骨骼肌的运动适应机制

背景：骨骼肌运动适应机制的研究对提高运动成绩,预防和治疗一些代谢紊乱性疾病具有重要意义。 目的：探讨骨骼肌运动适应的机制。 方法：应用计算机检索PubMed数据库和中文期刊全文数据库2011-03前发表的相关文章,检索词分别为“skeletal muscle, exercise, adaptation, cytoskeleton, dystrophin”和“骨骼肌,运动,适应,骨架蛋白,肌营养不良蛋白”,共检索到56篇文献,纳入所述内容与骨骼肌运动适应机制相关的文献,排除重复性研究,保留31篇进行综述。 结果与结论：激烈的运动使肌肉结构和细胞代谢产生应激反应,包括肌肉损伤和氧化应激反应。高强度的离心运动可造成肌肉超微结构损伤,但运动性肌损伤后存在肌肉再重建反应。运动训练可促进健康的个体对一氧化氮系统产生各种各样的适应,通过各种机制增强骨骼肌的生物学有效性,这些适应性变化可有效增加运动能力,对心血管系统具有保护作用。目前,大多数人类骨骼肌运动适应机制还没有被发现。     

运动训练肌肉拉伤动物模型构建的相关问题

背景：肌肉拉伤是常见的运动损伤之一,肌肉拉伤的动物模型是对其进行科学研究的重要途径。 目的：分析与总结肌肉拉伤的机制和动物模型建立的相关问题。 方法：计算机检索中国期刊全文数据库、Highwire以及PubMed 数据库1980-01/2010-12的相关文章,中文检索词为“肌肉拉伤、动物模型”,英文检索词为“muscle strain, animal model”。纳入与肌肉拉伤动物模型构建密切相关的研究。 结果与结论：初检得到168篇文献,共保留31篇文献进行综述。目前国内外已有学者建立了一些骨骼肌损伤的动物模型,这些模型的建立对于骨骼肌的深入研究起到了极为重要的作用,但是肌肉急性拉伤动物模型的建立方法与运动实践相去甚远。因此,如何更有效地模拟高速运动状态下肌肉急性拉伤,建立一种符合运动实践特点的肌肉急性拉伤动物模型有其重要的实践价值。 关键词：肌肉拉伤;运动;动物模型;骨骼肌损伤;机制 doi:10.3969/j.issn.1673-8225.2012.02.036     

抗生素骨水泥与人工关节置换后的翻修

背景：抗生素骨水泥是预防和治疗人工关节置换以及翻修后感染的重要方法。 目的：综述抗生素骨水泥的研究进展以及人工关节置换后翻修。 方法：通过计算机检索Pubmed数据库、中国知网数据库、中国生物医学文献数据库、维普期刊全文数据库、万方数据库,时间范围在1978年至2012年,中文检索词“骨水泥”、“抗生素骨水泥”、“感染”、“关节置换”;英文检索词“bone cement”、“antibiotic bone cement”、“infection”、“joint replacement”。 结果与结论：共检索到相关文献335篇。通过阅读标题、摘要以及全文进行初步筛选,最后保留29篇文献进行深入的分析。抗生素骨水泥目前已广泛应用于人工关节置换以及翻修后感染的治疗,可以降低初次关节置换和翻修后感染的风险。适量的抗生素与骨水泥混合后其材料特性和力学性能不会发生改变。不同抗生素在骨水泥中的释放率也存在不同,与骨水泥的孔隙率有着密切的关系,在骨水泥中加入能够增加孔隙率的添加剂,可以达到最终增加抗生素释放的目的。     

