Journal articles: 'Réactions de contraction de cycle'

1

Nalivaiko, P. V. "Cycle contraction in oriented graphs." Moscow University Mathematics Bulletin 65, no. 3 (June 2010): 116–18. http://dx.doi.org/10.3103/s0027132210030058.

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Chang, Yuan. "Financial Soundness Indicator, Financial Cycle, Credit Cycle and Business Cycle－Evidence from Taiwan." International Journal of Economics and Finance 8, no. 4 (March 23, 2016): 166. http://dx.doi.org/10.5539/ijef.v8n4p166.

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<p>Business cycle is the repeated expansions (from trough to peak) and contractions (from peak to trough) of real economic activity. Credit cycle is the cyclical process of the bank credit, ranging from short/long-term, loan to enterprise and loan to individual. Financial cycle reflects ups and downs in asset prices and financial institution's balance sheet. This paper examines the linkage among cycles as well as their lead-lag relationship. Theoretically, credit cycle is one of reasons driving business cycle, and financial cycle is a fundamental cause of credit cycle. Based on Taiwan’s quarterly data, this paper firstly identifies cyclical behavior of indicators of real economic activity, bank credit and assets prices in recent decade by defining expansion phases and contraction phases of cyclical variables. Second, this paper calculates concordance index to examine the degree of synchronization among cycles. Third, while the soundness for assets and liabilities of financial institution may drive financial cycle, this paper employs IMF’s Financial Soundness Indicator (FSI) as predictor of expansion and contraction phase of cyclical variables. Specifically, the paper assesses the health of bank’s balance sheet variables by Probit estimation on linkage between FSIs and expansion/contraction phase of cycle. Based on empirical evidence, the knowledge about the extent of assets/liability condition of financial institution corresponding to the expansion and contraction phase of financial, credit and business cycle is enhanced. Authority concerning about financial stability should oversight the performance of FSIs and then engage in prompt corrective actions when the level and volatility of those indicators sharply.</p>

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Bárány, Michael, Erzsébet Polyák, and Kate Bárány. "Protein phosphorylation during the contraction-relaxation-contraction cycle of arterial smooth muscle." Archives of Biochemistry and Biophysics 294, no. 2 (May 1992): 571–78. http://dx.doi.org/10.1016/0003-9861(92)90727-e.

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Moorthy, S. S., and Stephen F. Dierdorf. "Cardiac Cycle and Synchronous Left Hemidiaphragmatic Contraction." Anesthesia & Analgesia 71, no. 2 (August 1990): 206???207. http://dx.doi.org/10.1213/00000539-199008000-00026.

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Chung, Youngran, Robert Sharman, Richard Carlsen, Steven W. Unger, Douglas Larson, and Thomas Jue. "Metabolic fluctuation during a muscle contraction cycle." American Journal of Physiology-Cell Physiology 274, no. 3 (March 1, 1998): C846—C852. http://dx.doi.org/10.1152/ajpcell.1998.274.3.c846.

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Gated31P-nuclear magnetic resonance followed the metabolic fluctuation in rat gastrocnemius muscle during a contraction cycle. Within 16 ms after stimulation, the phosphocreatine (PCr) level drops 11.3% from its reference state. The PCr minimum corresponds closely to the time of maximum force contraction. Pi increases stoichiometrically, while ATP remains constant. During a twitch, PCr hydrolysis produces 3.1 μmol ATP/g tissue, which is substantially higher than the reported 0.3 μmol ATP ⋅ twitch−1 ⋅ g tissue−1 derived from steady-state experiments. The results reveal that a substantial energy fluctuation accompanies a muscle twitch.

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Niizeki, Kyuichi, and Yoshimi Miyamoto. "Phase-dependent heartbeat modulation by muscle contractions during dynamic handgrip in humans." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 4 (April 1, 1999): H1331—H1338. http://dx.doi.org/10.1152/ajpheart.1999.276.4.h1331.

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The influence of cardiac phase on the response of the cardiac pacemaker to dynamic hand contraction in eight healthy young men was studied to determine whether heart rate response to muscle contraction varied as a function of timing within the cardiac cycle. Changes in R-R interval (RRI) in response to muscle contraction were measured at various cardiac phases during heartbeat-synchronized handgrip at a rate of one contraction per two heartbeats. To extract the direct effect of the muscle contraction on the RRI, spontaneous slow variations and respiratory sinus arrhythmia were removed from the total RRI fluctuations in the frequency domain. Cross-correlograms between the extracted RRI fluctuations and muscle contraction showed that the coupling was strong when the muscle contraction occurred at the middle phase of the cardiac cycle. Muscle contraction at the systolic phase of the cardiac cycle had a tendency to produce a phase advance (shortening of RRI), whereas muscle contraction at the middle phase or later had a tendency to produce a phase delay (prolongation of RRI). The results showed the presence of a neuronal circuit that modulates the cardiac pacemaker activity depending on the timing of muscle contraction in the cardiac cycle.

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7

Buchler, B., S. Magder, and C. Roussos. "Effects of contraction frequency and duty cycle on diaphragmatic blood flow." Journal of Applied Physiology 58, no. 1 (January 1, 1985): 265–73. http://dx.doi.org/10.1152/jappl.1985.58.1.265.

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The effects of diaphragmatic contraction frequency (no. of intermittent tetanic contractions/min) at a given tension-time index and of duty cycle (contraction time/total cycle time) on diaphragmatic blood flow were measured in anesthetized mongrel dogs during bilateral supramaximal phrenic nerve stimulation. Diaphragmatic blood flow was measured by the radionuclide-labeled microsphere method. Contraction frequency was varied between 10 and 160/min at duty cycles of 0.25 and 0.75. Diaphragmatic blood flow increased with contraction frequency from 1.47 +/- 0.13 ml X min-1 X g-1 (mean +/- SE) at an average of 18/min to 2.65 +/- 0.16 ml X min-1 X g-1 at 74/min (P less than 0.01) with a duty cycle of 0.25 and from 1.32 +/- 0.19 ml X min-1 X g-1 at an average of 15/min to 1.96 +/- 0.15 ml X min-1 X g-1 at 80/min (P less than 0.02) with a duty cycle of 0.75. At higher contraction frequencies diaphragmatic blood flow did not increase further at both duty cycles. In addition, diaphragmatic blood flow was higher with a duty cycle of 0.25 than 0.75 at all contraction frequencies. We conclude that frequency of contraction is a major determinant of diaphragmatic blood flow and that high duty cycle impedes diaphragmatic blood flow.

