基于电阻抗扫描成像的乳腺癌检测方法

为了提高电阻抗成像在乳腺癌检测方面的性能,降低其假阳性率,提出了一种新的乳腺癌检测算子———异常能量指标(AEI)检测乳腺癌.通过对乳腺电阻抗成像进行建模并结合优化问题求解,提取乳腺癌病灶参数并进而构造AEI指标.与传统的基于临床医师视觉解释的图像检测方法相比,新方法可以获得更高的灵敏度、特异度和准确度.与基于参数的乳腺癌检测算法(HEDA算法和P算法)相比,AEI指标用于乳腺癌检测具有较高的灵敏度及特异度.临床数据实验表明,新方法可以有效地用于乳腺癌检测,具有较好的检测性能(灵敏度88.5%、特异度89.1%以及准确度88.9%).     

Cardiac-type excitation-contraction coupling in dysgenic skeletal muscle injected with cardiac dihydropyridine receptor cDNA

There are dihydropyridine (DHP)-sensitive calcium currents in both skeletal and cardiac muscle cells, although the properties of these currents are very different in the two cell types (for simplicity, we refer to currents in both tissues as L-type). The mechanisms of depolarization-contraction coupling also differ. As the predominant voltage-dependent calcium current of cardiac cells, the L-type current represents a major pathway for entry of extracellular calcium. This entry triggers the subsequent large release of calcium from the sarcoplasmic reticulum (SR). In contrast, depolarization of skeletal muscle releases calcium from the SR without the requirement for entry of extracellular calcium through L-type calcium channels. To investigate the molecular basis for these differences in calcium currents and in excitation-contraction (E-C) coupling, we expressed complementary DNAs for the DHP receptors from skeletal and cardiac muscle in dysgenic skeletal muscle. We compared the properties of the L-type channels produced and showed that expression of a cardiac calcium channel in skeletal muscle cells results in E-C coupling resembling that of cardiac muscle.     

Immunostaining of skeletal and cardiac muscle surface membrane with antibody against Duchenne muscular dystrophy peptide

Duchenne muscular dystrophy (DMD) is a debilitating X-linked muscle disease. We have used sequence information from complementary DNA clones, derived from the gene that is deleted in DMD patients, to generate an antiserum that stains the surface membrane of intact human and mouse skeletal muscle, but not that of DMD patients and mdx mice. Here we identify the protein reacting with this antiserum as a single component of relative molecular mass 210,000 (Mr = 210K) that fractionates with a low-ionic strength extract of intact human and mouse skeletal muscle. It is therefore distinct from the 400 K protein found in the heavy microsomal fraction of normal muscle and identified as a putative product of the DMD gene. We also analyse further the disease specificity of the antiserum. Positive staining is seen in normal controls, and in samples from patients with a wide range of muscular dystrophies other than DMD. Becker muscular dystrophy, which is allelically related to DMD, was the only other exception, and gave a sporadic staining pattern. The demonstration of a specific defect in the surface membrane of DMD muscle fibres substantiates the hypothesis that membrane lesions may initiate muscle degradation in DMD.     

MAP and kinesin-dependent nuclear positioning is required for skeletal muscle function

The basic unit of skeletal muscle in all metazoans is the multinucleate myofibre, within which individual nuclei are regularly positioned. The molecular machinery responsible for myonuclear positioning is not known. Improperly positioned nuclei are a hallmark of numerous diseases of muscle, including centronuclear myopathies, but it is unclear whether correct nuclear positioning is necessary for muscle function. Here we identify the microtubule-associated protein ensconsin (Ens)/microtubule-associated protein 7 (MAP7) and kinesin heavy chain (Khc)/Kif5b as essential, evolutionarily conserved regulators of myonuclear positioning in Drosophila and cultured mammalian myotubes. We find that these proteins interact physically and that expression of the Kif5b motor domain fused to the MAP7 microtubule-binding domain rescues nuclear positioning defects in MAP7-depleted cells. This suggests that MAP7 links Kif5b to the microtubule cytoskeleton to promote nuclear positioning. Finally, we show that myonuclear positioning is physiologically important. Drosophila ens mutant larvae have decreased locomotion and incorrect myonuclear positioning, and these phenotypes are rescued by muscle-specific expression of Ens. We conclude that improper nuclear positioning contributes to muscle dysfunction in a cell-autonomous fashion.     