衰老骨骼肌蛋白质的合成与抵抗**

背景：老年人随增龄出现的骨骼肌丢失现象称为骨骼肌衰老,通常表现为骨骼肌质量的丢失和力量的下降。其主要原因是衰老骨骼肌对骨骼肌蛋白合成刺激(补充蛋白质和运动)的敏感性下降,也即衰老出现了“蛋白质合成抵抗”现象。 目的：从概念、可能机制和干预手段等方面对衰老骨骼肌蛋白质合成抵抗进行综述,为探究营养和运动等干预手段来预防和延缓骨骼肌衰老提供理论依据。 方法：应用计算机检索Pubmed数据库和中国期刊网2000年1月至2011年12月相关文献。英文检索词为“skeletal muscle, aging,resistance training,protein”;中文检索词为“骨骼肌衰老,抗阻运动,蛋白质”。纳入标准：①观点明确,论点论据可靠的实验性文章。②与骨骼肌衰老以及相关内容的文章。排除标准：①与文章目的无关的内容。②重复性研究。 结果与结论：随着年龄的增长,老年人骨骼肌对较低浓度的氨基酸敏感性下降,蛋白质合成速率减弱,即出现“蛋白质合成抵抗”。研究表明蛋白质补充及抗阻运动可促进老年人骨骼肌蛋白质合成。而抗阻运动并结合蛋白质补充对老年人骨骼肌蛋白质合成的影响更加明显。但是老年人补充蛋白质的量,抗阻运动的强度以及何时补充蛋白质仍需做进一步的研究。     

人工全髋关节假体置换治疗运动性髋损伤的理论与实践☆

背景：全髋关节表面置换尽可能保持了髋关节原有的力学性能,置换后关节稳定性及活动度好,且无明显的年龄限制。 目的：探讨人工髋关节假体在髋关节运动损伤治疗中的临床应用,以及髋关节假体置换治疗的材料与方法进展。 方法：应用计算机检索1998-01/2011-10 PubMed数据库及中国知网数据库有关生物材料与组织工程髋关节的文献,英文检索词“hip joint injury,artificial hip joint,hip replacement,hip resurfacing arthroplasty”,中文检索词“髋关节损伤,人工髋关节,人工髋关节置换,全髋关节表面置换”。最终纳入符合标准的文献41篇。 结果与结论：严重髋关节运动损伤应行人工髋关节置换,以恢复患者的生活能力,甚至一定程度的运动能力。目前人工髋关节假体置换的关键因素在于假体材料,假体材料主要有金属材料、陶瓷材料高分子材料、新一代骨水泥等,各自具有一定优点与缺点,由于随访时间和临床观察周期较长,各种材料的疗效还需要进一步研究。计算机模拟髋关节的三维有限元分析成为研究的热点,将运动生物力学与材料科学结合,对新材料的研发与检验是制造满足组织工程学人工髋关节假体的要求,达到修复和重建目的的重要途径。     

基于微机电系统运动传感器在人体运动测量中的应用**

背景：基于微机电系统的运动传感器以其安装简易、使用便利、成本低廉的特点给人体运动测量变革带来了契机。 目的：分析总结运动传感器中适合人体运动测量的几型传感器,以及利用这些运动传感器取得的研究成果。 方法：应用计算机检索CNKI和ISI数据库中2005/2011-08关于基于微机电系统运动传感器技术的文章,在标题和摘要中以“微机电系统、运动传感器、人体运动”或“micro electro mechanical systems sensor,human motion,human movement”为检索词进行检索。选择内容与微机电系统运动传感器技术在人体运动测量中的应用相关的文章,且尽量选择近5年发表或发表在权威杂志的文章。 结果与结论：初检得到180篇文献,根据纳入标准选择34篇文章进行综述。人体运动测量中对各种运动传感器技术的关注和应用越来越多,运动传感器能够迅速简便地检测人体的运动信息,而其捕获的运动信息可广泛运用于各种临床领域。随着软硬件技术的不断发展将成为人体运动测量的主流手段。 关键词：运动传感器;微机电系统;人体运动测量;测量;应用;进展 doi:10.3969/j.issn.1673-8225.2012.09.041     