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8

Fowler, Mark R., and Godfrey L. Smith. "The cardiac contraction cycle: is Ca2+ going local?" Journal of Applied Physiology 107, no. 6 (December 2009): 1981–84. http://dx.doi.org/10.1152/japplphysiol.91168.2009.

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9

Levy, Hanoch, and David W. Low. "A contraction algorithm for finding small cycle cutsets." Journal of Algorithms 9, no. 4 (December 1988): 470–93. http://dx.doi.org/10.1016/0196-6774(88)90013-2.

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10

Grouiller, Annie. "Contraction de cycle dans la substitution d'un triflate osidique." Canadian Journal of Chemistry 64, no. 9 (September 1, 1986): 1709–10. http://dx.doi.org/10.1139/v86-281.

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Benzoate displacement of the 2-triflyl derivative of methyl 3-azido or 3-O-benzoyl-4-deoxy-α-DL-thero-pentopyranoside (1 or 4) occurs with a pyranose to furanose contraction reaction at C-2. This contraction is not observed with an azido displacement.

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11

Morris, Lee G., and Scott L. Hooper. "Mechanisms Underlying Stabilization of Temporally Summated Muscle Contractions in the Lobster (Panulirus) Pyloric System." Journal of Neurophysiology 85, no. 1 (January 1, 2001): 254–68. http://dx.doi.org/10.1152/jn.2001.85.1.254.

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Muscles are the final effectors of behavior. The neural basis of behavior therefore cannot be completely understood without a description of the transfer function between neural output and muscle contraction. To this end, we have been studying muscle contraction in the well-investigated lobster pyloric system. We report here the mechanisms underlying stabilization of temporally summating contractions of the very slow dorsal dilator muscle in response to motor nerve stimulation with trains of rhythmic shock bursts at a physiological intraburst spike frequency (60 Hz), physiological cycle periods (0.5–2 s), and duty cycles from 0.1 to 0.8. For temporal summation to stabilize, the rise and relaxation amplitudes of the phasic contractions each burst induces must equalize as the rhythmic train continues. Stabilization could occur by changes in rise duration, rise slope, plateau duration, and/or relaxation slope. We demonstrate a generally applicable method for quantifying the relative contribution changes in these characteristics make to contraction stabilization. Our data show that all characteristics change as contractions stabilize, but their relative contribution differs depending on stimulation cycle period and duty cycle. The contribution of changes in rise duration did not depend on period or duty cycle for the 1-, 1.5-, and 2-s period regimes, contributing ∼30% in all cases; but for the 0.5-s period regime, changes in rise duration increased from contributing 25% to contributing 50% as duty cycle increased from 0.1 to 0.8. At all cycle periods decreases in rise slope contributed little to stabilization at small duty cycles but increased to contributing ∼80% at high duty cycles. The contribution of changes in plateau duration decreased in all cases as duty cycle increased; but this decrease was greater in long cycle period regimes. The contribution of changes in relaxation slope also decreased in all cases as duty cycle increased; but for this characteristic, the decrease was greatest in fast cycle period regimes, and in these regimes at high duty cycles these changes opposed contraction stabilization. Exponential fits to contraction relaxations showed that relaxation time constant increased with total contraction amplitude; this increase presumably underlies the decreased relaxation slope magnitude seen in high duty cycle, fast cycle period regimes. These data show that changes in no single contraction characteristic can account for contraction stabilization in this muscle and suggest that predicting muscle response in other systems in which slow muscles are driven by rapidly varying neuronal inputs may be similarly complex.

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12

Josephson, Robert K. "Mechanical Power output from Striated Muscle during Cyclic Contraction." Journal of Experimental Biology 114, no. 1 (January 1, 1985): 493–512. http://dx.doi.org/10.1242/jeb.114.1.493.

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1. The mechanical power output of a synchronous insect muscle was determined by measuring tension as the muscle was subjected to sinusoidal length change and stimuli which occurred at selected phases of the length cycle. The area of the loop formed by plotting muscle tension against length over a full cycle is the work done on that cycle; the work done times the cycle frequency is the mechanical power output. The muscle was a flight muscle of the tettigoniid Neoconocephalus triops. The measurements were made at the normal wing-stroke frequency for flight (25 Hz) and operating temperature (30°C). 2. The power output with a single stimulus per cycle, optimal excursion amplitude, and optimal stimulus phase was 1.52 J kg−1 cycle−1 or 37W kg−1. The maximum power output occurs at a phase such that the onset of the twitch coincides with the onset of the shortening half of the length cycle. The optimum excursion amplitude was 5.5% rest length; with greater excursion, work output declined because of decreasing muscle force associated with the more rapid shortening velocity. 3. Multiple stimulation per cycle increases the power output above that available with twitch contractions. In this muscle, the maximum mechanical power output at 25 Hz was 76 W kg−1 which was achieved with three stimuli per cycle separated by 4-ms intervals and an excursion amplitude of 6.0% rest length. 4. The maximum work output during the shortening of an isotonic twitch contraction was about the same as the work done over a full sinusoidal shortening-lengthening cycle with a single stimulus per cycle and optimum excursion amplitude and phase.

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13

IWAMOTO, YOKO, JUNJIRO KUBO, MASAMITSU ITO, TAKASHI TAKEMIYA, and TOSHIO ASAMI. "VARIATION IN MAXIMAL VOLUNTARY CONTRACTION DURING THE MENSTRUAL CYCLE." Japanese Journal of Physical Fitness and Sports Medicine 51, no. 2 (2002): 193–201. http://dx.doi.org/10.7600/jspfsm1949.51.193.

