The Morphology of Repression: Dialectics between Chilean Students and State Force Actions 1

Author(s):  
Gabriela González Vaillant ◽  
Fernanda Page Poma
Keyword(s):  
1976 ◽  
Vol 231 (5) ◽  
pp. 1501-1508 ◽  
Author(s):  
MJ Siegman ◽  
TM Butler ◽  
SU Mooers ◽  
RE Davies

Mechanical responses to stretch and length-tension relations were examined in rabbit taenia coli, mesenteric vein, aorta, and myometrium and in guinea pig taenia coli made atonic by incubation in Krebs-bicarbonate solution at 20-22 degrees C. When stretched 10% of the length at which maximum active tension is observed (Lo) in 0.5 s, the muscles showed a transient large force (resistance to stretch) that decayed to a new constant level within minutes (stress relaxation). The resistance to stretch decreased markedly in Ca2+-free [disodium ethylene glycolbis-(beta-aminoethylether)-N,N-tetraacetic acid (EGTA)] Krebs but was restored in normal Krebs solution. Calcium removal did not affect the passive length-tension curve. The absence of Ca2+ did not change the steady-state force maintained by the muscle; thus stretch resistance was not due to tone. Blockade of Ca2+ influx associated with electrical activity with 5-[3,4-dimethoxyphenethyl)methylamino]-2-(3,4,5-trimethoxyphenyl-2-isoprop ylvaleronitrile (D-600) and of Ca2+ release from intracellular sites with thymol (1 mM) completely blocked contraction but did not alter the responses to stretch, thus dissociating the responses to stretch from these processes and tension development. The Ca2+-dependent stress relaxation showed a dependence on muscle length similar to that for active tension development. Except at long muscle lengths, where connective tissue markedly affects length-tension relations, most of the "viscoelasticity" of these smooth muscles is dependent on calcium and may be largely due to the straining of crossbridges that are attached, but not generating a net force, in the resting state.


1994 ◽  
Vol 72 (4) ◽  
pp. 1734-1744 ◽  
Author(s):  
M. Trulsson ◽  
R. S. Johansson

1. The encoding of force amplitude and force rate by human periodontal mechanoreceptive afferents was studied. Recordings were obtained from 19 single periodontal afferents in the inferior alveolar nerve with the use of tungsten microelectrodes. Loads consisting of a force increase (loading ramp), a phase of maintained force (static phase), and a force decrease (unloading ramp) were applied to the receptor bearing tooth, which was most often an incisor. The static forces applied ranged between 0.05 and 5 N, and the rate of force applied during the loading ramps ranged between 0.4 and 70 N/s. The forces were primarily applied in one of six directions (lingual, labial, mesial, distal, upward, or downward) that evoked the greatest discharge activity. 2. For each force application, the steady-state response was defined as the mean discharge rate during a 1-s period starting 0.5 s after the end of the loading ramp. Most afferents (15/19) exhibited a “hyperbolic” (viz., negatively accelerating) relationship between the amplitude of the stimulation force and the steady-state response, featuring a pronounced saturation tendency: the highest sensitivity to changes in static force was observed at force levels below 1 N. At higher force levels the sensitivity gradually diminished. Moreover, the dynamic sensitivity similarly decreased with increasing amplitude of static background force. For a subsample of afferents studied, comparable stimulus-response relationships were obtained in directions other than the most responsive one, but the discharge rates were lower. 3. In contrast to the response of most afferents, four (4/19) differed in that they consistently exhibited a nearly linear relationship between force amplitude and the steady-state response. Moreover, these afferents maintained their dynamic sensitivity as the amplitude of the background force was increased. 4. The steady-state response of all afferents was well described as a constant times F/ (F + c), where F represents the steady-state force, and c the force generating one-half the estimated maximum discharge rate that could be evoked by steady-state force stimulation. The c-parameter was on average 0.42 N (range 0.05–1.1 N) for the afferents exhibiting hyperbolic stimulus-response relationships. In contrast it ranged between 5 and 22 N for those exhibiting “nearly linear” relationships. A hypothetical model of the mechanics of the periodontal ligament supporting the F/(F + c) transform is proposed. 5. A general transfer function was developed to predict the instantaneous discharge rate of an individual afferent to arbitrary force profiles applied to the receptor bearing tooth.(ABSTRACT TRUNCATED AT 400 WORDS)


