足踝生物力学动态仿真实验台的多轴运动和力协同控制系统

目的 研究足踝生物力学动态仿真实验台的控制问题,提出一套完整的多轴控制算法使实验台在模拟自由度、时间和精度、负荷重量、调试效率等指标上与国际同行相比具有竞争力。方法 设计人体足踝步态实验台,通过5个伺服电机驱动的机构模拟步态的运动过程（5个自由度）。基于对整个步态过程中力加载的科学分析和合理简化,在Matlab中对此多自由度力加载的过程进行建模。提出运用PID迭代学习算法来控制力,并在Simulink中进行仿真分析。基于仿真的参数,在实际搭建的系统上验证该算法的有效性与可靠性。结果 经过4~5次的迭代学习,实验台可以在5 s时间内完成1个支撑相的模拟,3个方向的足底反力（Fz、Fy、Fx）都具有重复性和可控性,在50%的人体体重下Fz和Fy输出曲线与目标曲线的均方根误差分别收敛到20 N和8 N,小于模拟负载的10%。结论 迭代学习控制方法可使足踝步态模拟实验台具有较强的力学模拟能力,提高了实验台的智能性,为后续进一步提高模拟速度和精度奠定良好的基础,其研制对尸体足踝生物力学实验具有重要意义。     

足踝步态模拟机动力学特性仿真及实验验证

目的 研究足踝步态模拟机动力学特性,仿真着地相中的足底垂直、前后、水平3个足底反力,并在实验台中验证。方法 运用设计的5自由度步态模拟机,建立Adams虚拟样机和足踝模型（包含足部主要韧带和跖腱膜、足底软组织及跟腱力）,对其进行动力学仿真,并把仿真中的控制规律运用到实验台验证;将仿真和实验中测力板测得的足底反力与仿真和真实数据比较。结果 着地相进程中3个方向的足底反力与实际步态中吻合度较高,足部的韧带和跖腱膜、跟腱和软组织等对正确的步态有重要的影响,步态实验台能够很好重复仿真特性。结论 模拟机具备仿真人体步态着地相的能力,为活体无法进行测量的实验提供临床研究平台。     

降钙素治疗骨质疏松疗效的初步观察

降钙素治疗骨质疏松疗效的初步观察卢世璧，刘安民，张伯勋，郭义柱我院自１９８９年９月至１９９０年６月在临床上应用瑞士山德士药厂出品的人工合成降钙素治疗老年性骨质疏松症，初步取得了较满意疗效。现报道如下。对象及方法患者均为绝经后妇女，共２６例，年龄４５～...     

可溶性Fas对星形细胞瘤细胞凋亡的抑制作用

目的探讨可溶性Fas(sFas)对Fas系统介导的星形细胞瘤细胞凋亡的作用和与肿瘤分化程度的关系。方法采用双抗体夹心ELISA方法检测65例星形细胞瘤患者及25例对照组术前血清中sFas的表达水平,采用免疫成织化学方法检测其术后病理切片的Fas水平,运用TUNEL技术检测凋亡指数。结果星形细胞瘤患者中Fas的表达率为66.2％;sFas水平为(18.5±7.6)ng/L,显著高于对照组(6.2±2.3)ng/L(P<0.01);星形细胞瘤患者血清中sFas水平与Fas水平呈负相关;星形细胞瘤中sFas与肿瘤病理分级呈正相关;sFas与凋亡指数呈负相关(r=-0.896)。结论sFas可作为判断星形细胞瘤恶性程度的指标之一,sFas可以抑制Fas系统介导的星形细胞瘤细胞凋亡。     

洛阳鹤壁两地区唇腭裂调查及遗传分析

本文报道了河南省洛阳、鹤壁两地区２２万人群中有关唇裂和（或）腭裂调查及遗传学研究结果。先证者一级亲属患病率２０．６６‰，二级亲属３．１７‰，分别是群体患病率（０．４５‰）的４４倍和７倍。唇裂和（或）腭裂遗传度：一级亲属７１．８９％±７．３３％，二级亲属６６．４２％±２１．２３％，加权平均遗传度７１．３１％±６．９３％，说明遗传因素在其发病中起重要作用。     

河南省农村遗传性疾病调查

在河南省鹤壁和洛阳两地区农村进行了遗传性疾病调查,调查总人数223 263人,发现遗传病及与遗传有关的先天性疾病1 914人,其中单基因疾病57种,染色体病7种,多基因病23种,与遗传有关的先天性疾病38种,总的患病率为8.57‰。患病率高的前10种疾病依次是:非特异性智力低下、原发性癫痫、先天性聋哑、精神分裂症、唇裂上腭裂、先天性心脏病、腹股沟疝、多指及并指、支气管哮喘、先天愚型等。调查结果还表明:遗传病的患病率男性高于女性,0～14岁儿童高于15岁以上成人,山区、半山区高于平原,且均存在显著性差异。     

屈指肌腱损伤后修复的研究进展

屈指肌腱损伤修复后的功能较差,原因之一是屈指肌腱损伤后愈合的机理尚不明了,为此,国外学者进行了大量的实验与临床研究,近年来提出了不少新的观点。一、肌腱损伤后的修复方式: 早期怍者即对肌腱的愈合机理存有争议。Ammon(1837年)观察到腱端本身可再生出新的腱组织,而Adamn等则认为是鞘组     