运动与不同组织细胞凋亡*

背景：细胞凋亡程序可被运动刺激诱发启动造成细胞死亡。 目的：分析运动训练对不同组织细胞凋亡的影响,探讨运动训练引起的不同组织细胞凋亡与运动性疲劳,运动损伤,运动心脏重塑,运动性心肌微损伤,运动性免疫抑制的关系。 方法：应用计算机检索Medline数据库1990-01/2010-05期间运动训练与细胞凋亡关系的文章,检索词为“apoptosis”。同时检索Ginii数据库2000-01/2010-06期间运动训练与细胞凋亡关系的文章,检索词为“アポトーシス,運動”。同时计算机检索中国期刊全文数据库2000-01/2010-05期间运动训练与细胞凋亡相关的文章,检索词为“细胞凋亡,运动训练,骨骼肌,心肌,淋巴细胞,肝肾细胞”。 结果与结论：无论是单次运动还是系统运动训练,都可以对骨骼肌、心肌、肝肾及淋巴细胞的凋亡产生影响,并呈现细胞凋亡水平随运动强度的提高而提高,因此细胞凋亡与运动性骨骼肌微损伤,运动心脏重塑,运动性心肌微损伤,运动性免疫抑制的关系密切。 关键词：细胞凋亡;运动训练;骨骼肌细胞;心肌细胞;淋巴细胞 doi:10.3969/j.issn.1673-8225.2012.11.036     

细胞因子修饰的间充质干细胞

背景：将细胞治疗与基因治疗相结合,通过不同的细胞因子对间充质干细胞的修饰,不但可以赋予其新的能力,更能增强其本身的功能。但是在西北高原的低氧环境下,间充质干细胞的功能发挥就会受到一定的限制。 目的：文章综述了间充质干细胞近年来的研究进展,在与细胞因子联合应用后功能上的扩展,并寻找新的手段使其在高原低氧环境下充分发挥功能。 方法：应用计算机检索CNKI数据库和PUBMED数据库中关于间充质干细胞的文章,以“间充质干细胞;低氧诱导因子;肝细胞生长因子”或“mesenchymal stem cells; hypoxia inducible factor;hepatocyte growth factor”为检索词进行检索。检索文献总量为71篇,选择文章内容与间充质干细胞及其临床应用有关方面的文章,同一领域文献则选择近期发表或发表在权威杂志文章。 结果与结论：最终纳入35篇符合标准的文献。通过应用细胞因子的转染,将细胞因子的功能与间充质干细胞相结合,使得间充质干细胞的功能更全面,在高原低氧的恶劣环境下,依然能够有效的发挥临床效用,满足其临床上的治疗需求。     

肿瘤干细胞的研究进展

背景：肿瘤干细胞具有高度增殖和分化能力,但又不同于普通干细胞,此类干细胞还具有发展成为肿瘤的特性,因此备受学者们关注。 目的：综述近几年来肿瘤干细胞的特性以及与干细胞和肿瘤的关系及其临床意义。 方法：应用计算机检索2000-01/2010-11 PubMed数据库、中国期刊全文数据库、万方数据库相关肿瘤干细胞的文章,中文检索词为“肿瘤干细胞”,英文检索词为“tumor stem cell”。共检索到文献89篇,最终纳入符合标准的30篇文献。 结果与结论：目前国内肿瘤干细胞还处于基础研究阶段,国外肿瘤干细胞在实验研究方面已经取得了一定的进展,而且也在临床应用研究方面有一定的突破。普遍认为肿瘤组织中存在肿瘤干细胞,肿瘤干细胞对肿瘤的发生发展和肿瘤治疗都有重要的作用,对肿瘤干细胞治疗肿瘤的临床应用前景也非常乐观,但肿瘤干细胞特征以及与成体干细胞关系仍处于初步研究阶段。     