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14

Kuijsters, N., C. Rabotti, F. Sammali, M. Mischi, and B. Schoot. "Automatic Contraction Detection During the Menstrual Cycle By Electrohysterography." Journal of Minimally Invasive Gynecology 22, no. 6 (November 2015): S101. http://dx.doi.org/10.1016/j.jmig.2015.08.272.

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15

Sommer, M., G. Wöbker, and A. Ferbert. "Voluntary eyelid contraction modifies the blink reflex recovery cycle." Acta Neurologica Scandinavica 98, no. 1 (July 1998): 29–35. http://dx.doi.org/10.1111/j.1600-0404.1998.tb07374.x.

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16

Lehninger, Albert L. "THYROXINE AND THE SWELLING AND CONTRACTION CYCLE IN MITOCHONDRIA*." Annals of the New York Academy of Sciences 86, no. 2 (December 15, 2006): 484–93. http://dx.doi.org/10.1111/j.1749-6632.1960.tb42824.x.

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17

Sheng, Bin, and Yuefang Sun. "An improved linear kernel for the cycle contraction problem." Information Processing Letters 149 (September 2019): 14–18. http://dx.doi.org/10.1016/j.ipl.2019.05.003.

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18

Varian, Kenneth D., Ying Xu, Carlos A. A. Torres, Michelle M. Monasky, and Paul M. L. Janssen. "A random cycle length approach for assessment of myocardial contraction in isolated rabbit myocardium." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 5 (November 2009): H1940—H1948. http://dx.doi.org/10.1152/ajpheart.01289.2008.

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It is well known that the strength of cardiac contraction is dependent on the cycle length, evidenced by the force-frequency relationship (FFR) and the existence of postrest potentiation (PRP). Because the contractile strength of the steady-state FFR and force-interval relationship involve instant intrinsic responses to cycle length as well as slower acting components such as posttranslational modification-based mechanisms, it remains unclear how cycle length intrinsically affects cardiac contraction and relaxation. To dissect the impact of cycle length changes from slower acting signaling components associated with persisting changes in cycle length, we developed a novel technique/protocol to study cycle length-dependent effects on cardiac function; twitch contractions of right ventricular rabbit trabeculae at different cycle lengths were randomized around a steady-state frequency. Patterns of cycle lengths that resulted in changes in force and/or relaxation times can now be identified and analyzed. Using this novel protocol, taking under 10 min to complete, we found that the duration of the cycle length before a twitch contraction (“primary” cycle length) positively correlated with force. In sharp contrast, the cycle length one (“secondary”) or two (“tertiary”) beats before the analyzed twitch correlated negatively with force. Using this protocol, we can quantify the intrinsic effect of cycle length on contractile strength while avoiding rundown and lengthiness that are often complications of FFR and PRP assessments. The data show that the history of up to three cycle lengths before a contraction influences myocardial contractility and that primary cycle length affects cardiac twitch dynamics in the opposite direction from secondary/tertiary cycle lengths.

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19

Cohen, C., B. Darbois Texier, G. Laffaye, L. Auvray, and C. Clanet. "Weightlifting and the actomyosin cycle." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 471, no. 2184 (December 2015): 20150473. http://dx.doi.org/10.1098/rspa.2015.0473.

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How does a human lift a weight? Can we relate the dynamics of the lift to the molecular actin–myosin interactions responsible for muscle contraction? We address these questions with bench press experiments that we analyse with a theoretical model, based on the sliding filament theory. The agreement is fair, and we discuss its possible extension to medical diagnostics.

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Lang, S. A., and M. N. Levy. "Effects of vagus nerve on heart rate and ventricular contractility in chicken." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (May 1, 1989): H1295—H1302. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1295.

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We determined the effects of vagus nerve stimulation on cardiac cycle length and on ventricular contraction and relaxation in 18 chickens anesthetized with pentobarbital. Right vagus stimulation at a constant frequency of 35 Hz prolonged cycle length by 190%, whereas left vagus stimulation at the same frequency increased cycle length by 136%. When one burst of stimuli was delivered to the right vagus nerve each cardiac cycle, but the timing of the stimuli was changed within the cardiac cycle, the response of the avian pacemaker cells varied substantially with the timing of the stimuli. Right and left vagus stimulation at a constant frequency of 20 Hz depressed ventricular contraction by 62 +/- 6 and 52 +/- 6%, respectively, and depressed ventricular relaxation by 56 +/- 7 and 53 +/- 7%, respectively. These results indicate that in the chicken the chronotropic effects of right vagus stimulation are greater than those of left vagus stimulation, whereas right and left vagus stimulation are approximately equipotent on ventricular contraction and relaxation.

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21

Hu, F., A. Comtois, and A. E. Grassino. "Contraction-dependent modulations in regional diaphragmatic blood flow." Journal of Applied Physiology 68, no. 5 (May 1, 1990): 2019–28. http://dx.doi.org/10.1152/jappl.1990.68.5.2019.

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Blood flow (Q) of the diaphragm was measured simultaneously with Doppler probes placed on diaphragmatic veins and an artery and by direct volumetric measurements obtained from cannulation of diaphragmatic blood vessels. The Doppler converting coefficients obtained were 6.27, 7.25, 4.21, and 41.07 ml.min-1.kHz-1 for left phrenic artery flow (Qpha), phrenic vein flow (Qphv), internal mammary vein flow (Qimv), and azygos vein flow (Qazv), respectively. The time course of Qpha, Qphv, Qimv, and Qazv after imposed patterns of diaphragmatic contraction was measured in nine anesthetized dogs. Each pattern consisted of various combinations of transdiaphragmatic pressure (Pdi), frequency of pacing (f), and duty cycle obtained by bilateral phrenic nerve stimulation. The dogs were prepared with chests open and loosely casted abdomens. Qpha, Qphv, Qimv, and Qazv were measured at rest (control, passive diaphragm, mechanical ventilation) and at two submaximal levels of stimulation (30 and 60% of Pdimax). The f was 10 or 30 cycles/min and the duty cycle was 0.25, 0.50, and 0.75. The results show 1) Qpha, Qphv, Qimv, and Qazv reached stable values (equilibration) after 30-36 s of pacing; 2) the steady Qpha, Qphv, and Qimv were linearly related to Pdi, and they were related by a parabolic function to duty cycle, whereas Qazv was not significantly affected by Pdi and increased linearly as a function of the duty cycle; 3) the diaphragmatic blood drainage was approximately 60% through the intercostal veins leading into the azygos trunk, 25% through the phrenic vein, and 15% through the internal mammary vein during pacing of the diaphragm at a duty cycle of 0.50 and 60% Pdimax; and 4) for a given pacing pattern, Qpha and Qphv increased with f, but Qimv and Qazv did not.

