电脑前久坐易出现肌肉骨骼疼痛

一项新的研究显示，大学生花在电脑上的时间越长，越有可能在当天出现肌肉和骨骼疼痛的问题。[第一段]     

肌肉骨骼减少症发病机制及其运动防治效果

肌肉骨骼减少症（osteosarcopenia,OS）是一种多因素、多病因的退行性代谢综合征,其影响因素可能与衰老导致的机械、遗传、炎症因子、内分泌紊乱以及生活方式不规律相关。OS患者具有更高跌倒、骨折、活动障碍和死亡的风险,随着中国全球老龄化进程的加快,OS已经成为不容忽视的公共健康问题。近年来,国内外学者针对OS开展了大量的研究,但其发病机制仍不清楚。了解与OS相关的信号通路对进一步研究其发病机制和寻找治疗的新靶点具有重要意义。而运动作为现有效果强、持续性好的非药物治疗方式,能够增加老年人肌肉质量、提高骨密度、改善生活质量等,从而有效地预防和改善OS。本文主要就OS的流行病学、诊断标准、共同参与调节肌细胞与骨骼细胞代谢过程的相关信号通路（PI3K/Akt通路、Wnt/β-catenin通路、Notch通路、NF-κB通路）,以及不同运动方式对OS的干预效果等方面进行综述,以期为临床治疗OS提供理论依据,提高老年疾病的预防能力。     

NLRP3炎性小体在肌肉骨骼系统疾病中的作用

炎性小体是先天性免疫系统的受体和传感器,在许多疾病的发生和进展中起着关键的病理作用。近期研究表明,NOD样受体家族核苷酸结合寡聚化结构域样受体3 (NOD-like receptor thermal protein domain associated protein 3, NLRP3)炎性小体参与了对公共健康具有高度影响的疾病的发生,如肌肉骨骼系统疾病。肌肉骨骼系统疾病是主要由工作和周围环境引起或加重的肌肉、关节、骨骼等运动系统疾病,以及相关神经、循环系统损伤的疾病。NLRP3小体的激活可以诱导炎症及引发焦亡,造成机体进一步损伤。因此,以NLRP3炎性小体为切入点,开展对肌肉骨骼系统疾病的预防和治疗具有重要意义。研究炎症性疾病中NLRP3炎性小体活动的机制及作用已然成为新的研究方向。本文对NLRP3炎性小体的激活途径及机制进行了概述,并分析了NLRP3炎性小体在肌少症、骨质疏松症和关节炎等肌肉骨骼系统疾病中的作用,以期为肌肉骨骼系统疾病的治疗提供理论依据。     

二维心室建模和Brugada综合症仿真

本文以Tusscher提出的人体心室单细胞计算模型为基础,用计算机建模仿真的方法,构建一个心室壁组织的二维网格模型。通过修改细胞的离子通道参数,仿真了正常生理条件下和Brugada症状下三类心室细胞的动作电位和心电图波形。结果显示:Brugada症状下的心电图波形有明显的J波出现,ST-段抬高甚至T波倒置。这与临床医学上的报道基本符合,本研究为用计算机仿真建模研究Brugada综合症打下了基础。     

同胚模型——生物系统建模与仿真的一个发展方向

本文叙述了自系统论、控制论提出以来生物系统的建模与仿真的几种类型各自的优缺点,包括类比模型、黑箱模型、机能模型以及同胚模型,指出建立同胚模型是生命科学定量化较好的发展,最后提出了建立同胚模型的几种可能的方法。     

仿真领域的持续承诺

随着分子生物学领域的进步,基因组及相关计划的进展,系统生物学逐渐成为生命科学研究中的热点,生物系统方面的建模和仿真也成为目前系统生物学研究引人关注的内容之一。而第一代建模工具在应用的过程中存在许多缺陷,从而导致用户需求和工具建模能力之间存在巨大鸿沟。本文对第一代建模工具存在的问题进行了分析,并简单介绍了可以进行复杂仿真建模的新一代仿真工具。此外,文章对系统生物学的市场模式也进行了探讨。     

面向短QT综合征的药物作用建模与仿真研究

短QT综合征(short QT syndrome,SQTS)是以心电图QT间期、心室和心房不应期明显缩短为主要显性特征,并伴有晕厥、高发心源性猝死(sudden cardiac death,SCD)和恶性心律失常风险的一类遗传性心肌离子通道病.据目前资料信息,关于SQTS致病机理的报道比较多,而对SQTS药物治疗的报道罕见.为了揭示在SQTS下的药物作用,本文通过计算机仿真构建人体心室细胞和组织的药物作用模型,利用该模型,从亚细胞、细胞、组织三个尺度,模拟SQT1、SQT2和SQT3下的普罗帕酮药物作用过程,并仿真心电图的变化情况.仿真结果表明:在SQT1下普罗帕酮延长了动作电位时程(action potential duration,APD)和心电图QT间期,并降低T波幅值;相反,在SQT2和SQT3下普罗帕酮缩短了APD和QT间期.计算使用药物前后细胞间膜电压和APD空间离散度的变化,定量分析了普罗帕酮降低T波振幅的原因.总之,对SQT1,普罗帕酮有效;对SQT2和SQT3,普罗帕酮没有改变其致心律失常的危险.仿真结果为普罗帕酮用于临床治疗SQTS提供理论参考.     

