VEGF mRNA含量以及应用蛋白印迹法半定量脑组织VEGF含量。结果:大鼠在高原24 h后脑组织含水率明显增高(P<0.05),荧光素钠透过率显著增加(P<0.01);VEGF mRNA转录及其表达显著增高(P<0.001)。结论:VEGF表达在高原脑水肿形成中起重要作用。     

胸椎骨折合并胸外伤的外科治疗

目的　总结 17例胸椎骨折患者的特点与诊疗情况 ,为提高此类合并胸外伤患者的疗效提供有效的治疗方案。方法　分析了 17例胸椎骨折患者的临床特点、诊疗经过、近远期随访结果。结果　 14例 (82 .4 % )合并肋骨骨折 ,11例 (6 4 .7% )合并血气胸 ,10例 (5 8.8% )合并严重脊髓伤 ,3例 (30 % )远期脊髓伤为有用恢复。结论　胸椎骨折常合并肋骨骨折、血气胸、严重脊髓损伤 ,预后较差 ,为此应重视合并胸外伤的胸椎骨折的围手术期处理     

盐酸丁咯地尔治疗椎-基底动脉供血不足的效果

①目的　观察盐酸丁咯地尔对椎 基底动脉供血不足的治疗作用。②方法　将 82例椎 基底动脉供血不足病人随机分为两组 ,治疗组 4 2例 ,给予盐酸丁咯地尔 2 5 0mL静滴 ,每日 1次 ;对照组 4 0例 ,给予维脑路通0 .5g、胞二磷胆碱 0 .5 g静滴 ,每日 1次 ,均治疗 7d。检测两组治疗前后血液流变学和血流动力学指标的变化。 ③结果　治疗后治疗组全血高切黏度明显低于对照组 ,椎动脉平均血流速度 (VA)明显快于对照组 ,差异均有显著性(t=3.96 0 ,P <0 .0 1 ;t=2 .0 92 ,P <0 .0 5 )。治疗组治疗后全血高切、低切和血浆黏度明显低于治疗前 ,差异有显著性 (t=2 .74 6～ 2 .95 1 ,P <0 .0 1 ) ;VA、基底动脉平均血流速度 (BA)和外周血管阻力指数 (PI)高于治疗前 ,差异有显著性 (t=2 .732～ 5 .1 0 4 ,P <0 .0 1 )。对照组治疗后血浆黏度、PI明显低于治疗前 ,VA高于治疗前 ,差异均有显著性 (t=2 .1 6 8～ 2 .732 ,P <0 .0 5 ) ;全血高切、低切黏度、BA治疗前后差异无显著性 (t=0 .346～ 2 .0 0 8,P >0 .0 5 )。④结论　盐酸丁咯地尔对椎 基底动脉供血不足有良好的改善作用 ,其疗效明显优于维脑路通加胞二磷胆碱的治疗效果