屈指肌腱损伤修复术后早期活动作用的实验研究

选用白来亨鸡56只,建立肌腱损伤的模型并设计不同的术后活动方法及制动方法。为比较这些方法对损伤肌腱愈合及功能的影响,进行了实体显微镜、普通光学显微镜、扫描电镜等项观察,并测量了肌腱的滑动功能。结果表明:适量的术后早期活动可促进损伤肌腱的愈合,改善其滑动功能,而制动则不利于肌腱损伤的修复及功能的恢复。     

右美托咪定缓解神经病理性疼痛大鼠的痛觉过敏并抑制背根神经节内p-ERK信号通路的激活

目的 观察重复腹腔注射右美托咪定(DEX)对神经病理性疼痛大鼠的痛觉过敏和背根神经节(DRG)中ERK信号通路激活的影响.方法 给坐骨神经部分结扎(PSNL)神经病理性疼痛大鼠重复腹腔注射不同剂量的DEX.观察各组大鼠的机械、热痛觉过敏阈值.行为学测试完成后用免疫荧光和Western blot方法检测大鼠手术侧L5 DRG中p-ERK的表达.结果 (1)腹腔注射DEX 40 μg/kg 7、14 d均明显减轻PSNL诱导的机械、热痛觉过敏(P＜0.05).而腹腔注射DEX20μg/kg对PSNL大鼠疼痛行为学无明显影响.(2)重复腹腔注射40μg/kg DEX 7、14 d p-ERK的平均荧光强度比同一时间点的PSNL组明显减弱(P＜0.05),但仍明显高于对照组(P＜0.05).重复腹腔注射20μg/kg对PSNL大鼠p-ERK的平均荧光强度无明显影响(P＞0.05).(3)Westem blot 结果显示重复腹腔注射40μg/kg DEX 7、14 d明显抑制PSNL诱导的p-ERK的蛋白表达增多(P＜0.05).重复腹腔注射20μg/kg对PSNL大鼠p-ERK的蛋白表达无明显影响(P＞0.05).结论 重复腹腔注射DEX能够减轻神经损伤引起的痛觉过敏,抑制外周初级感觉神经系统中ERK信号通路的激活可能是其缓解的疼痛症状的机制之一.

Abstract：

Objective To investigate the effect of systemic administration of dexmedetomidine, a selective alpha 2 adrenergic receptor agonist, on mechanical and thermal hyperalgesia and dorsal root ganglia ERK activation induced by neuropathic pain. Methods Intraperitoneal injection of dexmedetomidine was repeatedly given once daily for 7 days or 14 days with the first injection one day before partial sciatic nerve ligation ( PSNL) surgery. Mechanical and thermal nociceptive thresholds were assessed in all animals. Then, animals were killed at corresponding time points, and the L5 DRG was removed for L5 DRG ERK activation status analysis by using immunoflurecence and Western blotting. Results (1) Partial sciatic never ligation produced a robust mechanical and thermal hyperalgisia and ERK activation of the L5 DRG in P7 and P14 groups. At the dose of 40 μg/kg, dexmedetomidine significantly attenuated PSNL-induced ipsilateral hyperalgesia on the day 7 and 14 after surgery. But the dose of 20 μg/kg of dexmedetomidine had no effect on pain behaviorl; (2) PSNL-induced up-regulation of mean fluorescence intensity of pERK on ipsilateral side of the L5 DRG was significantly suppressed by day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application, whereas 20 μg/kg dexmedetomidine had no effect; (3) Western blotting revealed that up-regulation of the protein expression of p-ERK on ipsilateral side of the L5 DRG was significantly inhibited on the day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application,whereas 20 μg/kg dexmedetomidine had no effect. Conclusion Systemic dexmedetomidine inhibits the activation of ERK signals in L5 DRG, which is possibly associated with its antihyperalgesia in rats with neuropathtic pain.     

右美托咪定缓解神经病理性疼痛大鼠的痛觉过敏并抑制背根神经节内p-ERK信号通路的激活

Objective To investigate the effect of systemic administration of dexmedetomidine, a selective alpha 2 adrenergic receptor agonist, on mechanical and thermal hyperalgesia and dorsal root ganglia ERK activation induced by neuropathic pain. Methods Intraperitoneal injection of dexmedetomidine was repeatedly given once daily for 7 days or 14 days with the first injection one day before partial sciatic nerve ligation ( PSNL) surgery. Mechanical and thermal nociceptive thresholds were assessed in all animals. Then, animals were killed at corresponding time points, and the L5 DRG was removed for L5 DRG ERK activation status analysis by using immunoflurecence and Western blotting. Results (1) Partial sciatic never ligation produced a robust mechanical and thermal hyperalgisia and ERK activation of the L5 DRG in P7 and P14 groups. At the dose of 40 μg/kg, dexmedetomidine significantly attenuated PSNL-induced ipsilateral hyperalgesia on the day 7 and 14 after surgery. But the dose of 20 μg/kg of dexmedetomidine had no effect on pain behaviorl; (2) PSNL-induced up-regulation of mean fluorescence intensity of pERK on ipsilateral side of the L5 DRG was significantly suppressed by day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application, whereas 20 μg/kg dexmedetomidine had no effect; (3) Western blotting revealed that up-regulation of the protein expression of p-ERK on ipsilateral side of the L5 DRG was significantly inhibited on the day 7, 14 post-PSNL following 40 μg/kg dexmedetomidine application,whereas 20 μg/kg dexmedetomidine had no effect. Conclusion Systemic dexmedetomidine inhibits the activation of ERK signals in L5 DRG, which is possibly associated with its antihyperalgesia in rats with neuropathtic pain.