味觉感受细胞离子通道和动作电位的建模与仿真

结合膜片钳测量的味觉感受细胞离子通道实验数据,提出了一个哺乳动物味觉感受细胞动作电位的数学模型.首先,建立了味觉感受细胞的电压门控Na＋通道和外向延迟整流K＋通道的模型,在此基础上建立了味觉感受细胞的单细胞计算模型.其次,仿真研究了味觉感受细胞在电刺激和酸味刺激下产生的动作电位,以及离子通道动力学特性对其的影响.该模型对于研究味觉感受细胞在味觉物质刺激下产生的动作电位及其离子通道的工作机制,以及味觉信息在外周神经的传递和信息编码具有指导意义。     

microRNAs在肌肉中的作用研究进展

microRNAs是一类非蛋白质编码小RNA,通常作用于靶基因mRNA的3′-UTR区引起靶基因的翻译抑制或降解。microRNAs的表达具有组织特异性,骨骼肌和心肌中有特异microRNAs的表达。microRNAs在肌肉的增殖、分化等发育过程中发挥重要的调节作用,并且microRNAs的表达异常与某些肌肉疾病的病理过程有关。现就microRNAs在肌肉中的作用研究进展作一综述。     

A Model of Human Muscle Energy Expenditure

A model of muscle energy expenditure was developed for predicting thermal, as well as mechanical energy liberation during simulated muscle contractions. The model was designed to yield energy (heat and work) rate predictions appropriate for human skeletal muscle contracting at normal body temperature. The basic form of the present model is similar to many previous models of muscle energy expenditure, but parameter values were based almost entirely on mammalian muscle data, with preference given to human data where possible. Nonlinear phenomena associated with submaximal activation were also incorporated. The muscle energy model was evaluated at varying levels of complexity, ranging from simulated contractions of isolated muscle, to simulations of whole body locomotion. In all cases, acceptable agreement was found between simulated and experimental energy liberation. The present model should be useful in future studies of the energetics of human movement using forward dynamic computer simulation.     

Activation in a Skeletal Muscle Contraction Model with a Modification for Insect Fibrillar Muscle

A sliding filament model for muscle contraction is extended by including an activation mechanism based on the hypothesis that the binding of calcium by a regulating protein in the myofibrils must occur before the rate constant governing the making of interactions between cross-bridges and thin filament sites can take on nonzero values. The magnitude of the rate constant is proportional to the amount of bound calcium. The model's isometric twitch and rise of force in an isometric tetanus are similar to the curves produced by real muscles. It redevelops force after a quick release in an isometric tetanus faster than the initial rise. Quick release experiments on the model during an isometric twitch show that the “active state” curve produced is different from the postulated calcium binding curve. The force developed by the model can be increased by a small quick stretch delivered soon after activation to values near the maximum generated in an isometric tetanus. Following the quick stretch, the force remains near the tetanic maximum for a long time even though the calcium binding curve rises to a peak and subsequently decays by about 50%. The model satisfies the constraint of shortening with a constant velocity under a constant load. Modifications can be made in the model so that it produces the delayed force changes following step length changes characteristic of insect fibrillar muscle.     

Finger Muscle Attachments for an OpenSim Upper-Extremity Model

We determined muscle attachment points for the index, middle, ring and little fingers in an OpenSim upper-extremity model. Attachment points were selected to match both experimentally measured locations and mechanical function (moment arms). Although experimental measurements of finger muscle attachments have been made, models differ from specimens in many respects such as bone segment ratio, joint kinematics and coordinate system. Likewise, moment arms are not available for all intrinsic finger muscles. Therefore, it was necessary to scale and translate muscle attachments from one experimental or model environment to another while preserving mechanical function. We used a two-step process. First, we estimated muscle function by calculating moment arms for all intrinsic and extrinsic muscles using the partial velocity method. Second, optimization using Simulated Annealing and Hooke-Jeeves algorithms found muscle-tendon paths that minimized root mean square (RMS) differences between experimental and modeled moment arms. The partial velocity method resulted in variance accounted for (VAF) between measured and calculated moment arms of 75.5% on average (range from 48.5% to 99.5%) for intrinsic and extrinsic index finger muscles where measured data were available. RMS error between experimental and optimized values was within one standard deviation (S.D) of measured moment arm (mean RMS error = 1.5 mm < measured S.D = 2.5 mm). Validation of both steps of the technique allowed for estimation of muscle attachment points for muscles whose moment arms have not been measured. Differences between modeled and experimentally measured muscle attachments, averaged over all finger joints, were less than 4.9 mm (within 7.1% of the average length of the muscle-tendon paths). The resulting non-proprietary musculoskeletal model of the human fingers could be useful for many applications, including better understanding of complex multi-touch and gestural movements.     

