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Force Responses (force + response)
Selected AbstractsReal-time Monitoring of Force Response Measured in Mechanically Stimulated Tissue-Engineered CartilageARTIFICIAL ORGANS, Issue 4 2009Orahn Preiss-Bloom Abstract:, Mechanical stimulation improves tissue-engineered cartilage development both in terms of biochemical composition and structural properties. However, the link between the compositional changes attributed to mechanical stimulation and the changing structural properties of the engineered cartilage is poorly understood. We hypothesize that transient events associated with construct stiffening can be documented and used to understand milestones in construct development. To do this, we designed and built a mechanical stimulation bioreactor that can continuously record the force response of the engineered construct in real time. This study documents the transient changes of the stiffness of tissue-engineered cartilage constructs over the first 14 days of their development under cyclic loading. Compressive strain stimulation (15%, 1 Hz) was applied to poly(ethylene glycol) (PEG) hydrogels seeded with primary articular chondrocytes. The average compressive modulus of strain-stimulated constructs was 12.7 ± 1.45 kPa after 2 weeks, significantly greater (P < 0.01) than the average compressive moduli of both unstimulated constructs (10.7 ± 0.94 kPa) and nonviable stimulated constructs (11.2 ± 0.91 kPa). The system was able to document that nearly all of the stiffness increase occurred over the last 2 days of the experiment, where live-cell constructs demonstrated a rapid 20% increase in force response. The system's ability to track significant increases in stiffness over time was also confirmed by Instron testing. These results present a novel view of the early mechanical development of tissue-engineering cartilage constructs and suggest that the real-time monitoring of force response may be used to noninvasively track the development of engineered tissue. [source] Bilateral teleoperation under time-varying communication time delay considering contact with environmentELECTRONICS & COMMUNICATIONS IN JAPAN, Issue 7 2009Noriko Iiyama Abstract With recent popularization of the Internet, bilateral control systems which are robust to fluctuant and unpredictable time delay are desirable. In such a situation, communication disturbance observer (CDOB) has been proposed as a control method for fluctuant and unpredictable time delay in bilateral teleoperation. It compensates time delay using disturbance observer by considering the effect of communication delay on the system as acceleration dimensional disturbance. Since this method cannot separate network disturbance from contact force exerted on a slave, force response of the slave transmitted to the master side is not precise. This paper presents a method for separating network disturbance from the contact force exerted on the slave. By producing the compensation value using separated network disturbance the force response value of the slave is transmitted to the master side more precisely. The validity of the proposed method is verified by experimental results. © 2009 Wiley Periodicals, Inc. Electron Comm Jpn, 92(7): 38,46, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/ecj.10051 [source] Contribution of central and peripheral factors to residual fatigue in Guillain,Barré syndromeMUSCLE AND NERVE, Issue 1 2007Marcel P.J. Garssen MD Abstract Many patients with Guillain,Barré syndrome (GBS) suffer from severe residual fatigue that has an uncertain basis. We determined the relative contribution of peripheral and central factors during a 2-min fatiguing sustained maximal voluntary contraction (MVC) in 10 neurologically well-recovered GBS patients and 12 age- and sex-matched healthy controls. Physiological fatigue was defined as the decline of voluntary force during an MVC of the biceps brachii. Relative amounts of peripheral fatigue and central activation failure were determined combining voluntary force and force responses to electrical stimulation. Surface electromyography was used to determine muscle-fiber conduction velocity. During the first minute of sustained MVC, peripheral fatigue developed more slowly in patients than in controls. Central fatigue only occurred in patients. The muscle-fiber conduction velocity was higher in patients. The initial MVC, decrease of MVC, initial force response, and initial central activation failure did not significantly differ between the groups. Although peripheral mechanisms cannot be excluded in the pathogenesis of residual fatigue after GBS, these