导航系统辅助下颈椎椎弓根螺钉置钉准确性的实验研究

目的：评价导航系统辅助下颈椎（C3～C7）椎弓根螺钉内固定置钉的准确性.方法：将32具成人尸体颈椎标本随机分为4组,分别采用盲法、透视法、透视导航法和CT导航法进行下颈椎椎弓根螺钉置入.术后采用标本大体解剖观察的方法评价置钉准确性.分优（螺钉完全在椎弓根内）、可（仅有螺纹穿出,对周围组织无损伤）和差（螺钉明显穿出）进行统计.结果：共置入螺钉318枚.盲法80枚,平均手术时间27min,优29枚（36 3%）、可21枚（26.3%）、差30枚（37.5%）;透视法78枚（有1例C4、C5右侧椎弓根均细小,不能容纳3.5mm螺钉）,平均手术时间112min,优35枚（44.9%）、可29枚（37.2%）、差14枚（17.9%）;透视导航法80枚,平均手术时间69min,优34枚（42.5%）,可36枚（45%）,差10枚（12.5%）;CT导航法80枚,平均手术时间98min,优70枚（87.5%）、可10枚（12.5%）.各组间手术时间均有显著性差异（P＜0.05）,透视法与透视导航法的置钉准确率间无显著性差异,其余各组间均有显著性差异（P＜0.05）.结论：单纯根据术前影像结果盲法行下颈椎椎弓根螺钉内固定不安全.透视法和透视导航法可提高置钉准确性,但手术风险仍较大,透视导航法比透视法置钉的手术时间缩短.CT导航法并未比透视法增加手术时间,但置钉准确性显著提高.     

A Clinical Study of Reversing Left Ventricular Hypertrophy in Hypertensive Patients by Adalat

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钾通道阻断剂对低氧/复氧诱导的培养海马神经元死亡的防护作用

目的研究钾通道阻断剂对单纯低氧/复氧诱导的培养海马神经元死亡的防护作用。方法培养8 d的海马神经元置于低氧环境(95% N2/5% CO2)6 h,复氧再培养直至72 h,复氧后0.5 h培养液内分别给予不同钾通道阻断剂,用细胞计数及MTT比色法检测神经元死亡情况。结果低氧/复氧诱导培养海马神经元出现迟发性死亡;四乙铵以剂量依赖性的方式防护低氧/复氧诱导的培养海马神经元免于死亡;大电导钙激活钾通道(BK通道)阻断剂iberiotoxin(IbTX)可完全消除低氧/复氧诱导的神经元死亡(P<0.001);A型钾通道阻断剂4-氨基吡啶不能防护低氧/复氧诱导的神经元免于死亡(P>0.05)。结论钾通道阻断剂四乙铵和IbTX能防护低氧/复氧诱导的培养海马神经元免于死亡,提示某些类型的钾通道尤其是BK通道活动增强可能参与了低氧/复氧诱导的培养海马神经元死亡。     

Ineffectiveness of organic calcium channel blockers in antagonizing long-term potentiation

Evidence has accumulated suggesting that the presence of calcium is critical for development of hippocampal long-term potentiation (LTP). However, there is a paucity of information about whether calcium's role in LTP is pre- or postsynaptic. In the present study, we examined the effectiveness of nitrendipine, verapamil, flunarizine and the benzodiazepine diazepam in: blocking voltage-dependent calcium channels; blocking synaptic transmission; and preventing development of LTP. Using the in vitro slice preparation, we obtained intracellular and extracellular recordings from guinea pig hippocampal CA1 pyramidal cells. At the cellular level, all 4 drugs were ineffective in blocking voltage-dependent calcium spikes (TTX resistant) and the calcium-dependent afterhyperpolarization. Verapamil and diazepam appeared to antagonize synaptic transmission, as reflected in smaller population spike amplitudes. Development of long-term potentiation was not affected by the presence of verapamil, flunarizine and diazepam. Nitrendipine appeared to reduce the percentage of slices exhibiting LTP; however, ethanol, the vehicle used to dissolve nitrendipine, was shown in separate experiments to reduce the percentage of slices exhibiting LTP. These results suggest that neither the organic calcium channel blockers--nitrendipine, verapamil, and flunarizine--nor micromolar concentrations of diazepam are potent blockers of extrasynaptic voltage-sensitive calcium channels in hippocampus. They thus cannot be used to demonstrate a specific pre- or postsynaptic calcium role in LTP.     

Molecular basis of severe myoclonic epilepsy in infancy

Severe myoclonic epilepsy (SMEI) or Dravet syndrome is caused by mutations of the SCN1A gene that encodes voltage-gated sodium channel alpha-1 subunit. Recently, we generated and characterized a knock-in (KI) mice with an SCN1A nonsense mutation that appeared in three independent SMEI patients. The SCN1A-KI mice well reproduced the SMEI disease phenotypes. Both homozygous and heterozygous knock-in mice developed epileptic seizures within the first postnatal month. In heterozygous knock-in mice, trains of evoked action potentials in inhibitory neurons exhibited pronounced spike amplitude decrement late in the burst but not in pyramidal neurons. We further showed that in wild-type mice the Nav1.1 protein is expressed dominantly in axons and moderately in somata of parbalbumin (PV) – positive inhibitory interneurons. Our immunohistochemical observations of the Nav1.1 are clearly distinct to the previous studies, and our findings has corrected the view of the Nav1.1 protein distribution. The data indicate that Nav1.1 plays critical roles in the spike output from PV interneurons and further, that the specifically altered function of these inhibitory circuits may contribute to epileptic seizures in the mice. These information should contribute to the understanding of molecular pathomechanism of SMEI and to develop its effective therapies.     