Author(s):  
R. Darin Ellis ◽  
Kentaro Kotani

A visco-elastic model of the mechanical properties of muscle was used to describe age-differences in the buildup of force in isometric elbow flexion. Given information from the literature on age-related physiological changes, such as decreasing connective-tissue elasticity, one would expect changes in the mechanical properties of skeletal muscle and their related model parameters. Force vs. time curves were obtained for 7 young (aged 21–27) and 7 old (aged 69–83) female subject. There were significant age group differences in steady-state force level and the best fitting model parameters. In particular, the viscous damping element of the model plays a large role in describing the increased time to reach steady-state force levels in the older subject group. Implications of this research include incorporating parameter differences into more complex models, such as crash impact models.


1997 ◽  
Vol 41 (01) ◽  
pp. 69-80
Author(s):  
Mark D. Bracco ◽  
Tomasz Wierzbicki

This paper studies the cutting by a wedge of advanced double hull (ADH) small-scale models. A total of six cutting experiments were performed with six different wedge geometries. Complex deformation patterns observed in the damaged specimens were simplified to obtain a closed-form upper bound for the steady-state cutting force. The ADH steady-state cutting force solution varied from 6% above to 12% below the experimental mean steady-state force. The absolute average error is 5%.


2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Joseph D Powers ◽  
Farid Moussavi-Harami ◽  
Maria Razumova ◽  
Jil Tardiff ◽  
Michael Regnier

At the subcellular level, the Frank-Starling law of the heart is described by an increase in calcium sensitivity and force with increased sarcomere length (SL). We examine how this relationship is affected by a dilated cardiomyopathy-associated mutation in tropomyosin (D230N, denoted Tm D230N ) by measuring contractility of intact and permeabilized cardiac muscle preparations at short (2.0 μm) and long (2.3 μm) SL. Transgenic mouse hearts containing the Tm D230N mutation have significantly dilated hearts and reduced cardiac output by ~6 months of age. Intact trabeculae were electrically stimulated and paced at 1 Hz with oxygenated solution (30°C) circulating through the experimental chamber, and permeabilized preparations were bathed in solutions (15°C) of progressively increased [Ca 2+ ] for measures of steady-state force. For intact muscle we found that the Tm D230N mutation results in significantly reduced twitch forces at SL 2.0 and 2.3 μm relative to wild-type (WT). Also, WT trabeculae displayed a significant increase in twitch force upon increase in SL (as expected) but Tm D230N trabeculae did not, demonstrating a loss of SL dependence of contraction. In permeabilized preparations, maximal activation (pCa 4.5) of both WT and Tm D230N preparations exhibited significant SL-dependent increases in force. However, at submaximal Ca 2+ (pCa 5.8), where the heart operates, WT preparations had significant increases in force with increasing length (comparing SL 2.0 to 2.3 μm), while this length-dependence of force augmentation in Tm D230N was absent. The increase in pCa 50 (pCa that produces half-maximal force) going from SL 2.0 to 2.3 μm was significantly less for Tm D230N preparations compared to WT, owing to a significantly smaller increase in pCa 50 at SL 2.3 μm (the pCa 50 at SL 2.0 μm was not significantly different between WT and Tm D230N ). These results suggest that the Tm D230N mutation limits an increase in the Ca 2+ sensitivity of contraction as the muscle lengthens by damping thin filament activation. To further examine length-dependent effects of the Tm D230N mutation, future experiments will test conditions that augment cross-bridge binding/inhibition, and other models of dilated cardiomyopathy that inhibit thin filament activation. Funding: HL111197


