神经肌肉电刺激下小腿肌肉的电学特性研究

目的 采用电阻抗成像（electrical impedance tomography,EIT）方法研究神经肌肉电刺激（neuromuscular electrical stimulation,NMES）下小腿肌肉的电学特性,旨在将EIT作为一种长期监测方法,从而可视化NMES训练对人类小腿肌肉的训练效果。方法 16名实验对象被随机分配到对照组（control group,CG,n=8）和最佳电压强度的NMES训练组（optimal voltage intensity training group,OG,n=8）。对照组保持正常生活方式并不进行NMES和其他的肌肉训练;NMES训练组中使用商业NMES设备对实验对象右小腿进行23 min的NMES训练,每周3次,为期5周。应用EIT测量在每周一训练开始前的电导率分布。并且采用生物电阻抗分析（bioelectrical impedance analysis,BIA）方法测量右腿细胞外含水量与身体总含水量的比率（ECW/TBW） βrl,及身体总含水量（TBW）τ。为了量化NMES在肌肉训练过程中的作用,使用配对样本t检验分析EIT重建图像的...     

虚拟现实平衡训练联合神经肌肉电刺激对前交叉韧带重建术后患者膝关节功能、腘绳肌肌力和步行功能的影响

摘要 目的：探讨虚拟现实平衡训练联合神经肌肉电刺激（NMES）对前交叉韧带重建术（ACLR）后患者膝关节功能、腘绳肌肌力和步行功能的影响。方法：选择2019年8月~2021年12月期间我院收治的前交叉韧带（ACL）损伤患者96例,并成功实施ACLR,采用随机数字表法分为对照组（n=48,常规康复训练、虚拟现实平衡训练）和研究组（n=48,常规康复训练、虚拟现实平衡训练联合NMES干预）。对比两组膝关节功能优良率、膝关节功能、腘绳肌肌力和步行功能。结果：研究组的临床膝关节功能优良率93.75%（45/48）高于对照组68.75%（33/48）,差异有统计学意义（P<0.05）。两组干预后膝关节功能评分、膝关节活动度对均升高,且研究组高于对照组（P<0.05）。两组干预后患侧腘绳肌等长肌力升高,且研究组高于对照组（P<0.05）,两组干预后健侧腘绳肌等长肌力对比无明显差异（P>0.05）。两组干预后步长、步速升高,且研究组高于对照组,患侧摆动相降低,且研究组低于对照组（P<0.05）。两组干预后被动活动察觉阀值、进行被动角度再生试验降低,且研究组低于对照组（P<0.05）。结论：虚拟现实平衡训练联合NMES应用于ACLR术后患者的疗效显著,有助于其膝关节功能恢复,提高腘绳肌肌力,改善步行功能。     

胃容积及胃食道液体状态变化的电学特性研究

目的 三维电阻抗成像(3D-EIT)结合二维电阻抗成像(2D-EIT)研究胃容积及胃食道液体状态变化的电学特性响应,旨在探究EIT技术应用于胃食道反流病监测的可能性。方法 8名受试者被要求在实验前4 h禁食,保证实验开始时胃部处于排空状态,实验开始后受试者被要求分两次喝下400 ml经口补水液,在摄入200 ml状态下和摄入400 ml状态下分别应用3D-EIT检测腹腔3D空间的电导率分布。为了定量说明不同状态下电学特性的变化,使用配对样本t检验分析3D-EIT重建3D图像的空间平均电导率(■)。采用数值仿真工具,建立两种尺寸胃容积模型验证,实验结果中胃容积变化是引起受试者腹腔3D空间内电导率变化的原因,并研究胃腔被不同比例补水液填充状态下电学特性的变化趋势,应用2D-EIT数值仿真进行电导率分布图像重建。结果 8名受试者腹腔3D-EIT实验中空间平均电导率■的配对样本t检验结果表明,空间平均电导率从C^{200 ml}状态下的■增加到C^{400 ml}状态下的■(n=8,P<0.05)。因此,受试者腹腔胃部区域空间平均电导率随胃容积增加而显著增...     

基于径向基函数神经网络的肺部加权频差电阻抗成像方法

目的 对肺通气过程进行床旁实时连续图像监控,是机械通气患者和临床医生的迫切需求。肺部电阻抗成像（EIT）可反映呼吸引起的胸腔电特性变化分布,在肺通气监测方面具有天然的优势。本文目的在于建立基于径向基函数神经网络（RBFNN）的肺部加权频差电阻抗成像（wfd-EIT）方法,实现对肺通气的高空间分辨率成像。方法 利用肺部wfd-EIT成像方法实时描绘胸腔电导率分布状况,再通过RBFNN将目标区域可视化并精准识别其边界信息。首先通过数值分析模拟,在各个激励频率利用COMSOL与MATLAB软件建立2 028个仿真样本,分为训练样本集和测试样本集,验证所提出成像方法的可行性和有效性。其次,为了验证仿真结果,建立肺部物理模型,选用具有低电导特性的生物组织模拟肺部通气区域,对其进行成像实验,并采用图像相关系数（ICC）和肺区域比（LRR）定量数据衡量成像方法的准确性。结果 wfd-EIT方法可以在任意时刻进行图像重建,并能够准确反映出目标区域的电特性分布;利用基于RBFNN的算法能够增强目标区域的成像精度,ICC可达0.94以上,更好地凸显其边界轮廓信息。结论 通过wfd-EIT成像方法,利用多频阻抗谱同步测量实现目标区域的快速可视化,并结合RBFNN网络逼近任意非线性函数的优点,实现对目标区域电特性变化的精准识别,为下一步进行临床肺通气的EIT图像监测奠定了理论和技术基础。     

