泥蚶肌肉凝集素的分离纯化及部分性质

泥蚶肌肉提取液经硫酸铵二步分级沉淀后,再经DEAE-Sepharose（Fast Flow）离子交换和SephacrylS-200-HR分子筛层析,从中分离纯化得到泥蚶肌肉凝集素．经测定,该凝集素分子量约为238kDa,为单个亚基的蛋白质,其相对分子量为60kDa,分子中含3．27％的糖．在氨基酸组成中,谷氨酸（Glu）含量最高,其次是丝氨酸（Ser）和天门冬氨酸（Asp）．泥蚶肌肉凝集素对人和动物红细胞均有凝集作用,其中对兔的红细跑的凝集活性最高．该凝集素对兔的红细胞的凝集活性不被测试的10种浓度为200mmol·L^-1的糖所抑制．pH6．0～7．0时具有较强活性;热稳定性较高,在30-50℃的温度范围内对兔红细胞的凝集仍保持原有活性,60℃以后活力下降;凝集活性依赖于Ca^2＋．     

髓鞘内不同浓度甘丙肽拮抗剂对屈肌运动的相反效应

目的 :了解脊髓中不同剂量甘丙肽拮抗剂M35和M40对甘丙肽抑制屈肌运动作用的影响。方法 :电刺激小腿腹神经引起小腿屈肌收缩时 ,观察髓鞘内联合注入甘丙肽和不同浓度拮抗剂时屈肌张力的改变。结果注入0 0 1、 0 0 3及 0 1μmol/LM35时 ,0 1μmol/L甘丙肽对屈肌张力抑制率从 - 2 9 2 %改变至± 15 1%、 - 2 5 %及 -17 8% ;但 1及 3μmol/L的M35使甘丙肽抑制率分别增强至 - 5 1 9%及 - 6 5 6 %。而给于 0 0 1及 0 0 3μmol/LM40时 ,甘丙肽抑制率增至 - 5 6 7%及 - 41 6 % ,0 3、 1及 3μmol/LM40使甘丙肽抑制率分别改变为 - 6 8%、 +12 2 %及 +30 4%。结论　低浓度M35为甘丙肽拮抗剂 ,高浓度M35有甘丙肽激动剂作用 ;低浓度M40为甘丙肽激动剂 ,高浓度M40有甘丙太拮抗剂效应。脊髓神经元可能存在不同甘丙肽亚型受体。     

增龄骨骼肌的机能特征及运动的其影响(综述)

骨骼肌在增龄或衰老时结构与生理机能发生一系列的变化。增龄骨骼肌的主要特征表现为肌肉萎缩、运动单位重建、绝对力量与单位面积的肌力下降 ,同时肌肉的最大输出功率与持续输出功率也下降。增龄骨骼肌与年轻骨骼肌相比更容易收缩时发生损伤且恢复较慢。同时某些运动可对增龄骨骼肌的结构与机能的变化施加一定的影响。     

缺血再灌注损伤--延迟性肌肉酸痛的可能机制

通过比较大量心肌、骨骼肌缺血再灌注损伤和骨骼肌延迟性酸痛的研究结果,提出缺血再灌注损伤是延迟性肌肉酸痛产生的机制这一假说,旨在为延迟性肌肉酸痛的进一步研究提供方向.     

EMSF肌肉功能电刺激应用的研究

本文通过国外对EMSF（肌肉功能电刺激）的研究应用及“力王”多年来的国内应用情况进行研究和分析，旨在拓展我国力量训练的有效方法。     

Lean mass as a total mediator of the influence of muscular fitness on bone health in schoolchildren: a mediation analysis

This report aims to analyse the independent association of lean mass and muscle fitness with bone mineral content (BMC) and bone mineral density (BMD), and to examine whether the relationship between muscle fitness and bone health is mediated by lean mass. Body composition (by dual energy X-ray absorptiometry (DXA)), muscle fitness, physical activity, age and height were measured in 132 schoolchildren (62 boys, aged 8–11 years). Analysis of covariance tested differences in bone-related variables by lean mass and muscle fitness, controlling for different sets of confounders. Linear regression models fitted for mediation analyses examined whether the association between muscle fitness and bone mass was mediated by lean mass. Children with good performance in handgrip and standing long jump had better and worse bone health, respectively. These differences disappeared after controlling for lean mass. Children with high lean mass had higher values in all bone-related variables. In addition, the relationship between muscle fitness and bone mass was fully mediated by lean mass. In conclusion, the relationship between upper-limbs muscle fitness and bone health seems to be dependent on lean mass but not on muscle fitness. Schoolchildren with high lean mass have more BMC and BMD in all regions. Lean mass mediates the association between muscle fitness and bone mass.     

跆拳道训练对儿童肌肉适能的影响研究

文章根据儿童生长发育的特点,采用符合儿童运动需求一般身体素质训练和专项训练相结合的方法,对实验组受试者实施为期6个月的跆拳道训练。研究严格遵循肌肉适能的指标测试方法,根据握力、立定跳远及仰卧起坐测试数据的变化,并通过实验组与对照组的横向对比,与自身的纵向对比,来揭示跆拳道训练对儿童肌肉适能影响。为儿童身体素质的提高提供合理有效的训练方法和手段,为儿童提高身体素质搭建了平台。     

Disruption of splicing-regulatory elements using CRISPR/Cas9 to rescue spinal muscular atrophy in human iPSCs and mice

We here report a genome-editing strategy to correct spinal muscular atrophy (SMA). Rather than directly targeting the pathogenic exonic mutations, our strategy employed Cas9 and guide-sgRNA for the targeted disruption of intronic splicing-regulatory elements. We disrupted intronic splicing silencers (ISSs, including ISS-N1 and ISS + 100) of survival motor neuron (SMN) 2, a key modifier gene of SMA, to enhance exon 7 inclusion and full-length SMN expression in SMA iPSCs. Survival of splicing-corrected iPSC-derived motor neurons was rescued with SMN restoration. Furthermore, co-injection of Cas9 mRNA from Streptococcus pyogenes (SpCas9) or Cas9 from Staphylococcus aureus (SaCas9) alongside their corresponding sgRNAs targeting ISS-N1 into zygotes rescued 56% and 100% of severe SMA transgenic mice (Smn^−/−, SMN2^tg/−). The median survival of the resulting mice was extended to >400 days. Collectively, our study provides proof-of-principle for a new strategy to therapeutically intervene in SMA and other RNA-splicing-related diseases.     

糖皮质激素引起肌肉萎缩细胞模型的建立

目的：建立高剂量或长期服用糖皮质激素会引起肌肉萎缩的细胞模型。方法：以BCA法（蛋白质浓度分析法）检测了用糖皮质激素地塞米松（DEX，100nM）孵育1～4天对C2C12肌管的蛋白总量的影响，以建立长期使用糖皮质激素引起肌肉萎缩的细胞模型。实验结果表明：孵育DEX1～4天分别使C2C12肌管蛋白总量下降为对照组的79．1％、63．1％、50．8％和41．7％。同时还比较了DEX孵育和停止更换培养基（模拟营养不良）两种细胞模型的特征，结果显示DEX孵育比停止更换培养基更迅速地引起蛋白总量下降。