浅谈综合布线系统接地设计

综合布线系统作为建筑智能化不可缺少的基础设施,其接地系统的好坏将直接影响到综合布线系统的运行质量,故而显得尤为重要。本文介绍了综合布线系统接地的结构及设计要求,并提出在接地设计中应注意的几个问题。     

乙炔黑吸附聚合制导电聚苯胺

用乙炔黑吸附化学聚合新工艺制备导电聚苯胺，可保持电导率不变，但转化率和堆密度提高，并明显改善了聚苯胺的颗粒形态和制膜加工性，使由其制备的聚苯胺复合正极膜和固体聚苯胺锂蓄电池的电化学性能得以改进。     

Finite element modelling of skeletal muscles coupled with fatigue

In this study, Hill's muscle theory coupled with fatigue was proposed to describe mechanical behaviours of skeletal muscles. The force developed by a fatigued muscle was described by a muscle fatigue formula which was a time function of the activation α_a and the stretch λ. The modified Hill's muscle theory was hence incorporated into a three-dimensional (3D) finite element model using the PAK finite element code. In this paper, the theoretical derivation of the 3D muscle model was firstly described. After presenting the method of establishing the finite element programme, a case example of studying the mechanical response of a frog gastrocnemius muscle was used to illustrate the applicability of the proposed methodology. The effects of the muscle fatigue on the deformation as well as the stress and strain distribution of the frog muscle subject to a cyclic activation function have been determined. An experiment capturing the real-time shape change of a frog muscle was also conducted to assess the applicability of the proposed method. A comparison between the deformed shapes of the predictive model and the frog muscles was also made. It was shown that the method is capable of providing a reasonable model for describing the mechanical behaviour of skeletal muscles.     

Role of pH and Ionic Strength on Water Relationships in Washed Minced Chicken-breast Muscle Gels

ABSTRACT The relationship between pH, ionic strength, and water balance of chicken-breast muscle gels was investigated. An increase in gel pH (pH 6.4 to 7.4) without added NaCl led to dramatic increases in water-holding capacity and water uptake (P < 0.05). Gels at 150 mM NaCl exhibited less ability to adsorb water than salt-free gels (P < 0.05 at pH 6.8 to 7.4) and had lower water-holding capacities (P < 0.05) and fold scores at and below pH 7. Varying salt concentration of the gel-bathing solutions had dramatic effect on the water uptake of the gels. The results show that strong water-absorbing gels can be produced at low ionic strengths and suggest that the negative charge of the muscle proteins is the driving force for water uptake and retention.     

气动人工肌肉手臂的神经网络Smith预估控制

针对含时滞d的1关节气动人工肌肉(PAM)手臂,用三层递归神经网络(RNN),建立PAM手臂包含时滞的模型(即非线性Smith预估器),并超前d步预测PAM手臂的输出角度.将此超前d步的预测值作为反馈量,与设定值相比较得到的误差作为PID控制器输入量,实现Smith预估PID控制.同时每一步都用RNN模型当前时刻的输出值与PAM手臂当前时刻实际输出值之差的平方做为RNN权值的在线调整准则对RNN预测模型的权值进行在线调整,以自适应PAM手臂的不确定性和时变性.使用Matlab通过串口和研华亚当模块对实物PAM手臂进行控制,控制效果表明所提出的Smith预估PID控制算法比常规PID控制算法的性能有显著提高,证明所提出的算法是有效的和切实可行的.     

Early Lipid Raft-Related Changes: Interplay between Unilateral Denervation and Hindlimb Suspension

Muscle disuse and denervation leads to muscle atrophy, but underlying mechanisms can be different. Previously, we have found ceramide (Cer) accumulation and lipid raft disruption after acute hindlimb suspension (HS), a model of muscle disuse. Herein, using biochemical and fluorescent approaches the influence of unilateral denervation itself and in combination with short-term HS on membrane-related parameters of rat soleus muscle was studied. Denervation increased immunoexpression of sphingomyelinase and Cer in plasmalemmal regions, but decreased Cer content in the raft fraction and enhanced lipid raft integrity. Preliminary denervation suppressed (1) HS-induced Cer accumulation in plasmalemmal regions, shown for both nonraft and raft-fractions; (2) HS-mediated decrease in lipid raft integrity. Similar to denervation, inhibition of the sciatic nerve afferents with capsaicin itself increased Cer plasmalemmal immunoexpression, but attenuated the membrane-related effects of HS. Finally, both denervation and capsaicin treatment increased immunoexpression of proapoptotic protein Bax and inhibited HS-driven increase in antiapoptotic protein Bcl-2. Thus, denervation can increase lipid raft formation and attenuate HS-induced alterations probably due to decrease of Cer levels in the raft fraction. The effects of denervation could be at least partially caused by the loss of afferentation. The study points to the importance of motor and afferent inputs in control of Cer distribution and thereby stability of lipid rafts in the junctional and extrajunctional membranes of the muscle.     

Treatment of Stress Urinary Incontinence with Muscle Stem Cells and Stem Cell Components: Chances,Challenges and Future Prospects

Urinary incontinence (UI) is a major problem in health care and more than 400 million people worldwide suffer from involuntary loss of urine. With an increase in the aging population, UI is likely to become even more prominent over the next decades and the economic burden is substantial. Among the different subtypes of UI, stress urinary incontinence (SUI) is the most prevalent and focus of this review. The main underlying causes for SUI are pregnancy and childbirth, accidents with direct trauma to the pelvis or medical treatments that affect the pelvic floor, such as surgery or irradiation. Conservative approaches for the treatment of SUI are pelvic physiotherapy, behavioral and lifestyle changes, and the use of pessaries. Current surgical treatment options include slings, colposuspensions, bulking agents and artificial urinary sphincters. These treatments have limitations with effectiveness and bear the risk of long-term side effects. Furthermore, surgical options do not treat the underlying pathophysiological causes of SUI. Thus, there is an urgent need for alternative treatments, which are effective, minimally invasive and have only a limited risk for adverse effects. Regenerative medicine is an emerging field, focusing on the repair, replacement or regeneration of human tissues and organs using precursor cells and their components. This article critically reviews recent advances in the therapeutic strategies for the management of SUI and outlines future possibilities and challenges.     

