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Passive Forces (passive + force)
Selected AbstractsReliability of dynamometric passive properties of the pelvic floor muscles in postmenopausal women with stress urinary incontinenceNEUROUROLOGY AND URODYNAMICS, Issue 8 2008Mélanie Morin Abstract The passive properties of the pelvic floor muscles (PFM) might play a role in stress urinary incontinence (SUI) pathophysiology. Aim To investigate the test,retest reliability of the dynamometric passive properties of the PFM in postmenopausal SUI women. Methods Thirty-two SUI postmenopausal women were convened to two sessions 2 weeks apart. In each session, the measurements were repeated twice. The pelvic floor musculature was evaluated in four different conditions: (1) forces recorded at minimal aperture (initial passive resistance); (2) passive resistance at maximal aperture; (3) five lengthening and shortening cycles (Forces and passive elastic stiffness (PES) were evaluated at different vaginal apertures. Hysteresis was also calculated.); (4) Percentage of passive resistance loss after 1 min of sustained stretching was computed. The generalizability theory was used to calculate two reliability estimates, the dependability indices (,) and the standard error of measurement (SEM), for one session involving one measurement or the mean of two measurements. Results Overall, the reliability of the passive properties was good with indices of dependability of 0.75,0.93. The SEMs for forces and PES were 0.24,0.67 N and 0.03,0.10 N/mm, respectively, for mean, maximal and 20-mm apertures, representing an error between 13% and 23%. Passive forces at minimal aperture showed lower reliability (,,=,0.51,0.57) compared with other vaginal openings. The aperture at a common force of 0.5 N was the only parameter demonstrating a poor reliability (,,=,0.35). Conclusion This new approach for assessing PFM passive properties showed enough reliability for highly recommending its inclusion in the PFM assessment of SUI postmenopausal women. Neurourol. Urodynam. 27:819,825, 2008, © 2008 Wiley-Liss, Inc. [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] Compliant grasping with passive forcesJOURNAL OF FIELD ROBOTICS (FORMERLY JOURNAL OF ROBOTIC SYSTEMS), Issue 5 2005Cai-Hua Xiong Because friction is central to robotic grasp, developing an accurate and tractable model of contact compliance, particularly in the tangential direction, and predicting the passive force closure are crucial to robotic grasping and contact analysis. This paper analyzes the existence of the uncontrollable grasping forces (i.e., passive contact forces) in enveloping grasp or fixturing, and formulates a physical model of compliant enveloping grasp. First, we develop a locally elastic contact model to describe the nonlinear coupling between the contact force with friction and elastic deformation at the individual contact. Further, a set of "compatibility" equations is given so that the elastic deformations among all contacts in the grasping system result in a consistent set of displacements of the object. Then, combining the force equilibrium, the locally elastic contact model, and the "compatibility" conditions, we formulate the natural compliant model of the enveloping grasp system where the passive compliance in joints of fingers is considered, and investigate the stability of the compliant grasp system. The crux of judging passive force closure is to predict the passive contact forces in the grasping system, which is formulated into a nonlinear least square in this paper. Using the globally convergent Levenberg-Marquardt method, we predict contact forces and estimate the passive force closure in the enveloping grasps. Finally, a numerical example is given to verify the proposed compliant enveloping grasp model and the prediction method of passive force closure. © 2005 Wiley Periodicals, Inc. [source] Imbalance of plasma membrane ion leak and pump relationship as a new aetiological basis of certain disease statesJOURNAL OF INTERNAL MEDICINE, Issue 6 2003G. Ronquist Abstract. The basis for life is the ability of the cell to maintain ion gradients across biological membranes. Such gradients are created by specific membrane-bound ion pumps [adenosine triphosphatases (ATPases)]. According to physicochemical rules passive forces equilibrate (dissipate) ion gradients. The cholesterol/phospholipid ratio of the membrane and the degree of saturation of phospholipid fatty acids are important factors for membrane molecular order and herewith a determinant of the degree of non-specific membrane leakiness. Other operative principles, i.e. specific ion channels can be opened and closed according to mechanisms that are specific to the cell. Certain compounds called ionophores can be integrated in the plasma membrane and permit specific inorganic ions to pass. Irrespective of which mechanism ions leak across the plasma membrane the homeostasis may be kept by increasing ion pumping (ATPase activity) in an attempt to restore the physiological ion gradient. The energy source for this work seems to be glycolytically derived ATP formation. Thus an increase in ion pumping is reflected by increased ATP hydrolysis and rate of glycolysis. This can be measured as an accumulation of breakdown products of ATP and end-products of anaerobic glycolysis (lactate). In certain disease entities, the balance between ATP formation and ion pumping may be disordered resulting in a decrease in inter alia (i.a.) cellular energy charge, and an increase in lactate formation and catabolites of adenylates. Cardiac syndrome X is proposed to be due to an excessive leakage of potassium ions, leading to electrocardiographic (ECG) changes, abnormal Tl-scintigraphy of the heart and anginal pain (induced by adenosine). Cocksackie B3 infections, a common agent in myocarditis might also induce an ionophore-like effect. Moreover, Alzheimer's disease is characterized by the formation of extracellular amyloid deposits in the brain of patients. Perturbation of cellular membranes by the amyloid peptide during the development of Alzheimer's disease is one of several mechanisms proposed to account for the toxicity of this peptide on neuronal membranes. We have studied the effects of the peptide and fragments thereof on 45Ca2+ -uptake in human erythrocytes and the energetic consequences. Treatment of erythrocytes with the ,1,40 peptide, results in qualitatively similar nucleotide pattern and decrease of energy charge as the treatment with Ca2+ -ionophore A23187. Finally, in recent studies we have revealed and published in this journal that a rare condition, Tarui's disease or glycogenosis type VII, primarily associated with a defect M-subunit of phosphofructokinase, demonstrates as a cophenomenon an increased leak of Ca2+ into erythrocytes. [source] | ||||||||||