results suggest that central changes are involved. This study thus provides further insight into the factors contributing to residual fatigue in GBS patients. Muscle Nerve, 2007 [source] Distinct effects of subcellular glycogen localization on tetanic relaxation time and endurance in mechanically skinned rat skeletal muscle fibresTHE JOURNAL OF PHYSIOLOGY, Issue 14 2009J. Nielsen In vitro experiments indicate a non-metabolic role of muscle glycogen in contracting skeletal muscles. Since the sequence of events in excitation,contraction (E,C) coupling is known to be located close to glycogen granules, at specific sites on the fibre, we hypothesized that the distinct compartments of glycogen have specific effects on muscle fibre contractility and fatigability. Single skeletal muscle fibres (n= 19) from fed and fasted rats were mechanically skinned and divided into two segments. In one segment glycogen localization and volume fraction were estimated by transmission electron microscopy. The other segment was mechanically skinned and, in the presence of high and constant myoplasmic ATP and PCr, electrically stimulated (10 Hz, 0.8 s every 3 s) eliciting repeated tetanic contractions until the force response was decreased by 50% (mean ±s.e.m., 81 ± 16, range 22,252 contractions). Initially the total myofibrillar glycogen volume percentage was 0.46 ± 0.07%, with 72 ± 3% in the intermyofibrillar space and 28 ± 3% in the intramyofibrillar space. The intramyofibrillar glycogen content was positively correlated with the fatigue resistance capacity (r2= 0.32, P= 0.02). Intermyofibrillar glycogen was inversely correlated with the half-relaxation time in the unfatigued tetanus (r2= 0.25, P= 0.03). These results demonstrate for the first time that two distinct subcellular populations of glycogen have different roles in contracting single muscle fibres under conditions of high myoplasmic ATP. [source] Disruption of excitation,contraction coupling and titin by endogenous Ca2+ -activated proteases in toad muscle fibresTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Esther Verburg This study investigated the effects of elevated, physiological levels of intracellular free [Ca2+] on depolarization-induced force responses, and on passive and active force production by the contractile apparatus in mechanically skinned fibres of toad iliofibularis muscle. Excitation,contraction (EC) coupling was retained after skinning and force responses could be elicited by depolarization of the transverse-tubular (T-) system. Raising the cytoplasmic [Ca2+] to ,1 ,m or above for 3 min caused an irreversible reduction in the depolarization-induced force response by interrupting the coupling between the voltage sensors in the T-system and the Ca2+ release channels in the sarcoplasmic reticulum. This uncoupling showed a steep [Ca2+] dependency, with 50% uncoupling at ,1.9 ,m Ca2+. The uncoupling occurring with 2 ,m Ca2+ was largely prevented by the calpain inhibitor leupeptin (1 mm). Raising the cytoplasmic [Ca2+] above 1 ,m also caused an irreversible decline in passive force production in stretched skinned fibres in a manner graded by [Ca2+], though at a much slower relative rate than loss of coupling. The progressive loss of passive force could be rapidly stopped by lowering [Ca2+] to 10 nm, and was almost completely inhibited by 1 mm leupeptin but not by 10 ,m calpastatin. Muscle homogenates preactivated by Ca2+ exposure also evidently contained a diffusible factor that caused damage to passive force production in a Ca2+ -dependent manner. Western blotting showed that: (a) calpain-3 was present in the skinned fibres and was activated by the Ca2+exposure, and (b) the Ca2+ exposure in stretched skinned fibres resulted in proteolysis of titin. We conclude that the disruption of EC coupling occurring at elevated levels of [Ca2+] is likely to be caused at least in part by Ca2+ -activated proteases, most likely by calpain-3, though a role of calpain-1 is not excluded. [source] Real-time Monitoring of Force Response Measured in Mechanically Stimulated Tissue-Engineered CartilageARTIFICIAL ORGANS, Issue 4 2009Orahn Preiss-Bloom Abstract:, Mechanical stimulation improves tissue-engineered cartilage development both in terms of biochemical composition and structural properties. However, the link between the compositional changes attributed to mechanical stimulation and the changing structural properties of the engineered cartilage is poorly understood. We hypothesize that transient events associated with construct stiffening can be documented and used to understand milestones in construct development. To do this, we designed