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Membrane response

From the foregoing examination of deflection of a pressurized strip of a thin film, it is evident that the pressure is resisted less by bending stress and more by membrane stress as the pressure p increases beyond the reference pressure pr defined in (5.59). In terms of midpoint deflection wq, membrane effects come into play when wq and they tend to dominate response for WQ h. Within this range, the full span of the film within the bulge may be viewed as being divided into two regimes of behavior, as illustrated in [Pg.393]

Within the range of behavior described by (5.67), the center point deflection of the bulge wq is found to depend on pressure according to [Pg.394]

Within a region of extent small compared to a near the edges of the bulge at a = a, it is expected that gradients in deformation fields are relatively large. On this basis, only the gradient terms in (5.61) are maintained, that is, transverse deflection near a = a is assumed to be governed by [Pg.395]

The resulting unique solution exhibits two features of particular interest, namely, the curvature w a) = /2 (/if/a )(12p/p ) / at the edge of the bulge, from which the edge bending moment can be calculated according [Pg.395]

A main objective in developing the boundary layer solution is to determine the bending moment at the edge of the bulge, which is needed to determine the driving force for further delamination of the film. The bending moment is determined from the solution to be [Pg.396]


Ion-selective electrodes (ISEs) with ionophore-based membranes allow for quantification of a large number of analytes in various matrixes. Tailoring of the composition of the membranes to comply with the analytical task, requires advanced theory of membrane response. Most of theoretical descriptions include nonrealistic extra-thermodynamic assumptions, in the first place it is assumed that some kind of species strongly predominate in membranes. Ideally, a rigorous theory of ISE response should be based on strict thermodynamics. However, real ISE membranes are too complex. Therefore, known attempts aimed at rigorous thermodynamic description of ISEs proved to be fraritless. [Pg.305]

Class II drugs are classical (3-adrenoceptor antagonists such as propranolol, atenolol, metoprolol or the short-acting substance esmolol. These drugs reduce sinus rate, exert negative inotropic effects and slow atrioventricular conduction. Automaticity, membrane responsiveness and effective refractory period of Purkinje fibres are also reduced. The typical extracardiac side effects are due to (3-adrenoceptor blockade in other organs and include bronchospasm, hypoglycemia, increase in peripheral vascular resistance, depressions, nausea and impotence. [Pg.100]

Gormezano, 1., and Harvey, J. A. (1980) Sensory and associative effects of LSD in classical conditioning of rabbit (oryctolagus cuniculus) nictitating membrane response. J. Comp. Physiol. Psychol., 94 641-649. [Pg.53]

Harvey, J. A., Gormezano, I., and Cool, V. A. (1982) Effects of d-lysergic acid diethylamide, d-2-bromo-lysergic acid diethylamide, d, l-2-5-dimethoxy-4-methylamphetamine and d-am-phetamine on classical conditioning of the rabbit nictitating membrane response. J. Pharmacol. Exp. Then, 221 289-294. [Pg.242]

Figure 5.2). Panels can be quite strong since this is a very efficient structural action however, end anchorage is extremely important to achieving significant capacity. Resistance to blast loads of more than 2-4 psi (14-28 kPa) will normally require tensile membrane response. [Pg.164]

The metal building cladding will fail in flexure at a low overpressure unless girt spacings are low. Tensile membrane response is possible however, care must be paid to detailing to ensure that membrane response can be achieved. Tension membrane response can also be exhibited by girts and purlins. For this example problem, alt elements will be designed for flexure. [Pg.232]

The simplest practicable approach considers the membrane as a continuous, nonporous phase in which water of hydration is dissolved.In such a scenario, which is based on concentrated solution theory, the sole thermodynamic variable for specifying the local state of the membrane is the water activity the relevant mechanism of water back-transport is diffusion in an activity gradient. However, pure diffusion models provide an incomplete description of the membrane response to changing external operation conditions, as explained in Section 6.6.2. They cannot predict the net water flux across a saturated membrane that results from applying a difference in total gas pressures between cathodic and anodic gas compartments. [Pg.398]

Another family of cell adhesion molecules, the integrins, are the components of plasma membranes responsible for maintaining the link between cells and their extracellular associations. This link is not only mechanical but allows communication. [Pg.8]

Pharmacology Therapeutic concentrations of lidocaine attenuate phase 4 diastolic depolarization, decrease automaticity and cause a decrease or no change in excitability and membrane responsiveness. Action potential duration and effective refractory period (ERP) of Purkinje fibers and ventricular muscle are decreased, while the ratio of ERP to action potential duration is increased. Lidocaine raises ventricular fibrillation threshold. AV nodal conduction time is unchanged or shortened. Lidocaine increases the electrical stimulation threshold of the ventricle during diastole. [Pg.444]

Although there is no direct connection between the rules discussed in Chap. 4 for the monovalent-divalent ion selectivity of ligands in liquid membranes and the electrochemical selectivity behavior of these membranes (cf. Eqs. (22) and (31)), the effect of solvent on Na+/Ca2+ selectivity (Fig. 22) is remarkably similar to the calculated effect shown in Fig. 18 (actually for K+/Ba2+ preference). The discrimination against Mg2+ and especially HaO+ is considerably better for the electrode discussed here 117) than for liquid ion-exchange membranes responsive to Ca2+ (123). [Pg.156]