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22

Muthu, P., J. M. Talent, I. Gryczynski, and J. Borejdo. "Cross-Bridge Duty Cycle in Isometric Contraction of Skeletal Myofibrils†." Biochemistry 47, no. 20 (May 2008): 5657–67. http://dx.doi.org/10.1021/bi7023223.

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23

Isenberg, G., S. Han, A. Schiefer, and M. F. Wendt-Gallitelli. "Changes in mitochondrial calcium concentration during the cardiac contraction cycle." Cardiovascular Research 27, no. 10 (October 1, 1993): 1800–1809. http://dx.doi.org/10.1093/cvr/27.10.1800.

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Cachon, Monique, Claude Greuet, Jacky Cosson, and Philippe Huitorel. "Analysis of the mechanism of dinoflagellate flagella contraction-relaxation cycle." Biology of the Cell 76, no. 1 (January 1992): 33–42. http://dx.doi.org/10.1016/0248-4900(92)90192-4.

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25

VerPlank, Lynn, and Rong Li. "Cell Cycle-regulated Trafficking of Chs2 Controls Actomyosin Ring Stability during Cytokinesis." Molecular Biology of the Cell 16, no. 5 (May 2005): 2529–43. http://dx.doi.org/10.1091/mbc.e04-12-1090.

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Cytokinesis requires the coordination of many cellular complexes, particularly those involved in the constriction and reconstruction of the plasma membrane in the cleavage furrow. We have investigated the regulation and function of vesicle transport and fusion during cytokinesis in budding yeast. By using time-lapse confocal microscopy, we show that post-Golgi vesicles, as well as the exocyst, a complex required for the tethering and fusion of these vesicles, localize to the bud neck at a precise time just before spindle disassembly and actomyosin ring contraction. Using mutants affecting cyclin degradation and the mitotic exit network, we found that targeted secretion, in contrast to contractile ring activation, requires cyclin degradation but not the mitotic exit network. Analysis of cells in late anaphase bearing exocyst and myosin V mutations show that both vesicle transport and fusion machineries are required for the completion of cytokinesis, but this is not due to a delay in mitotic exit or assembly of the contractile ring. Further investigation of the dynamics of contractile rings in exocyst mutants shows these cells may be able to initiate contraction but often fail to complete the contraction due to premature disassembly during the contraction phase. This phenotype led us to identify Chs2, a transmembrane protein targeted to the bud neck through the exocytic pathway, as necessary for actomyosin ring stability during contraction. Chs2, as the chitin synthase that produces the primary septum, thus couples the assembly of the extracellular matrix with the dynamics of the contractile ring during cytokinesis.

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Smith, D. A. "The theory of sliding filament models for muscle contraction. II. Biochemically-based models of the contraction cycle." Journal of Theoretical Biology 146, no. 2 (September 1990): 157–75. http://dx.doi.org/10.1016/s0022-5193(05)80133-x.

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Koba, Satoshi, Kenshi Yoshinaga, Sayaka Fujita, Michio Miyoshi, and Tatsuo Watanabe. "Exercise pressor reflex function in female rats fluctuates with the estrous cycle." Journal of Applied Physiology 113, no. 5 (September 1, 2012): 719–26. http://dx.doi.org/10.1152/japplphysiol.00396.2012.

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In women, sympathoexcitation during static handgrip exercise is reduced during the follicular phase of the ovarian cycle compared with the menstrual phase. Previous animal studies have demonstrated that estrogen modulates the exercise pressor reflex, a sympathoexcitatory mechanism originating in contracting skeletal muscle. The present study was conducted in female rats to determine whether skeletal muscle contraction-evoked reflex sympathoexcitation fluctuates with the estrous cycle. The estrous cycle was judged by vaginal smear. Plasma concentrations of estrogen were significantly ( P < 0.05) higher in rats during the proestrus phase of the estrus cycle than those during the diestrus phase. In decerebrate rats, either electrically induced 30-s continuous static contraction of the hindlimb muscle or 30-s passive stretch of Achilles tendon (a maneuver that selectively stimulates mechanically sensitive muscle afferents) evoked less renal sympathoexcitatory and pressor responses in the proestrus animals than in the diestrus animals. Renal sympathoexcitatory response to 1-min intermittent (1- to 4-s stimulation to relaxation) bouts of static contraction was also significantly less in the proestrus rats than that in the diestrus rats. In ovariectomized female rats, 17β-estradiol applied into a well covering the dorsal surface of the lumbar spinal cord significantly reduced skeletal muscle contraction-evoked responses. These observations demonstrate that the exercise pressor reflex function and its mechanical component fluctuate with the estrous cycle in rats. Estrogen may cause these fluctuations through its attenuating effects on the spinal component of the reflex arc.

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Rogers, Anna M., Natasha R. Saunders, Kyra E. Pyke, and Michael E. Tschakovsky. "Rapid vasoregulatory mechanisms in exercising human skeletal muscle: dynamic response to repeated changes in contraction intensity." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 3 (September 2006): H1065—H1073. http://dx.doi.org/10.1152/ajpheart.00368.2006.