and built a mechanical stimulation bioreactor that can continuously record the force response of the engineered construct in real time. This study documents the transient changes of the stiffness of tissue-engineered cartilage constructs over the first 14 days of their development under cyclic loading. Compressive strain stimulation (15%, 1 Hz) was applied to poly(ethylene glycol) (PEG) hydrogels seeded with primary articular chondrocytes. The average compressive modulus of strain-stimulated constructs was 12.7 ± 1.45 kPa after 2 weeks, significantly greater (P < 0.01) than the average compressive moduli of both unstimulated constructs (10.7 ± 0.94 kPa) and nonviable stimulated constructs (11.2 ± 0.91 kPa). The system was able to document that nearly all of the stiffness increase occurred over the last 2 days of the experiment, where live-cell constructs demonstrated a rapid 20% increase in force response. The system's ability to track significant increases in stiffness over time was also confirmed by Instron testing. These results present a novel view of the early mechanical development of tissue-engineering cartilage constructs and suggest that the real-time monitoring of force response may be used to noninvasively track the development of engineered tissue. [source] Effects of chlorpromazine on excitation,contraction coupling events in fast-twitch skeletal muscle fibres of the ratBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2004R Wagner Single mechanically skinned fibres from the rat extensor digitorum longus muscle, which allow access to intracellular compartments, were used to examine the effects of 0.5,100 ,M chlorpromazine hydrochloride (CPZ) on the major steps of the excitation,contraction (E,C) coupling to elucidate the involvement of skeletal muscle in the neuroleptic malignant syndrome (NMS). At 1 ,M, CPZ caused a 20,30% increase in the force response induced by t-system depolarisation and a marked increase in the rate of caffeine-induced SR Ca2+ release. At [CPZ]2.5 ,M, there was an initial increase followed by a marked decrease of the t-system depolarisation-induced force responses, while the potentiating effect on the caffeine-induced SR Ca2+ release remained. These effects were reversible. CPZ had no effect on the maximum Ca2+ -activated force, but caused reversible, concentration-dependent increases in the Ca2+ sensitivity of the contractile apparatus at [CPZ] 10 ,M, with a 50% predicted shift of 0.11 pCa (,log [Ca2+]) units at 82.3 ,M CPZ. CPZ did not alter the rate of SR-Ca2+ loading at 1 and 10 ,M, but reversibly reduced it by ,40% at 100 ,M by reducing the SR Ca2+ pump. Nevertheless, the SR Ca2+ content was greater when fibres became unresponsive to t-system-induced depolarisation in the presence than in the absence of 100 ,M CPZ. The results show that CPZ has concentration-dependent stimulatory and inhibitory effects on various steps of the E,C coupling, which can explain the involvement of skeletal muscle in NMS and reconcile previous divergent data on CPZ effects on muscle. British Journal of Pharmacology (2004) 141, 624,633. doi:10.1038/sj.bjp.0705655 [source] On the accuracy of simplified methods for the analysis of isolated bridgesEARTHQUAKE ENGINEERING AND STRUCTURAL DYNAMICS, Issue 3 2001P. Franchin Abstract To foster the use of seismic isolation in structures, existing guidelines strive to formulate design methods which are simple and accessible to non-specialized engineers. On the other hand, not all of the simplifying provisions adopted by the norms can be said to have been adequately tested to provide a consistent level of accuracy. The study attempts, in particular, to elucidate three aspects related to the methods of analysis for linear or linearized isolated bridges on which little or no advice can be found in the norms. The first one is about the way one has to account for the fact that damping matrices of isolated bridges are never of proportional type. The present study demonstrates, through a number of typical applications, that classical modal analysis, using real modes and the diagonal terms of the modal damping matrices, still provide a fully acceptable approximation. The second and third aspects are related to the use of linearization expressions extended to the analysis of hyperstatic bridges. Parametric analyses conducted in the study show that none of the formulas in current use gives satisfactory results for both the displacement and the force responses, a requirement for a reliable design of an isolated bridge. How to use the equivalent linear parameters, and in particular the isolators equivalent damping ratios, in the