Quinidine administration results in a dose-dependent depression of membrane responsiveness in atrial muscle fibers. The maximum rate of phase 0 depolarization and the amplitude of phase 0 are depressed equally at all membrane potentials. Quinidine also decreases atrial muscle excitability in such a way that a larger current stimulus is needed for initiation of an active response. These actions of quinidine often are referred to as its local anesthetic properties. [Pg.171]

Serum concentrations have a major influence on the activity of quinidine on cardiac tissue. Low extracellular K+ concentrations antagonize the depressant effects of quinidine on membrane responsiveness, whereas high extracellular K+ concentrations increase quinidine s ability to depress membrane responsiveness. This dependency may explain why hypokalemic patients are often unresponsive to the antiarrhythmic effects of quinidine and are prone to develop cardiac rhythm disorders. [Pg.171]

Disopyramide reduces membrane responsiveness in atrial muscle and the amplitude of the action potential. Excitability of atrial muscle is decreased. These changes decrease atrial muscle conduction velocity. Action potential duration in atrial muscle fibers is prolonged by disopyramide administration. This occurrence increases ERR Postrepolarization refractoriness does not occur with disopyramide, and it appears to differ from quinidine and procainamide in this respect. [Pg.174]

Disopyramide administration reduces membrane responsiveness in Purkinje fibers and ventricular muscle and reduces the action potential amplitude. Even greater depression may occur in damaged or injured myocardial cells. Action potentials are prolonged after disopyramide administration, and this results in an increase in the ERPs of His-Purkinje and ventricular muscle tissue. Unlike procainamide and quinidine, disopyramide does not produce postrepolarization refractoriness. [Pg.174]

The electrophysiological properties of lidocaine in atrial muscle resemble those produced by quinidine. Membrane responsiveness, action potential amplitude, and atrial muscle excitability are all decreased. These changes result in a decrease in conduction velocity. However, the depression of conduction velocity is less marked than that caused by quinidine or procainamide. Action potential duration of atrial muscle fibers is not altered by lidocaine at either normal or subnormal extracellular K+ levels. The ERP of atrial myocardium either remains the same or increases slightly after lidocaine administration. [Pg.176]

Lidocaine reduces action potential amplitude and membrane responsiveness. Significant shortening of the action potential duration and ERP occurs at lower con-... [Pg.176]

Flecainide decreases the maximal rate of depolarization in atrial tissue and shifts the membrane responsiveness curve to the right. [Pg.180]

Propranolol has local anesthetic properties and exerts actions similar to those of quinidine on the atrial membrane action potential. Membrane responsiveness and action potential amphtude are reduced, and excitability is decreased conduction velocity is reduced. Because these concentrations are similar to those that produce p-blockade, it is impossible to determine whether the drug acts by specific receptor blockade or via a membrane-stabilizing effect. [Pg.182]

Propranolol decreases Purkinje fiber membrane responsiveness and reduces action potential amplitude. His-Purkinje tissue excitability also is reduced. These changes result in a decrease in His-Purkinje conduction velocity. However, these electrophysiological alterations are observed at propranolol concentrations in excess of those normally used in therapy. The most striking electrophysiological property of propranolol at usual therapeutic concentrations is a depression of catecholamine-stimulated automaticity. [Pg.182]

Doses of 2-PAM larger than 40 mg/kg, as well as TMB-4 and toxogonin, produced a temporary block of the cardiac response to vagal stimulation and of the nictitating membrane response to preganglionic, but not postganglionic, stimulation. There was transient hypotension due to block of ganglionic transmission.9,63,71... [Pg.29]

TASTE SENSATIONS BASED ON GENERAUZED MEMBRANE RESPONSES... [Pg.14]

Aspartame, sweetness production, 28-30 Aspartic acid, as food material, 138-147 Aspartic acid dipeptides, taste, 141-142r Astringpncy, sensation based on generalized membrane responses, 16-18 Automated data analysis and pattern recognition tool kit, 102... [Pg.342]

Cheeses, conjugated dienoic derivatives of linoleic acid, 263,267r Chelators, 57-58 Chemesthesis, sensation based on generalized membrane response, 15,16/ Chemesthetic stimulants, description, 21 Chemical analysis of seafood freshness indicators, 250... [Pg.343]

Cooling, sensation based on generalized membrane response, 15-18 Copper sulfate, use for control of off-flavor metabolites, 327 Cysticercus species, ionizing radiation, 296,298f... [Pg.344]

Flagellum 0.1 x 12,000 nm Protein structure arises from membrane. Responsible for motility... [Pg.265]


See other pages where Membrane response is mentioned: [Pg.514]    [Pg.135]    [Pg.93]    [Pg.46]    [Pg.53]    [Pg.176]    [Pg.175]    [Pg.71]    [Pg.135]    [Pg.164]    [Pg.172]    [Pg.655]    [Pg.342]    [Pg.64]    [Pg.655]    [Pg.77]    [Pg.257]    [Pg.363]    [Pg.219]    [Pg.282]   


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