纳入标准：有关成肌细胞的生物学特性、在骨骼肌收缩中的应用、在基因治疗中应用方面的文献。
Inclusive criteria: Literature about the biological characteristics of myoblast, the application in skeletal muscle contraction and gene treatment.
血液中咖啡因水平的增加会阻碍腺苷的作用，导致血管收缩，最终则可能导致心脏病发作。埃尔-索海米说，在这项研究中，大约有55%的人携带有减缓咖啡因代谢的基因。
Increased levels of circulating caffeine may block adenosine's action, causing blood vessels to constrict, subsequently triggering a heart attack, says El-Sohemy.
目的：总结成肌细胞在骨骼肌收缩功能和细胞基因治疗研究中的应用。
OBJECTIVE: To summarize the application of myoblast in skeletal muscle contraction and gene treatment research.
结论：成肌细胞可以为骨骼肌在收缩功能上的研究提供一个很好的研究平台，其在基因治疗研究中的应用也为肌组织工程的研究奠定了基础。
CONCLUSION: Myoblast provides a research platform for skeletal muscle contraction function, which also lays a foundation for the muscle tissue engineering research in gene treatment.
为研究慢性低氧及跑台训练对大鼠骨骼肌肌球蛋白重链(mhc)亚型基因表达的影响，对揭示肌肉收缩蛋白性能的变化机制具有特定的意义。
The purpose of this paper is to investigate the influences on the gene expression of myosin heavy chain (MHC) isoforms of skeletal muscle in rats by chronic hypoxia and exercise training.
肥厚性心肌病与缺血性心脏病无关，但是50%的病例具有家族性并且与基因突变有关。突变基因一般为心脏收缩过程先关基因。
Hypertrophic cardiomyopathy is not related to ischemic heart disease but 50% of cases are familial and may be related to genetic mutations in genes encoding for cardiac contractile elements.
结果：正常胆囊有11047条基因表达，其前10位高表达基因与平滑肌收缩及物质转运有关。
Results: There were a total of11047genes expressed in the normal gallbladder, and the first10highly expressed genes were related to the function of smooth muscle contraction and materials transport.
新的研究证实，该基因加新的9种基因可以调节心脏收缩期，以QT间期来衡量。
The new study identifies that gene plus nine new ones that modify the timing of heart contractions, a measure known as the QT interval.
因此，我们检测了左心室收缩功能障碍并继发肿瘤坏死因子(TNF1.6)过表达的转基因老鼠腺苷水平和选择性ar的表达。
Therefore, we assessed adenosine levels and selective ar expression in transgenic mice with left ventricular systolic dysfunction secondary to overexpression of tumor necrosis factor - (TNF 1.6).
因此，我们检测了左心室收缩功能障碍并继发肿瘤坏死因子(TNF1.6)过表达的转基因老鼠腺苷水平和选择性ar的表达。
Therefore, we assessed adenosine levels and selective ar expression in transgenic mice with left ventricular systolic dysfunction secondary to overexpression of tumor necrosis factor - (TNF 1.6).
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