Regulatory Light Chains in Cardiac Development and Disease

The role of regulatory light chains (RLCs) in cardiac muscle function has been elucidated progressively over the past decade. The RLCs are among the earliest expressed markers during cardiogenesis and persist through adulthood. Failing hearts have shown reduced RLC phosphorylation levels and that restoring baseline levels of RLC phosphorylation is necessary for generating optimal force of muscle contraction. The signalling mechanisms triggering changes in RLC phosphorylation levels during disease progression remain elusive. Uncovering this information may provide insights for better management of heart failure patients. Given the cardiac chamber-specific expression of RLC isoforms, ventricular RLCs have facilitated the identification of mature ventricular cardiomyocytes, opening up possibilities of regenerative medicine. This review consolidates the standing of RLCs in cardiac development and disease and highlights knowledge gaps and potential therapeutic advancements in targeting RLCs.     

The “Angiogenic Switch” and Functional Resources in Cyclic Sports Athletes

Regular physical activity in cyclic sports can influence the so-called “angiogenic switch”, which is considered as an imbalance between proangiogenic and anti-angiogenic molecules. Disruption of the synthesis of angiogenic molecules can be caused by local changes in tissues under the influence of excessive physical exertion and its consequences, such as chronic oxidative stress and associated hypoxia, metabolic acidosis, sports injuries, etc. A review of publications on signaling pathways that activate and inhibit angiogenesis in skeletal muscles, myocardium, lung, and nervous tissue under the influence of intense physical activity in cyclic sports. Materials: We searched PubMed, SCOPUS, Web of Science, Google Scholar, Clinical keys, and e-LIBRARY databases for full-text articles published from 2000 to 2020, using keywords and their combinations. Results: An important aspect of adaptation to training loads in cyclic sports is an increase in the number of capillaries in muscle fibers, which improves the metabolism of skeletal muscles and myocardium, as well as nervous and lung tissue. Recent studies have shown that myocardial endothelial cells not only respond to hemodynamic forces and paracrine signals from neighboring cells, but also take an active part in heart remodeling processes, stimulating the growth and contractility of cardiomyocytes or the production of extracellular matrix proteins in myofibroblasts. As myocardial vascularization plays a central role in the transition from adaptive heart hypertrophy to heart failure, further study of the signaling mechanisms involved in the regulation of angiogenesis in the myocardium is important in sports practice. The study of the “angiogenic switch” problem in the cerebrovascular and cardiovascular systems allows us to claim that the formation of new vessels is mediated by a complex interaction of all growth factors. Although the lungs are one of the limiting systems of the body in cyclic sports, their response to high-intensity loads and other environmental stresses is often overlooked. Airway epithelial cells are the predominant source of several growth factors throughout lung organogenesis and appear to be critical for normal alveolarization, rapid alveolar proliferation, and normal vascular development. There are many controversial questions about the role of growth factors in the physiology and pathology of the lungs. The presented review has demonstrated that when doing sports, it is necessary to give a careful consideration to the possible positive and negative effects of growth factors on muscles, myocardium, lung tissue, and brain. Primarily, the “angiogenic switch” is important in aerobic sports (long distance running). Conclusions: Angiogenesis is a physiological process of the formation of new blood capillaries, which play an important role in the functioning of skeletal muscles, myocardium, lung, and nervous tissue in athletes. Violation of the “angiogenic switch” as a balance between proangiogenic and anti-angiogenic molecules can lead to a decrease in the functional resources of the nervous, musculoskeletal, cardiovascular, and respiratory systems in athletes and, as a consequence, to a decrease in sports performance.     

Molecular Mechanisms of the Deregulation of Muscle Contraction Induced by the R90P Mutation in Tpm3.12 and the Weakening of This Effect by BDM and W7

Point mutations in the genes encoding the skeletal muscle isoforms of tropomyosin can cause a range of muscle diseases. The amino acid substitution of Arg for Pro residue in the 90th position (R90P) in γ-tropomyosin (Tpm3.12) is associated with congenital fiber type disproportion and muscle weakness. The molecular mechanisms underlying muscle dysfunction in this disease remain unclear. Here, we observed that this mutation causes an abnormally high Ca²⁺-sensitivity of myofilaments in vitro and in muscle fibers. To determine the critical conformational changes that myosin, actin, and tropomyosin undergo during the ATPase cycle and the alterations in these changes caused by R90P replacement in Tpm3.12, we used polarized fluorimetry. It was shown that the R90P mutation inhibits the ability of tropomyosin to shift towards the outer domains of actin, which is accompanied by the almost complete depression of troponin’s ability to switch actin monomers off and to reduce the amount of the myosin heads weakly bound to F-actin at a low Ca²⁺. These changes in the behavior of tropomyosin and the troponin–tropomyosin complex, as well as in the balance of strongly and weakly bound myosin heads in the ATPase cycle may underlie the occurrence of both abnormally high Ca²⁺-sensitivity and muscle weakness. BDM, an inhibitor of myosin ATPase activity, and W7, a troponin C antagonist, restore the ability of tropomyosin for Ca²⁺-dependent movement and the ability of the troponin–tropomyosin complex to switch actin monomers off, demonstrating a weakening of the damaging effect of the R90P mutation on muscle contractility.