组织工程心脏瓣膜支架材料的研究和展望

背景：当前应用于临床的生物瓣和机械瓣都存在着一定缺陷,而组织工程心脏瓣膜将避免这些问题成为理想的生物瓣膜替代物。 目的：综述近年来组织工程心脏瓣膜支架材料的研究进展及面临的问题。 方法：应用计算机检索1990至2011年万方数据库相关文章,检索词为“组织工程,心脏瓣膜,支架材料”,并限定文章语言种类为中文。同时计算机检索1990至2011年 PubMed数据库相关文章,检索词为“tissue engineering,heart valve,scaffold materials”,并限定文章语言种类为English。共检索到文献147篇,最终纳入符合标准的文献61篇。 结果与结论：人工心脏瓣膜置换是目前治疗心脏瓣膜性病变的主要外科治疗手段,但现有机械瓣和生物瓣都不是理想的心脏瓣膜置换物,在耐久性,增长潜力,相容性,抗感染方面有着显著的缺陷。组织工程心脏瓣膜是一个活体器官,并具有和自体心脏瓣膜同样的生长,修复和重建能力,这一新概念的提出为构建理想的心脏瓣替换物带来了希望。     

Calorie restriction extends yeast life span by lowering the level of NADH

Calorie restriction (CR) extends life span in a wide variety of species. Previously, we showed that calorie restriction increases the replicative life span in yeast by activating Sir2, a highly conserved NAD-dependent deacetylase. Here we test whether CR activates Sir2 by increasing the NAD/NADH ratio or by regulating the level of nicotinamide, a known inhibitor of Sir2. We show that CR decreases NADH levels, and that NADH is a competitive inhibitor of Sir2. A genetic intervention that specifically decreases NADH levels increases life span, validating the model that NADH regulates yeast longevity in response to CR.     

Mitochondrial function as a determinant of life span

Average human life expectancy has progressively increased over many decades largely due to improvements in nutrition, vaccination, antimicrobial agents, and effective treatment/prevention of cardiovascular disease, cancer, etc. Maximal life span, in contrast, has changed very little. Caloric restriction (CR) increases maximal life span in many species, in concert with improvements in mitochondrial function. These effects have yet to be demonstrated in humans, and the duration and level of CR required to extend life span in animals is not realistic in humans. Physical activity (voluntary exercise) continues to hold much promise for increasing healthy life expectancy in humans, but remains to show any impact to increase maximal life span. However, longevity in Caenorhabditis elegans is related to activity levels, possibly through maintenance of mitochondrial function throughout the life span. In humans, we reported a progressive decline in muscle mitochondrial DNA abundance and protein synthesis with age. Other investigators also noted age-related declines in muscle mitochondrial function, which are related to peak oxygen uptake. Long-term aerobic exercise largely prevented age-related declines in mitochondrial DNA abundance and function in humans and may increase spontaneous activity levels in mice. Notwithstanding, the impact of aerobic exercise and activity levels on maximal life span is uncertain. It is proposed that age-related declines in mitochondrial content and function not only affect physical function, but also play a major role in regulation of life span. Regular aerobic exercise and prevention of adiposity by healthy diet may increase healthy life expectancy and prolong life span through beneficial effects at the level of the mitochondrion.     

Beyond interventions: caloric restriction as a scientific model

Caloric restriction is a major component of most life-style interventions. Beyond its use as an intervention tool, caloric restriction can also serve as a scientific model to study important research questions. Caloric restriction in nonhuman animals can dramatically extend the life span, and this can also be tested in humans. In addition to conducting randomized controlled trials of caloric restriction, there is much knowledge to be gained by studying already existing conditions of very long-term caloric restriction. The Cronies, members from the Calorie Restriction Society, are one such model. In addition to studying biological markers relevant to aging in the Cronies, we can also study them to understand what makes them so successful at long-term eating behavior change. This information is invaluable given the difficulties people from the general population face in adhering to calorie reduction interventions.     