context of a modal analysis, is treated next. This problem is seldom if ever mentioned in the norms where at most a formula is given for constructing modal damping ratios based on the damping ratios of the isolators. A rational, approximate procedure is discussed in this paper, applicable to all types of structures with non-proportional damping, which in the case of bridges can be shown to reduce to the expression provided in the Japanese bridge design guidelines. Copyright © 2001 John Wiley & Sons, Ltd. [source] Effects of dofetilide on cardiovascular tissues from normo- and hypertensive ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2002Sheila A. Doggrell The aim was to test whether dofetilide has some potential for use in the treatment of heart failure. Dofetilide at ,3 times 10,5 M had no effect on the quiescent Wistar Kyoto (WKY) rat aorta, mesenteric and intralobar arteries, or the spontaneous contractions of the WKY rat portal vein. Dofetilide at 10,6 to 3 times 10,5 M relaxed the KCl-contracted aorta. Dofetilide at 10,9 -10,7 M augmented the force of contraction of left ventricle strips from 12- and 18-month-old WKY rats at 2 Hz. Spontaneously hypertensive rats (SHRs) at 12 and 17,21 months of age are models of cardiac hypertrophy and failure, respectively. The augmentation of force at 2 Hz with dofetilide was similar on 12-and 18-month-old WKY rats and 12-month-old SHRs but reduced on the 18-month-old SHR left ventricle. At a higher more physiological frequency, 4 Hz, the threshold concentration of dofetilide required to augment the force responses of 21-month-old SHR left ventricles was markedly increased and the maximum augmenting effect was decreased. Dofetilide at 10,7 -10,5 M reduced the rate of the 17-month-old WKY rat right atrium, and had a similar effect on age-matched SHR right atrium. In summary, dofetilide is a positive inotrope and negative chronotrope in the rat. However, as the positive inotropic effect is not observed with clinically relevant concentrations at a physiological rate in heart failure, dofetilide is unlikely to be useful as a positive inotrope in the treatment of heart failure. [source] Contribution of central and peripheral factors to residual fatigue in Guillain,Barré syndromeMUSCLE AND NERVE, Issue 1 2007Marcel P.J. Garssen MD Abstract Many patients with Guillain,Barré syndrome (GBS) suffer from severe residual fatigue that has an uncertain basis. We determined the relative contribution of peripheral and central factors during a 2-min fatiguing sustained maximal voluntary contraction (MVC) in 10 neurologically well-recovered GBS patients and 12 age- and sex-matched healthy controls. Physiological fatigue was defined as the decline of voluntary force during an MVC of the biceps brachii. Relative amounts of peripheral fatigue and central activation failure were determined combining voluntary force and force responses to electrical stimulation. Surface electromyography was used to determine muscle-fiber conduction velocity. During the first minute of sustained MVC, peripheral fatigue developed more slowly in patients than in controls. Central fatigue only occurred in patients. The muscle-fiber conduction velocity was higher in patients. The initial MVC, decrease of MVC, initial force response, and initial central activation failure did not significantly differ between the groups. Although peripheral mechanisms cannot be excluded in the pathogenesis of residual fatigue after GBS, these results suggest that central changes are involved. This study thus provides further insight into the factors contributing to residual fatigue in GBS patients. Muscle Nerve, 2007 [source] Effect of ADP on slow-twitch muscle fibres of the rat: implications for muscle fatigueTHE JOURNAL OF PHYSIOLOGY, Issue 1 2006W. A. Macdonald Slow-twitch mechanically skinned fibres from rat soleus muscle were bathed in solutions mimicking the myoplasmic environment but containing different [ADP] (0.1 ,m to 1.0 mm). The effect of ADP on sarcoplasmic reticulum (SR) Ca2+ -content was determined from the magnitude of caffeine-induced force responses, while temporal changes in SR Ca2+ -content allowed determination of the effective rates of the SR Ca2+ -pump and of the SR Ca2+ -leak. The SR Ca2+ -pump rate, estimated at pCa (,log10[Ca2+]) 7.8, was reduced by 20% as the [ADP] was increased from 0.1 to 40 ,m, with no further alteration when the [ADP] was increased to 1.0 mm. The SR Ca2+ -leak rate constant was not altered by increasing [ADP] from 0.1 to 40 ,m, but was increased by 26% when the [ADP] was elevated to 1.0 mm. This ADP-induced SR Ca2+ -leak was insensitive to ruthenium red