1982 ◽  
Vol 242 (3) ◽  
pp. C146-C158 ◽  
Author(s):  
R. A. Meiss

Controlled length changes were imposed on mesotubarium superius and ovarian ligament smooth muscles from the reproductive tracts of female rabbits in constant estrus. Stretches of up to 35% of the muscle length were applied during isometric contraction, relaxation, and steady-state force levels. Force was continuously monitored and was plotted as a function of length. During constant velocity stretches there was an initial steep rise in force, a rapid downward deviation from the initial slope, and a long region with a constant upward slope. Stretches made during contraction showed smaller initial rises in force and steeper linear portions than did identical comparison stretches made during relaxation. The value of the slope was independent of the prior developed force, but it did depend on whether the muscle was contracting or relaxing. During contraction and steady-state force levels, the slope was independent of the stretch rate, but it was strongly rate dependent during relaxation. Changes in the stretch rate during stretch caused associated changes in muscle force; the relationship was curvilinear and was exaggerated during relaxation. The findings are placed in the context of a sliding-filament--cross-bridge hypothesis.


1991 ◽  
Vol 261 (2) ◽  
pp. C253-C258 ◽  
Author(s):  
E. Suematsu ◽  
M. Resnick ◽  
K. G. Morgan

The mechanism of contraction of vascular smooth muscle by prostaglandin F2 alpha (PGF2 alpha) was examined by simultaneous measurement of the intracellular Ca2+ concentration [( Ca2+]i), force, and myosin light-chain (MLC) phosphorylation in ferret aorta. In the presence of 2.5 mM extracellular Ca2+, PGF2 alpha (10(-5)M) produced a tonic contraction with a transient spike in [Ca2+]i, followed by a relatively small sustained increase in [Ca2+]i (from a basal level of 2.32 +/- 0.07 x 10(-7) to 2.72 +/- 0.05 x 10(-7) M). In Ca(2+)-free bathing media, PGF2 alpha also produced a tonic contraction with a small spike in [Ca2+]i, indicating a release of Ca2+ from intracellular store sites, followed by no significant increase in [Ca2+]i. Ca(2+)-force curves were constructed by plotting the calibrated steady-state aequorin light signal against the resulting steady-state force. The curve was significantly shifted to the left by PGF2 alpha. PGF2 alpha also shifted the Ca(2+)-phosphorylation curve to the left. These results suggest that PGF2 alpha causes contraction by both elevating [Ca2+]i and decreasing the Ca2+ requirement for MLC phosphorylation. The data are consistent with a mechanism where there is either an increase in activity of MLC kinase or a decrease in phosphatase activity. Additionally, there was a smaller, but statistically significant, effect to increase force at any one phosphorylation level, pointing to the possibility of regulation of contractile force separate from MLC phosphorylation.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ricarda M. Haeger ◽  
Dilson E. Rassier

AbstractWhen a muscle is stretched during a contraction, the resulting steady-state force is higher than the isometric force produced at a comparable sarcomere length. This phenomenon, also referred to as residual force enhancement, cannot be readily explained by the force-sarcomere length relation. One of the most accepted mechanisms for the residual force enhancement is the development of sarcomere length non-uniformities after an active stretch. The aim of this study was to directly investigate the effect of non-uniformities on the force-producing capabilities of isolated myofibrils after they are actively stretched. We evaluated the effect of depleting a single A-band on sarcomere length non-uniformity and residual force enhancement. We observed that sarcomere length non-uniformity was effectively increased following A-band depletion. Furthermore, isometric forces decreased, while the percent residual force enhancement increased compared to intact myofibrils (5% vs. 20%). We conclude that sarcomere length non-uniformities are partially responsible for the enhanced force production after stretch.


Author(s):  
Anthony R. Rosales ◽  
Sean P. Ross ◽  
Paul Helquist ◽  
Per-Ola Norrby ◽  
Matthew S. Sigman ◽  
...  

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