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We tested the hypothesis that vasoregulatory mechanisms exist in humans that can rapidly adjust muscle blood flow to repeated increases and decreases in exercise intensity. Six men and seven women (age, 24.4 ± 1.3 yr) performed continuous dynamic forearm handgrip contractions (1- to 2-s contraction-to-relaxation duty cycle) during repeated step increases and decreases in contraction intensity. Three step change oscillation protocols were examined: Slow (7 contractions per contraction intensity × 10 steps); Fast (2 contractions per contraction intensity × 15 steps); and Very Fast (1 contraction per contraction intensity × 15 steps). Forearm blood flow (FBF; Doppler and echo ultrasonography), heart rate (ECG), and mean arterial pressure (arterial tonometry) were examined for the equivalent of a cardiac cycle during each relaxation phase (FBFrelax). Mean arterial pressure and heart rate did not change during repeated step changes ( P = 0.352 and P = 0.190). For both Slow and Fast conditions, relaxation phase FBFrelax adjusted immediately and repeatedly to both increases and decreases in contraction intensity, and the magnitude and time course of FBFrelax changes were virtually identical. For the Very Fast condition, FBFrelax increased with the first contraction and thereafter slowly increased over the course of repeated contraction intensity oscillations. We conclude that vasoregulatory mechanisms exist in human skeletal muscle that are capable of rapidly and repeatedly adjusting muscle blood flow with ongoing step changes in contraction intensity. Importantly, they demonstrate symmetry in response magnitude and time course with increasing versus decreasing contraction intensity but cannot adjust to very fast exercise intensity oscillations.

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DEMONT, M. EDWIN, and JOHN M. GOSLINE. "Mechanics of Jet Propulsion in the Hydromedusan Jellyfish, Polyorchis Penicillatus: II. Energetics of the Jet Cycle." Journal of Experimental Biology 134, no. 1 (January 1, 1988): 333–45. http://dx.doi.org/10.1242/jeb.134.1.333.

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The mechanical energy generated by the contraction of the subumbrellar swimming muscles to power the jet cycle in the hydromedusan jellyfish Polyorchis penicillatus (Eschscholtz, 1829) was measured. This energy was experimentally partitioned into three components during the contraction. The sum of these components was taken to be the mechanical energy generated by the muscles during the jet cycle and was between 8.9×10−5 and 1.4×10−4J per contraction. Energy from one of these components is stored as strain energy in the mesoglea and powers the refilling phase. The mesoglea can clearly act as an effective elastic structure to antagonize the contraction of the swimming muscles completely, and it may be designed to function at some optimum. The mechanical significance of elastic energy storage systems in jet-propelled animals is discussed, and this significance is clearly displayed in Polyorchis. The unusually long-duration action potential of the swimming muscles may be an important component of the swimming mechanism, allowing the muscles to store energy in an elastic structure at the end of the contraction phase when little hydrodynamic thrust is developed. It is suggested that the action potential of vertebrate cardiac muscle may have a similar mechanical function.

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Hogan, Michael C., Bruno Grassi, Michele Samaja, Creed M. Stary, and L. B. Gladden. "Effect of contraction frequency on the contractile and noncontractile phases of muscle venous blood flow." Journal of Applied Physiology 95, no. 3 (September 2003): 1139–44. http://dx.doi.org/10.1152/japplphysiol.00226.2003.

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The purpose of this study was to test the hypothesis that increasing muscle contraction frequency, which alters the duty cycle and metabolic rate, would increase the contribution of the contractile phase to mean venous blood flow in isolated skeletal muscle during rhythmic contractions. Canine gastrocnemius muscle ( n = 5) was isolated, and 3-min stimulation periods of isometric, tetanic contractions were elicited sequentially at rates of 0.25, 0.33, and 0.5 contractions/s. The O2 uptake, tension-time integral, and mean venous blood flow increased significantly ( P < 0.05) with each contraction frequency. Venous blood flow during both the contractile (106 ± 6, 139 ± 8, and 145 ± 8 ml·100 g-1·min-1) and noncontractile phases (64 ± 3, 78 ± 4, and 91 ± 5 ml·100 g-1·min-1) increased with contraction frequency. Although developed force and duration of the contractile phase were never significantly different for a single contraction during the three contraction frequencies, the amount of blood expelled from the muscle during an individual contraction increased significantly with contraction frequency (0.24 ± 0.03, 0.32 ± 0.02, and 0.36 ± 0.03 ml·N-1·min-1, respectively). This increased blood expulsion per contraction, coupled with the decreased time in the noncontractile phase as contraction frequency increased, resulted in the contractile phase contribution to mean venous blood flow becoming significantly greater (21 ± 4, 30 ± 4, and 38 ± 6%) as contraction frequency increased. These results demonstrate that the percent contribution of the muscle contractile phase to mean venous blood flow becomes significantly greater as contraction frequency (and thereby duty cycle and metabolic rate) increases and that this is in part due to increased blood expulsion per contraction.

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Lee, Wing-Kee, Malte Spielmann, Ulrich Bork, and Frank Thévenod. "Cd2+-induced swelling-contraction dynamics in isolated kidney cortex mitochondria: role of Ca2+ uniporter, K+ cycling, and protonmotive force." American Journal of Physiology-Cell Physiology 289, no. 3 (September 2005): C656—C664. http://dx.doi.org/10.1152/ajpcell.00049.2005.

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The nephrotoxic metal Cd2+ causes mitochondrial damage and apoptosis of kidney proximal tubule cells. A K+ cycle involving a K+ uniporter and a K+/H+ exchanger in the inner mitochondrial membrane (IMM) is thought to contribute to the maintenance of the structural and functional integrity of mitochondria. In the present study, we have investigated the effect of Cd2+ on K+ cycling in rat kidney cortex mitochondria. Cd2+ (EC50 ∼19 μM) induced swelling of nonenergized mitochondria suspended in isotonic salt solutions according to the sequence KCl = NaCl > LiCl ≫ choline chloride. Cd2+-induced swelling of energized mitochondria had a similar EC50 value and showed the same cation dependence but was followed by a spontaneous contraction. Mitochondrial Ca2+ uniporter (MCU) blockers, but not permeability transition pore inhibitors, abolished swelling, suggesting the need for Cd2+ influx through the MCU for swelling to occur. Complete loss of mitochondrial membrane potential (ΔΨm) induced by K+ influx did not prevent contraction, but addition of the K+/H+ exchanger blocker, quinine (1 mM), or the electroneutral protonophore nigericin (0.4 μM), abolished contraction, suggesting the mitochondrial pH gradient (ΔpHm) driving contraction. Accordingly, a quinine-sensitive partial dissipation of ΔpHm was coincident with the swelling-contraction phase. The data indicate that Cd2+ enters the matrix through the MCU to activate a K+ cycle. Initial K+ load via a Cd2+-activated K+ uniporter in the IMM causes osmotic swelling and breakdown of ΔΨm and triggers quinine-sensitive K+/H+ exchange and contraction. Thus Cd2+-induced activation of a K+ cycle contributes to the dissipation of the mitochondrial protonmotive force.

