肌

The mechanism might be related to the degression of glucocorticoids and the activation of glycogen synthase.

肌肽增强应激负荷小鼠肝糖原合成能力，其作用机制可能与肌肽降低体内糖皮质激素水平、激活糖原合酶有关。

Phytase was a kind of enzyme for hydrolyzing phytate to release myoinositol and inorganic phosphate, which would promote the utilization of phosphate, reduce the drainage of phosphate in the dejecta and reduce the environmental pollution.

植酸酶是催化植酸及植酸盐水解成肌醇与磷酸的一类酶的总称。植酸酶添加在饲料中，会将其中的植酸水解成肌醇和磷酸，从而提高了磷的利用率，降低了粪便中磷的排放量，减少了植酸磷对环境的污染。

The training can also exercise the back of the top of the deltoid and trapezius.

这项训练还可以锻炼背部上方的三角肌和斜方肌。

The onset latencies of the antagonist trunk muscles relative to the deltoid muscle were analyzed to determine the effects of group, target height and load.

躯干拮抗肌的起始潜伏期与三角肌的关系取决于试验的组别，目标的高度及负荷的不同。

Objective:To explore the morphological changes in orbicularis oculi muscle and orbicularis oris muscle after denervation.

目的：探讨不同程度失神经支配后，眼轮匝肌和口轮匝肌的形态学变化。

Objective Facial nerve denervation can cause a series of symptoms.

目的 面神经麻痹后将引起一系列面肌瘫痪症状，面肌的机能和组织学都将随着时间的不同而发生不同程度的病理变化。

Compression of nerve roots often produces objective sensory changes early, with paresthesia and loss of sensating detectable in the affected dermatome.

神经根受压常很早即产生客观的感觉变化，在受影响的皮节区有感觉异常及感觉缺失，神经根持续受压，可发生运动肌无力，若累及腰4神根，可见膝腱反射减弱和轻度股四头肌无力，小腿肌肉感觉减退。

Compre ion of nerve roots often produces objective se ory changes early, with paresthesia and lo of se ating detectable in the affected dermatome. With continued root compre ion. Motor weakne may develop. With involvement of the L4 root, the patellar tendon reflex may be diminished and slight quadrice weakne may be o erved.

神经根受压常很早即产生客观的感觉变化，在受影响的皮节区有感觉异常及感觉缺失，神经根持续受压，可发生运动肌无力，若累及腰4神根，可见膝腱反射减弱和轻度股四头肌无力，小腿肌肉感觉减退。

After developing 48 hours, hepatocytes enters 2.0 mM t-butyl hydroperxide or 2.0 mM diamide to induced cell blebbing. The samples collected at 0, 15, 30, 60 minutes to analyze cell about membrane protein thiol deletion; the leakage of lactate dehydrodenase; the change of glutathione; the lipid peroxidation; the variation of actin and tubulin, and use Confocal fluorescent microscope to observe the change of actin and tubulin in rat hepatocytes.

肝细胞在48小时培养后，分别加入2.0mM t-buty1 hydroperoxide或2.0 mM diamide诱发细胞膜小泡生成，并分别於0、15、30、60分钟取样，分析细胞膜硫醇流失程度；乳酸去氢□渗漏；□胱甘□浓度变化；脂质过氧化；肌动蛋白与管蛋白变化；并利用雷射共轭焦萤光显微镜观察肝细胞中肌动蛋白及管蛋白的变化。

The result indicates the t-BHP or diamide both cause the mass loss about the membrane protein thiol in hepatocytes, the fast oxidization about glutathione in hepatocytes, the leakage of lactate dehydrodenase, but the level of t-BHP is larger than of diamide. In the aspect of lipid peroxidation, only the t-BHP produces apparent change. As to actin and tubulin, they both find fall-off and present time-dependency effects. The result in Confocal fluorescent microscope also show these two cytoskeletal proteins are related to cell blebbing, but they don''t play the same role during the porcess. Tubulin may be more important than actin. If the study predispose dithiothreitol before adding t-BHP or diamide, then the damage by the diamide is repressed, but just partly protection for the damage by t-BHP.

结果显示t-BHP或diamide均可造成细胞膜蛋白硫醇大量流失与胞内GSH快速氧化，亦显著导致乳酸去氢□渗漏，但t-BHP诱发的渗漏程度大於diamide；在脂质过氧化方面，则仅t-BHP处理组产生明显的脂质氧化情形；至於肌动蛋白与管蛋白单体均可见减少且呈现时间依赖效应；在雷射共轭焦萤光显微镜观察中，亦显现这两种架构蛋白与细胞膜起泡有关，但两者在小泡生成的过程中扮演的角色并不完成相同，可能管蛋白较肌动蛋白重要；如果细胞在t-BHP或diamide加入前预先以dithiothreitol处理，则diamide 所造成的伤害显著的受到抑制，但DTT对t-BHP所诱发的伤害则仅有部分保护效果。

For a big chunk of credit-card losses; the number of filings (and thus charge-off rates) would be rising again, whether

年美国个人破产法的一个改动使得破产登记急速下降，而后引起了信用卡大规模的亏损。

Eph. 4:23 And that you be renewed in the spirit of your mind

弗四23 而在你们心思的灵里得以更新