but was abolished by 2,5-di(tert-butyl)-1,4-hydroquinone (TBQ), indicating that the leak pathway is via the SR Ca2+ -pump and not the SR Ca2+ -release channel. The decrease in SR Ca2+ -pump rate and SR Ca2+ -leak rate when [ADP] was increased led to a 40% decrease in SR Ca2+ -loading capacity. Elevation of [ADP] had only minor direct effects on the contractile apparatus of slow-twitch fibres. These results suggest that ADP has only limited depressing effects on the contractility of slow-twitch muscle fibres. This is in contrast to the marked effects of ADP on force responses in fast-twitch muscle fibres and may contribute to the fatigue-resistant nature of slow-twitch muscle fibres. [source] Disruption of excitation,contraction coupling and titin by endogenous Ca2+ -activated proteases in toad muscle fibresTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Esther Verburg This study investigated the effects of elevated, physiological levels of intracellular free [Ca2+] on depolarization-induced force responses, and on passive and active force production by the contractile apparatus in mechanically skinned fibres of toad iliofibularis muscle. Excitation,contraction (EC) coupling was retained after skinning and force responses could be elicited by depolarization of the transverse-tubular (T-) system. Raising the cytoplasmic [Ca2+] to ,1 ,m or above for 3 min caused an irreversible reduction in the depolarization-induced force response by interrupting the coupling between the voltage sensors in the T-system and the Ca2+ release channels in the sarcoplasmic reticulum. This uncoupling showed a steep [Ca2+] dependency, with 50% uncoupling at ,1.9 ,m Ca2+. The uncoupling occurring with 2 ,m Ca2+ was largely prevented by the calpain inhibitor leupeptin (1 mm). Raising the cytoplasmic [Ca2+] above 1 ,m also caused an irreversible decline in passive force production in stretched skinned fibres in a manner graded by [Ca2+], though at a much slower relative rate than loss of coupling. The progressive loss of passive force could be rapidly stopped by lowering [Ca2+] to 10 nm, and was almost completely inhibited by 1 mm leupeptin but not by 10 ,m calpastatin. Muscle homogenates preactivated by Ca2+ exposure also evidently contained a diffusible factor that caused damage to passive force production in a Ca2+ -dependent manner. Western blotting showed that: (a) calpain-3 was present in the skinned fibres and was activated by the Ca2+exposure, and (b) the Ca2+ exposure in stretched skinned fibres resulted in proteolysis of titin. We conclude that the disruption of EC coupling occurring at elevated levels of [Ca2+] is likely to be caused at least in part by Ca2+ -activated proteases, most likely by calpain-3, though a role of calpain-1 is not excluded. [source] Effects of chlorpromazine on excitation,contraction coupling events in fast-twitch skeletal muscle fibres of the ratBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2004R Wagner Single mechanically skinned fibres from the rat extensor digitorum longus muscle, which allow access to intracellular compartments, were used to examine the effects of 0.5,100 ,M chlorpromazine hydrochloride (CPZ) on the major steps of the excitation,contraction (E,C) coupling to elucidate the involvement of skeletal muscle in the neuroleptic malignant syndrome (NMS). At 1 ,M, CPZ caused a 20,30% increase in the force response induced by t-system depolarisation and a marked increase in the rate of caffeine-induced SR Ca2+ release. At [CPZ]2.5 ,M, there was an initial increase followed by a marked decrease of the t-system depolarisation-induced force responses, while the potentiating effect on the caffeine-induced SR Ca2+ release remained. These effects were reversible. CPZ had no effect on the maximum Ca2+ -activated force, but caused reversible, concentration-dependent increases in the Ca2+ sensitivity of the contractile apparatus at [CPZ] 10 ,M, with a 50% predicted shift of 0.11 pCa (,log [Ca2+]) units at 82.3 ,M CPZ. CPZ did not alter the rate of SR-Ca2+ loading at 1 and 10 ,M, but reversibly reduced it by ,40% at 100 ,M by reducing the SR Ca2+ pump. Nevertheless, the SR Ca2+ content was greater when fibres became unresponsive to t-system-induced depolarisation in the presence than in the absence of 100 ,M CPZ. The results show that CPZ has concentration-dependent stimulatory and inhibitory effects on various steps of the E,C coupling, which can explain the involvement of skeletal muscle in NMS and reconcile previous divergent data on CPZ effects on muscle. British Journal of Pharmacology (2004) 141, 624,633. doi:10.1038/sj.bjp.0705655 [source] | |||||||||||||