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Lutjemeier, Barbara J., Leonardo F. Ferreira, David C. Poole, Dana Townsend, and Thomas J. Barstow. "Muscle microvascular hemoglobin concentration and oxygenation within the contraction–relaxation cycle." Respiratory Physiology & Neurobiology 160, no. 2 (February 2008): 131–38. http://dx.doi.org/10.1016/j.resp.2007.09.005.

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Markofski, Melissa M., and William A. Braun. "Influence of Menstrual Cycle on Indices of Contraction-Induced Muscle Damage." Journal of Strength and Conditioning Research 28, no. 9 (September 2014): 2649–56. http://dx.doi.org/10.1519/jsc.0000000000000429.

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Hammer, Shane M., Jesse C. Craig, Ryan M. Broxterman, and Thomas J. Barstow. "Oxygen Utilization During The Contraction-Relaxation Cycle Of Intermittent Forearm Exercise." Medicine & Science in Sports & Exercise 48 (May 2016): 746–47. http://dx.doi.org/10.1249/01.mss.0000487241.04360.2a.

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Broxterman, Ryan M., Carl J. Ade, Jesse C. Craig, Samuel L. Wilcox, and Thomas J. Barstow. "Muscle Oxygenation Characteristics Within the Contraction-Relaxation Cycle for Handgrip Exercise." Medicine & Science in Sports & Exercise 46 (May 2014): 757. http://dx.doi.org/10.1249/01.mss.0000495767.69902.69.

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Tchirikov, Mikhail, Ulrich Peiper, and Hobe J. Schroder. "Contraction kinetics of isolated human myometrium during menstrual cycle and pregnancy." BJOG: An International Journal of Obstetrics and Gynaecology 107, no. 1 (January 2000): 62–67. http://dx.doi.org/10.1111/j.1471-0528.2000.tb11580.x.

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&NA;. "Symposium Entitled: “Calcium: Excitation-Contraction Coupling And The Cross-Bridge Cycle”." Medicine & Science in Sports & Exercise 27, Supplement (May 1995): S101. http://dx.doi.org/10.1249/00005768-199505001-00567.

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Segal, Dagan, Assaf Zaritsky, Eyal D. Schejter, and Ben-Zion Shilo. "Feedback inhibition of actin on Rho mediates content release from large secretory vesicles." Journal of Cell Biology 217, no. 5 (March 1, 2018): 1815–26. http://dx.doi.org/10.1083/jcb.201711006.

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Secretion of adhesive glycoproteins to the lumen of Drosophila melanogaster larval salivary glands is performed by contraction of an actomyosin network assembled around large secretory vesicles, after their fusion to the apical membranes. We have identified a cycle of actin coat nucleation and disassembly that is independent of myosin. Recruitment of active Rho1 to the fused vesicle triggers activation of the formin Diaphanous and actin nucleation. This leads to actin-dependent localization of a RhoGAP protein that locally shuts off Rho1, promoting disassembly of the actin coat. When contraction of vesicles is blocked, the strict temporal order of the recruited elements generates repeated oscillations of actin coat formation and disassembly. Interestingly, different blocks to actin coat disassembly arrested vesicle contraction, indicating that actin turnover is an integral part of the actomyosin contraction cycle. The capacity of F-actin to trigger a negative feedback on its own production may be widely used to coordinate a succession of morphogenetic events or maintain homeostasis.

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Lippincott, J., K. B. Shannon, W. Shou, R. J. Deshaies, and R. Li. "The Tem1 small GTPase controls actomyosin and septin dynamics during cytokinesis." Journal of Cell Science 114, no. 7 (April 1, 2001): 1379–86. http://dx.doi.org/10.1242/jcs.114.7.1379.

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Cytokinesis in budding yeast involves an actomyosin-based ring which assembles in a multistepped fashion during the cell cycle and constricts during cytokinesis. In this report, we have investigated the structural and regulatory events that occur at the onset of cytokinesis. The septins, which form an hour-glass like structure during early stages of the cell cycle, undergo dynamic rearrangements prior to cell division: the hourglass structure splits into two separate rings. The contractile ring, localized between the septin double rings, immediately undergoes contraction. Septin ring splitting is independent of actomyosin ring contraction as it still occurs in mutants where contraction fails. We hypothesize that septin ring splitting may remove a structural barrier for actomyosin ring to contract. Because the Tem1 small GTPase (Tem1p) is required for the completion of mitosis, we investigated its role in regulating septin and actomyosin ring dynamics in the background of the net1-1 mutation, which bypasses the anaphase cell cycle arrest in Tem1-deficient cells. We show that Tem1p plays a specific role in cytokinesis in addition to its function in cell cycle progression. Tem1p is not required for the assembly of the actomyosin ring but controls actomyosin and septin dynamics during cytokinesis.

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CHEN, CHUAN-SHOW. "BIOMECHANICAL STUDY ON A NEW TRAINING MACHINE AND METHOD FOR POWER AND STRENGTH." Journal of Mechanics in Medicine and Biology 05, no. 02 (June 2005): 243–51. http://dx.doi.org/10.1142/s0219519405001448.