ProTx-I and ProTx-II: gating modifiers of voltage-gated sodium channels.

The tarantula venom peptides ProTx-I and ProTx-II inhibit voltage-gated sodium channels by shifting their voltage dependence of activation to a more positive potential, thus acting by a mechanism similar to that of potassium channel gating modifiers such as hanatoxin and VSTX1. ProTx-I and ProTx-II inhibit all sodium channel (Nav1) subtypes tested with similar potency and represent the first potent peptidyl inhibitors of TTX-resistant sodium channels. Like gating modifiers of potassium channels, ProTx-I and ProTx-II conform to the inhibitory cystine knot motif, and ProTx-II was demonstrated to bind to sodium channels in the closed state. Both toxins have been synthesized chemically, and ProTx-II, produced by recombinant means, has been used to map the interaction surface of the peptide with the Nav1.5 channel. In comparison, beta-scorpion toxins activate sodium channels by shifting the voltage dependence of activation to more negative potentials, and together these peptides represent valuable tools for exploring the gating mechanism of sodium channels.     

CFTR stabilizes ENaC at the plasma membrane

CFTR was reported to regulate ENaC channel opening, decreasing ENaC activity in airways and increasing it in sweat ducts. We generated MDCK-I cell lines stably expressing tagged alphabetagammaENaC+CFTR or ENaC alone, and developed an assay to quantify cell-surface half-life of ENaC. Surprisingly, we found that co-expressed CFTR stabilizes ENaC at the plasma membrane, suggesting that CFTR regulates ENaC stability, not just opening.     

投影法植入椎弓根螺钉的可行性

目的探讨通过椎弓根的投影法植入椎弓根螺钉的可行性及临床应用价值。方法通过对椎弓根的解剖及椎弓根投影的影像解剖研究,探讨通过椎弓根投影植入椎弓根螺钉的可行性,临床上前瞻性地利用该法植入胸椎椎弓根螺钉50枚,腰椎椎弓根86枚,术后CT复查。胸椎植入的成功率与经典Margel法对比,腰椎植入的成功率与经典的AO法对比,利用SPSS13.0的Pearson Chi-Squaretest对结果进行统计分析,分析该法与AO及Margel法的成功率是否存在显著差异。结果椎弓根的投影就是椎弓根行径在X线片及CT片上的投影,临床利用椎弓根的投影法植入胸椎螺钉16例50枚,Margel法31例74枚,投影法植入腰椎螺钉23例86枚,AO法32例142枚,投影法胸椎的成功率明显高于Margel法,腰椎的成功率与AO法没有明显的显著性差异。结论椎弓根投影法植入螺钉的方法是可靠、可行的。     

单节段与双节段椎弓根螺钉固定胸腰椎单椎体骨折的生物力学比较

目的:比较单节段与双节段椎弓根螺钉固定术固定胸腰椎单椎体骨折的生物力学效果。方法:在16具新鲜小牛胸腰椎标本(T11-L3)的L1椎体上制作不完全爆裂骨折模型,分为两组,分别行单节段与双节段椎弓根螺钉固定,对固定后的标本施加扭矩为4Nm的疲劳载荷共2000次,加载频率为0.5Hz,经脊柱三维运动测量系统测量正常、损伤、固定和周期性加载后固定节段前屈/后伸、左/右侧弯和左/右旋转运动时固定节段的运动范围。结果:单节段固定组前屈、后伸、侧屈、旋转稳定指数(SPI)分别为0.78、0.80、0.92、0.83,双节段固定组SPI分别为0.88、0.89、0.95、0.85,在前屈方向单节段固定组明显小于双节段固定组(P<0.01);疲劳后,单节段固定组SPI在前屈、后伸、侧屈、旋转方向分别降低0.05、0.03、0.05、0.11,降低值均大于双节段固定组,且在旋转和侧屈方向有显著性差异(旋转:P<0.01;侧屈:P<0.05)。结论:两种术式均可重建脊柱骨折即刻稳定性,效果无明显差异。在旋转、侧屈方向,双节段椎弓根螺钉固定术抗疲劳载荷效果优于单节段固定术。     

Regulation of single potassium channels by serotonin in the cell bodies of the tail mechanosensory neurons ofAplysia californica

Sensory neurons in the pleural ganglion ofAplysia mediate the afferent portion of the tail withdrawal reflex. Previous work has shown that in these neurons and in the siphon sensory neurons ofAplysia, serotonin modulates a steady-state non-inactivating potassium current called the S current. Using the technique of patch clamping, we have examined the kinetics of single potassium channels and found that they share the properties of the S potassium channel of the siphon sensory neurons. This channel has an elementary slope conductance of73 ± 9.98pS(x±S.E.M.) and shows Goldman rectification. It is active at the resting potential and does not inactivate with maintained depolarization. Bath application of serotonin in a majority of experiments decreased the functional number of channels in the patch.