Channel Gating Dependence on Pore Lining Helix Glycine Residues in Skeletal Muscle Ryanodine Receptor

Type 1 ryanodine receptors (RyR1s) release Ca²⁺ from the sarcoplasmic reticulum to initiate skeletal muscle contraction. The role of RyR1-G4934 and -G4941 in the pore-lining helix in channel gating and ion permeation was probed by replacing them with amino acid residues of increasing side chain volume. RyR1-G4934A, -G4941A, and -G4941V mutant channels exhibited a caffeine-induced Ca²⁺ release response in HEK293 cells and bound the RyR-specific ligand [³H]ryanodine. In single channel recordings, significant differences in the number of channel events and mean open and close times were observed between WT and RyR1-G4934A and -G4941A. RyR1-G4934A had reduced K⁺ conductance and ion selectivity compared with WT. Mutations further increasing the side chain volume at these positions (G4934V and G4941I) resulted in reduced caffeine-induced Ca²⁺ release in HEK293 cells, low [³H]ryanodine binding levels, and channels that were not regulated by Ca²⁺ and did not conduct Ca²⁺ in single channel measurements. Computational predictions of the thermodynamic impact of mutations on protein stability indicated that although the G4934A mutation was tolerated, the G4934V mutation decreased protein stability by introducing clashes with neighboring amino acid residues. In similar fashion, the G4941A mutation did not introduce clashes, whereas the G4941I mutation resulted in intersubunit clashes among the mutated isoleucines. Co-expression of RyR1-WT with RyR1-G4934V or -G4941I partially restored the WT phenotype, which suggested lessening of amino acid clashes in heterotetrameric channel complexes. The results indicate that both glycines are important for RyR1 channel function by providing flexibility and minimizing amino acid clashes.     

ERK信号通道调控大鼠气道平滑肌细胞的增殖与凋亡

 为了了解ERK信号通道对正常大鼠气道平滑肌细胞(airway smooth muscle cells, ASMCs)增殖与凋亡的调控. 通过对正常大鼠ASMCs原代培养,4～7代用于实验,以ERK激动剂表皮生长因子（EGF）和抑制剂PD98059干预ASMCs生长,采用RT-PCR和免疫荧光染色观察ASMCs上ERK mRNA和蛋白的表达,MTT法、^３Ｈ-TdR掺入法检测ASMC增殖,Hoechst染色和Annexin-Ⅴ FITC PI双染色法检测细胞凋亡,Western免疫印迹检测ERK1/2、磷酸化ERK1/2和procaspase-3蛋白的表达.结果发现ASMCs上存在ERK mRNA和蛋白的表达,与空白对照组比较,PD98059干预后ASMCs的Ａ_４９０值和细胞DNA合成量均减少(Ｐ<0.05),细胞凋亡指数、早期凋亡细胞百分率均增高(Ｐ<0.05),ERK1/2、磷酸化ERK1/2表达和ERK活化率均降低, procaspase-3蛋白的表达增高.EGF干预后ASMCs的Ａ_４９０值和细胞DNA合成量均增高(Ｐ<0.05),细胞凋亡指数、早期凋亡细胞百分率均下降(Ｐ<0.05),ERK1/2、磷酸化ERK1/2表达和ERK活化率均增高, procaspase-3蛋白的表达降低.P+E组无明显差异(P>0.05).ERK信号通道参与大鼠ASMCs增殖和凋亡的调控,ERK对大鼠ASMCs凋亡的调控与procaspase-3蛋白有关,这一发现将有助于对哮喘ASMCs异常增殖调控机制的深入研究.     

Uncoupling Protein 1 and Sarcolipin Are Required to Maintain Optimal Thermogenesis,and Loss of Both Systems Compromises Survival of Mice under Cold Stress

The importance of brown adipose tissue as a site of nonshivering thermogenesis has been well documented. Emerging studies suggest that skeletal muscle is also an important site of thermogenesis especially when brown adipose tissue function is lacking. We recently showed that sarcolipin (SLN), an uncoupler of the sarco(endo)plasmic reticulum Ca²⁺ ATPase (SERCA) pump, could contribute to heat production in skeletal muscle. In this study, we sought to understand how loss of UCP1 or SLN is compensated during cold exposure and whether they are both necessary for thermogenesis. Toward this goal, we generated a UCP1;SLN double knock-out (DKO) mouse model and challenged the single and DKO mice to acute and long-term cold exposures. Results from this study show that there is up-regulation of SLN expression in UCP1-KO mice, and loss of SLN is compensated by increased expression of UCP1 and browning of white adipose tissue. We found that the DKO mice were viable when reared at thermoneutrality. When challenged to acute cold, the DKO were extremely cold-sensitive and became hypothermic. Paradoxically, the DKO mice were able to survive gradual cold challenge, but these mice lost significant weight and depleted their fat stores, despite having higher caloric intake. These studies suggest that UCP1 and SLN are required to maintain optimal thermogenesis and that loss of both systems compromises survival of mice under cold stress.