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Strength and power are important in sports competition, and increasing ability of explosive muscle contraction force is key to winning for sports performance in events like jumping or throwing. In this study, Passive Repeated Plyometric (PRP) training method and the machine were designed. This machine allow one to training for top gear power with high frequency and without danger as compared with the conventional way of training like common way of plyomerics or using machine for isotonic muscle contraction. The PRP has it specific effects, which can be summarized as follow: 1. Motor driving PRP machine allow athlete training with high frequency, up to 300 rpm (0.2 Hz), especially for lower extremities to increase thrust force and force of body trunk. 2. PRP training method bring about the stretching reflex and elastic energy to recruit into a powerful muscle contraction. 3. This training machine formed a natural and powerful muscle contraction by stretching and shortening in a cycle of contraction, which is called stretching-shortening cycle or SSC. 4. Well-documented evidence from both theoretical and practical were achieved in 1998 Bangkok Asian game and the following Pusan2002 applying to track & field and basketball players.

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Shepherd, N., and F. Kavaler. "Direct control of contraction force of single frog atrial cells by extracellular ions." American Journal of Physiology-Cell Physiology 251, no. 5 (November 1, 1986): C653—C661. http://dx.doi.org/10.1152/ajpcell.1986.251.5.c653.

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We describe a method by which the ionic surround of an isolated frog heart cell can be changed within a small fraction of a contraction cycle while continuously measuring contraction force. With this method, we have investigated the effect on force development of changing the extracellular concentrations of Ca [( Ca]o) and Na [( Na]o) in the period between electrically driven contractions and during the rising phase of a contraction. Raising or lowering either [Ca]o or [Na]o more than 300 ms prior to a stimulus caused peak force of the next contraction to be changed 100% of the way to the steady-state value characteristic of the new ionic concentrations. Similar maneuvers at later times relative to the stimulus caused progressively smaller changes. Lowering [Ca]o from 2 to 1 mM or raising [Na]o from 78 to 110 mM 100 ms after stimulation brought twitch force 35 and 67% of the way to the new steady states, respectively. We conclude that extracellular Ca is the source of activator Ca in these cells and that extracellular Na plays a role in regulation of the intracellular Ca concentration early in the contraction cycle.

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Abarca, Sergio F., and Michael T. Montgomery. "Are Eyewall Replacement Cycles Governed Largely by Axisymmetric Balance Dynamics?" Journal of the Atmospheric Sciences 72, no. 1 (January 1, 2015): 82–87. http://dx.doi.org/10.1175/jas-d-14-0151.1.

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Abstract The authors question the widely held view that radial contraction of a secondary eyewall during an eyewall replacement cycle is well understood and governed largely by the classical theory of axisymmetric balance dynamics. The investigation is based on a comparison of the secondary circulation and derived tangential wind tendency between a full-physics simulation and the Sawyer–Eliassen balance model. The comparison is made at a time when the full-physics model exhibits radial contraction of the secondary eyewall during a canonical eyewall replacement cycle. It is shown that the Sawyer–Eliassen model is unable to capture the phenomenology of secondary eyewall radial contraction because it predicts a net spindown of the boundary layer tangential winds and does not represent the boundary layer spinup mechanism that has been articulated in recent work.

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Iridiastadi, Hardianto, and Maury A. Nussbaum. "Muscular Fatigue and Endurance During Intermittent Static Efforts: Effects of Contraction Level, Duty Cycle, and Cycle Time." Human Factors: The Journal of the Human Factors and Ergonomics Society 48, no. 4 (December 2006): 710–20. http://dx.doi.org/10.1518/001872006779166389.

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Nakamura, Y., N. Hayashi, and I. Muraoka. "Temporal Effect of Muscle Contraction on Respiratory Sinus Arrhythmia." Methods of Information in Medicine 36, no. 04/05 (October 1997): 268–70. http://dx.doi.org/10.1055/s-0038-1636879.

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Abstract:The purpose of this investigation was to compare the heart rate variability at respiratory frequency (HRVRF) in muscle contractions during the inspiratory phase with that during the expiratory phase. Eight volunteers performed pedaling on a cycle ergometer, twice a cycle of respiration (4 sec) against a load of 0.25 Nm/kg BW, of which the timing was adjusted to twice during the inspiration phase (I), once during the expiration, once during the inspiration (El), or twice during the expiration phase (E). Spectral analysis was applied to the R-R intervals of each condition. The amplitude of HRVRF in E was less than half of I (9 ± 2 msec versus 23 ±2 msec). The results indicate that the timing of muscle contraction can affect the heart rate variability even at the frequency band of respiration.

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Gilchrist, Simon, and Egon Zakrajšek. "Credit Spreads and Business Cycle Fluctuations." American Economic Review 102, no. 4 (June 1, 2012): 1692–720. http://dx.doi.org/10.1257/aer.102.4.1692.

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Using micro-level data, we construct a credit spread index with considerable predictive power for future economic activity. We decompose the credit spread into a component that captures firm-specific information on expected defaults and a residual component–– the excess bond premium. Shocks to the excess bond premium that are orthogonal to the current state of the economy lead to declines in economic activity and asset prices. An increase in the excess bond premium appears to reflect a reduction in the risk-bearing capacity of the financial sector, which induces a contraction in the supply of credit and a deterioration in macroeconomic conditions.

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Couvrette2, Amélie, and Chantal Plourde. "Au-delà de la séparation : perceptions de mères incarcérées sur leurs relations avec leurs enfants depuis la détention1." Criminologie 52, no. 1 (May 6, 2019): 301–23. http://dx.doi.org/10.7202/1059550ar.