Newer approaches in increasing life span

Based on ideal conditions technical life span of human kind is approximately 110-120 years. Although number of studies including calorie restriction and antiparkinsonism drug (deprenyl) have indicated increased life span in animals, it is premature to expect them to increase life span in man. However, current studies like activation of immune system with DHEA in man and anticipation of antioxidant therapy contributing to increased life span are encouraging. Practice of meditation particularly TM and balanced diet might be contributory.     

Caloric restriction in humans: potential pitfalls and health concerns

To date, the only intervention that has consistently been shown to slow the rate of aging, and to increase mean and maximum lifespan in short-lived species, is life-long calorie restriction. It is yet unclear whether long-term calorie restriction in longer lived species (i.e. primates and humans) will have a similar effect. In humans, several studies investigating short-term calorie restriction or "weight loss" programs suggest beneficial outcomes on parameters of cardiovascular disease. Studies on long-term calorie restriction are performed on a self-selected group of human subjects and show similar effects. However, few studies are currently investigating the quality of life and potential pitfalls of long-term calorie restriction in humans. It is likely that some of the physiological and psychological effects of caloric restriction that occur in animals may impact the human life very differently. For certain, calorie restriction has a plethora of health benefits in mammals, such as a reduction in age-related diseases such as cancer. However, despite the "magic" of CR, this intervention in humans may present itself with a number of health concerns, which may not be applicable to or impact the life of experimental animals, but may do so in humans. These potential pitfalls and "side effects" are not clearly addressed in the literature and will be a focus of this review.     

Relationship between protein O-linked glycosylation and insulin-stimulated glucose transport in rat skeletal muscle following calorie restriction or exposure to O-(2-acetamido-2-deoxy-d-glucopyranosylidene)amino-N-phenylcarbamate

AIMS AND BACKGROUND: Protein O-linked glycosylation is regulated in vivo by the concentration of hexosamine substrates. Calorie restriction (60% of ad libitum intake) for 20 days causes decreased UDP-N-acetylhexosamine levels and increased insulin-mediated glucose transport in rat skeletal muscle. Conversely, prolonged incubation (19 h) of muscle with O-(2-acetamido-2-deoxy-D-glucopyranosylidene)amino-N-phenyl-carbamate (PUGNAc; an inhibitor of N-acetyl-beta-D-glucosaminidase) is characterized by increased O-linked glycosylation and insulin resistance. We aimed to determine the calorie restriction effect on O-linked glycosylation and characterize the temporal relationship between PUGNAc-induced O-linked glycosylation and insulin resistance. HYPOTHESIS: A calorie restriction protocol characterized by decreased muscle hexosamine levels will result in a global reduction in O-linked glycosylated proteins in muscle, and PUGNAc-induced insulin resistance will coincide with increased O-linked glycosylation. METHODS: Plantaris muscle and liver from rats (ad libitum or calorie restricted) were analysed for O-linked glycosylation using two antibodies against different O-linked N-acetylglucosamine epitopes. Also, rat epitrochlearis muscles were incubated for 8.5 h +/- 100 mum PUGNAc prior to measurement of [(3)H]-3-O-methylglucose transport and O-linked glycosylation. RESULTS: Calorie restriction did not alter protein O-linked glycosylated levels in muscle or liver. Incubation with PUGNAc for 8.5 h resulted in increased in O-linked glycosylation but unaltered basal or insulin-stimulated glucose transport. CONCLUSIONS: The delay between O-linked glycosylation and insulin resistance in muscle incubated with PUGNAc suggests an indirect, relatively slow mechanism for insulin resistance. The effect of calorie restriction on insulin action in muscle is unlikely to be the direct result of a global change in protein O-linked glycosylation.     