Model for the Action of Calcium in Muscle

CALCIUM ions play an important part in contraction^1–3, but little is known of the way that changes in internal calcium actually control the events that lead to the development of tension. Most experiments involving calcium have been performed under steady state conditions at different stabilized calcium concentrations^4–9 and can only give limited information as to the action of calcium. Recently, tension transient experiments have been described at either constant calcium concentration^6,7 or when the calcium concentration was varying in a known manner^10,11. From these and related experiments, a model for the kinetics of calcium has been deduced which predicts not only the time course of tension development from just a knowledge of the free calcium concentration, but which is also able to correlate the ATPase, tension and calcium binding responses in the steady state. The model considers that two calciums act as separate effectors with a de-repressant action in the same functional unit.     

An Ecological Risk Management and Capacity Building Model

Worldwide, natural and human ecosystems are increasingly subjected to natural hazards due to global environmental change. Because these threats reflect interaction between social and ecological systems, effective Disaster Risk Reduction (DRR) can best be accomplished by increasing community capacity to mitigate, cope with, adapt to, and recover from hazard consequences by developing DRR strategies that accommodate natural and human ecosystem interdependency. One reason of the widespread ineffectiveness in preparedness has been the neglect of environment/community interactions, and how community and individual variables interact with each other. To address this gap an all-hazard and inter-disciplinary literature review was conducted that synergized and integrated individual-level and environment/community-level factors. Based on the review a social-ecological model was developed. This model identifies a multitude of variables operating across a wide range of dimensions (i.e., individual, historical, physical/natural, social, spiritual/religious, economic, political) and different scales (i.e., individual, household, community organisations, businesses, local government, state government). Based on the review a holistic ecological all-hazard inter-disciplinary risk management and capacity building model was developed that describes how these factors interact to influence risk management and adaptive capacities. This holistic model provides a foundation and rationale for facilitating the capacity of all stakeholders in at-risk areas to develop comprehensive social-ecological relationships and researchers to investigate human-environment interactions in depth.     

The Three Filament Model of Skeletal Muscle Stability and Force Production

Ever since the 1950s, muscle force regulation has been associated with the cross-bridge interactions between the two contractile filaments, actin and myosin. This gave rise to what is referred to as the "two-filament sarcomere model". This model does not predict eccentric muscle contractions well, produces instability of myosin alignment and force production on the descending limb of the force-length relationship, and cannot account for the vastly decreased ATP requirements of actively stretched muscles. Over the past decade, we and others, identified that a third myofilament, titin, plays an important role in stabilizing the sarcomere and the myosin filament. Here, we demonstrate additionally how titin is an active participant in muscle force regulation by changing its stiffness in an activation/force dependent manner and by binding to actin, thereby adjusting its free spring length. Therefore, we propose that skeletal muscle force regulation is based on a three filament model that includes titin, rather than a two filament model consisting only of actin and myosin filaments.     

Slow Conduction in Cardiac Muscle: A Biophysical Model

Mechanisms of slow conduction in cardiac muscle are categorized and the most likely identified. Propagating action potentials were obtained experimentally from a synthetically grown strand of cardiac muscle (around 50 μm by 30 mm) and theoretically from a one-dimensional cable model that incorporated varying axial resistance and membrane properties along its length. Action potentials propagated at about 0.3 m/s, but in some synthetic strands there were regions (approximately 100 μm in length) where the velocity decreased to 0.002 m/s. The electrophysiological behavior associated with this slow conduction was similar to that associated with slow conduction in naturally occurring cardiac muscle (notches, Wenckebach phenomena, and block). Theoretically, reasonable changes in specific membrane capacitance, membrane activity, and various changes in geometry were insufficient to account for the observed slow conduction velocities. Conduction velocities as low as 0.009 m/s, however, could be obtained by increasing the resistance (r_i) of connections between the cells in the cable; velocities as low as 0.0005 m/s could be obtained by a further increase in r_i made possible by a reduction in membrane activity by one-fourth, which in itself decreased conduction velocity by only a factor of 1/1.4. As a result of these findings, several of the mechanisms that have been postulated, previously, are shown to be incapable of accounting for delays such as those which occur in the synthetic strand as well as in the atrioventricular (VA) node.