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Cette recherche qualitative exploratoire s’intéresse aux perceptions de mères détenues quant aux effets de leur incarcération sur leurs relations avec leurs enfants. L’étude documente également les conséquences qu’elles perçoivent à la suite de cette incarcération ainsi que les réactions de leurs enfants. Quinze mères incarcérées dans un établissement de détention ont été rencontrées. L’analyse montre qu’un ensemble de conditions, l’instabilité et la violence conjugale, la consommation de substances psychoactives et les restrictions quant à la garde des enfants étaient présentes avant l’incarcération et que celles-ci affectaient la relation entre la mère et ses enfants. Mais pour les mères rencontrées, l’incarcération s’impose comme un élément supplémentaire complexifiant une relation déjà tendue entre la mère et ses enfants. Les réactions des enfants à la nouvelle détention et les conséquences de celle-ci dans leur relation avec leur mère ont été largement décrites. Alors qu’elles blâment leurs propres mères pour leurs choix déviants et qu’elles reconnaissent avoir placé leurs enfants à risque, elles se placent comme élément de solution aux problèmes de délinquance et de consommation que leurs enfants pourraient développer. Pour elles, elles arriveront à briser ce cycle.

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Mullins, Paula D., and Vladimir E. Bondarenko. "Mathematical model for β1-adrenergic regulation of the mouse ventricular myocyte contraction." American Journal of Physiology-Heart and Circulatory Physiology 318, no. 2 (February 1, 2020): H264—H282. http://dx.doi.org/10.1152/ajpheart.00492.2019.

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The β1-adrenergic regulation of cardiac myocyte contraction plays an important role in regulating heart function. Activation of this system leads to an increased heart rate and stronger myocyte contraction. However, chronic stimulation of the β1-adrenergic signaling system can lead to cardiac hypertrophy and heart failure. To understand the mechanisms of action of β1-adrenoceptors, a mathematical model of cardiac myocyte contraction that includes the β1-adrenergic system was developed and studied. The model was able to simulate major experimental protocols for measurements of steady-state force-calcium relationships, cross-bridge release rate and force development rate, force-velocity relationship, and force redevelopment rate. It also reproduced quite well frequency and isoproterenol dependencies for intracellular Ca2+ concentration ([Ca2+]i) transients, total contraction force, and sarcomere shortening. The mathematical model suggested the mechanisms of increased contraction force and myocyte shortening on stimulation of β1-adrenergic receptors is due to phosphorylation of troponin I and myosin-binding protein C and increased [Ca2+]i transient resulting from activation of the β1-adrenergic signaling system. The model was used to simulate work-loop contractions and estimate the power during the cardiac cycle as well as the effects of 4-aminopyridine and tedisamil on the myocyte contraction. The developed mathematical model can be used further for simulations of contraction of ventricular myocytes from genetically modified mice and myocytes from mice with chronic cardiac diseases. NEW & NOTEWORTHY A new mathematical model of mouse ventricular myocyte contraction that includes the β1-adrenergic system was developed. The model simulated major experimental protocols for myocyte contraction and predicted the effects of 4-aminopyridine and tedisamil on the myocyte contraction. The model also allowed for simulations of work-loop contractions and estimation of the power during the cardiac cycle.

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Mat Dzahir, Mohd Azuwan, Tatsuya Nobutomo, and Shin Ichiroh Yamamoto. "Development of Gait Training System Powered by Antagonistic Mono-and Bi-Articular Actuators Using Contraction Model Control Scheme." Applied Mechanics and Materials 393 (September 2013): 525–31. http://dx.doi.org/10.4028/www.scientific.net/amm.393.525.

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The use of Pneumatic Muscle Actuator (PMA) in medical robots for rehabilitation has changed due to the requirements for a compliant, light weight and user-friendly robotic system. In this paper, a control system for controlling the bi-articular actuators (PMA) is proposed. Based on the information obtained from the positional input data (hip and knee joint angles), a contraction model is derived using mathematical equations to determine the contraction patterns of antagonistic mono-and bi-articular actuators, and then implemented it into the control system. Anterior and posterior muscle activation levels are introduced into the model to manipulate its magnitude. There are two tests for the control system; first is with antagonistic mono-articular actuators alone; second is along with antagonistic bi-articular actuators. The contraction model control scheme was tested on a healthy subject in a robot assisted walk test, and satisfactory performance was obtained. The result showed that, the cycle time of the gait training system is improved up to 3 seconds gait cycle compared to 5 seconds gait cycle used in previous research. However, a little time shift and inertia occurred when the controller is tested at faster gait cycle time of 2 seconds and 1 second. Thus, the potential field and iterative learning control are suggested to improve the gait cycle of the system.

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Stallone, J. N., J. T. Crofton, and L. Share. "Sexual dimorphism in vasopressin-induced contraction of rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (February 1, 1991): H453—H458. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h453.

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Previously, we reported that, in the rat, pressor responsiveness to vasopressin (VP) is higher in males than in females during most phases of the estrous cycle. To explore the role of the vasculature in this phenomenon, we examined vascular reactivity to VP in thoracic aortas of male rats and female rats during each phase of the estrous cycle. Aortic rings were prepared from age-matched male and female Sprague-Dawley rats and mounted for isometric tension recording. Maximal response of female aortas to VP (4,246 +/- 163 mg/mg ring dry wt) was more than twice (P less than 0.001) that of male aortas (1,877 +/- 215 mg/mg ring wt). Sensitivity of female aortas to VP was substantially higher (P less than 0.001) than that of male aortas (EC50: 10.9 +/- 0.7 vs. 19.0 +/- 1.6 nM, respectively). Maximal rate of tension development (dT/dtmax) during contraction with VP was nearly twofold higher (P less than 0.01) in female aortas (536 +/- 23 mg/min) than in male aortas (300 +/- 19 mg/min). Maximal response, sensitivity, and dT/dtmax of female aortas did not vary significantly during the estrous cycle. Maximal response of female aortas to phenylephrine (PE; 1,251 +/- 93 mg/mg ring wt) was half that (P less than 0.001) of male aortas (2,546 +/- 194 mg/mg ring wt); sensitivity to PE did not differ significantly (EC50: 0.33 +/- 0.02 vs. 0.38 +/- 0.06 microM, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

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Xiaojuan Guo, Yaqin Zhao, and Binsheng Yang. "Regulation of centrin self-assembly investigated by fluorescence resonance light scattering." RSC Advances 7, no. 17 (2017): 10206–14. http://dx.doi.org/10.1039/c6ra26865j.

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Journal articles on the topic 'Réactions de contraction de cycle'

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