运动与骨骼肌中的基因表达

通过献资料法阐述了运动对骨骼肌基因表达的影响,以便深入理解骨骼肌的工作原理,为客观指导运动训练提供依据．     

心肌3种应力的并联桥本构模型

为了深入研究心肌的力学性质,通过理论推导,提出了心肌的并联桥本构模型。该模型包含心肌的被动力、主动力和生长应力三种模型。被动力模型是一个各向异性的非线性弹性模型,其力学性质主要决定于心肌的纤维方向的力学性质;结合自由钙离子浓度演化方程和横桥动力学模型,发展了心肌的主动力模型,在周期化钙离子浓度场的基础上,得到随时间周期变化的主动应力;提出了生长应力的概念,建立基于生长因子表达变化的生长应力模型。研究结果表明,并联桥本构模型完备地反映了心肌的被动力、主动力和生长应力3种应力状态模型。     

Regions of the skeletal muscle dihydropyridine receptor critical for excitation-contraction coupling

It is thought that in skeletal muscle excitation-contraction (EC) coupling, the release of Ca2+ from the sarcoplasmic reticulum is controlled by the dihydropyridine (DHP) receptor in the transverse tubular membrane, where it serves as the voltage sensor. We have shown previously that injection of an expression plasmid carrying the skeletal muscle DHP receptor complementary DNA restores EC coupling and L-type calcium current that are missing in skeletal muscle myotubes from mutant mice with muscular dysgenesis. This restored coupling resembles normal skeletal muscle EC coupling, which does not require entry of extracellular Ca2+. By contrast, injection into dysgenic myotubes of an expression plasmid carrying the cardiac DHP receptor cDNA produces L-type calcium current and cardiac-type EC coupling, which does require entry of extracellular Ca2+. To identify the regions responsible for this important functional difference between the two structurally similar DHP receptors, we have expressed various chimaeric DHP receptor cDNAs in dysgenic myotubes. The results obtained indicate that the putative cytoplasmic region between repeats II and III of the skeletal muscle DHP receptor is an important determinant of skeletal-type EC coupling.     

骨骼肌急性拉伤与修复的组织学探讨

指出了骨骼肌急性拉伤的生物力学原因.对骨骼肌损伤与修复的组织学基础进行了分析和探讨.结论表明:预防为主是减少肌肉拉伤最有效的方法;冰敷疗法无实验依据和理论支持,使用时一定要十分谨慎;热疗法是较安全、可靠的方法.     

人骨骼肌双向电泳条件优化及部分蛋白质鉴定

目的建立和优化人骨骼肌组织双向电泳模型,为深入探讨骨骼肌萎缩的分子机制提供方法上的保障。方法使用两性离子去垢剂CHAPS和SB3-10,并配合不同浓度的离液剂抽提骨骼肌蛋白质,并通过双向电泳对蛋白质进行分离,用基质辅助激光解析电离飞行时间质谱(MALDI-TOF)对选取的蛋白质进行鉴定。结果优化过的双向电泳模型可在一张凝胶上分离800多个蛋白质点,通过MALDI-TOF鉴定出HUMANserine/threonine protein kinase KKIALRE等4种低丰度蛋白质。结论多种去垢剂和离液剂的组合使用才能获得对组织中蛋白质较好的抽提效果。获得的人骨骼肌双向电泳图谱是对人类骨骼肌蛋白质组学数据库的有益补充,为使用比较蛋白质组学方法筛选人肌病关键蛋白质提供了实践和理论基础。     

Primary structure of the receptor for calcium channel blockers from skeletal muscle

The complete amino-acid sequence of the receptor for dihydropyridine calcium channel blockers from rabbit skeletal muscle is predicted by cloning and sequence analysis of DNA complementary to its messenger RNA. Structural and sequence similarities to the voltage-dependent sodium channel suggest that in the transverse tubule membrane of skeletal muscle the dihydropyridine receptor may act both as voltage sensor in excitation-contraction coupling and as a calcium channel.