Adult-onset calorie restriction attenuates kainic acid excitotoxicity in the rat hippocampal slice

Lifelong calorie restriction is the only known intervention that has been shown to consistently increase life span and reduce the effects of aging on the brain. Given the difficulties of replicating lifelong calorie restriction within human populations, we have sought to assess the effects of short-term adult-onset calorie restriction upon acute excitotoxic insults in the rat hippocampus. Adult animals (approximately 6 months of age) underwent calorie restriction (alternate day feeding) for 7-10 weeks. Utilizing both electrophysiological and immunocytochemical techniques, we report that calorie restriction had no effect upon long-term potentiation (LTP), a measure of neuronal function. In control animals, application of kainic acid (20 microM) resulted in only 35% recovery of CA1 population spikes post-insult. However calorie-restricted animals showed significantly improved recovery after kainic acid treatment (64%). This data was supported by immunocytochemical studies which noted widespread loss of microtubule-associated protein (MAP 2) immunoreactivity in control slices following treatment with kainic acid; however MAP 2 staining was preserved in the CA1 and CA3 regions of calorie-restricted animals. Interestingly there was no significant difference in the recovery of population spikes between groups when slices were treated with N-methyl-d-aspartate (15 microM). We conclude that short-term adult-onset calorie restriction does not alter normal neuronal function and serves to protect the hippocampus from acute kainic acid excitotoxicity.     

Longevity of exercising male rats: effect of an antioxidant supplemented diet

Food restriction increases maximal life span in rodents. Male rats that exercise in voluntary running wheels do not have an increase in maximal longevity despite a relative caloric deficit. In contrast, sedentary rats that are food restricted so as to cause the same caloric deficit have an extension of maximal longevity. It seemed possible that exercise-induced oxidative stress might prevent a maximum life span-extending effect of a caloric deficit to manifest itself. This study was done to determine if antioxidants would allow a maximal longevity-extending effect of exercise to manifest itself in male rats. The antioxidant diet had no effect on longevity of the runners (Antiox., 951±158 days versus control 937±171 days), or of the sedentary controls (875±127 versus 858±152 days). As in previous studies, wheel running modestly increased average longevity (≈9%), but had no effect on maximal life span. The finding that antioxidants had no effect on longevity of the wheel runners supports the interpretation that the caloric deficit induced by exercise in male rats does not have a life-extending effect that is countered by oxidative tissue damage.     

Glutathione is necessary to ensure benefits of calorie restriction during ageing in Saccharomyces cerevisiae

Calorie restriction increases longevity of mammals and yeasts but this mechanism remains unclear. In this study, the role of glutathione on lifespan extension induced by calorie restriction was investigated by using a Saccharomyces cerevisiae strain deficient in glutathione synthesis (gsh1). We observed an increase in chronological lifespan of calorie-restricted gsh1 mutant cells, compared to WT (wild type) strain, which was associated with a reduction in the levels of oxidative stress biomarkers. The gsh1 strain showed an increase in cell yield under calorie restriction that was associated with a higher pyruvate kinase activity and a reduction in oxygen consumption and aconitase activity. This indicates that the respiratory metabolism is decreased in gsh1 mutant cells. The lifespan extension of gsh1 mutant cells did not represent an advantage at long term, since old cells of gsh1 strain showed a higher frequency of petite mutants. In addition, aged WT cells outlast aged gsh1 mutant cells in direct competition assays in a fresh medium. These results suggest that glutathione is required for the beneficial effects of calorie restriction on cellular longevity.     

Genes determining yeast replicative life span in a long-lived genetic background

Here we describe the replicative life spans of more than 50 congenic Saccharomyces cerevisiae strains, each carrying a mutation previously implicated in yeast aging. This analysis provides a direct comparison, in a single, long-lived strain background, of a majority of reported yeast aging genes. Of the eleven deletion mutations previously reported to increase yeast life span, we find that deletion of FOB1, deletion of SCH9, and deletion of GPA2, GPR1, or HXK2 (three genetic models of calorie restriction) significantly enhanced longevity. In addition, over-expression of SIR2 or growth on low glucose increased life span. These results define a limited number of genes likely to regulate replicative life span in a strain-independent manner, and create a basis for future epistasis analysis to determine genetic pathways of aging.