Contraction inward

The open surface of a liquid tends to contract inwards towards the bulk of the liquid, as if it were covered with an elastic skin. This phenomenon is termed surface tension. Surfactant... 

Stage III Void formation continues, but bubble collapse dominates and causes the bubbles to contract (inward) and the graphite foam to shrink dimensionally and volumetrically (i.e., densification). 

X= 2) or (P = 0, X = 3) and the distinction between these possibilities is most satisfactorily based upon independent evidence, such as microscopic observations. The growth of compact nuclei inevitably results in the consumption of surfaces and when these outer faces, the sites of nucleation, have been eliminated, j3 necessarily is zero this may result in a diminution of n. The continued inward advance of the reaction interface at high a results in a situation comparable with the contracting volume reaction (discussed below) reference to this similarity was also made in consideration of the Mampel approach discussed above. Shapes of the deceleratory region of a time curves for nucleation and growth reactions and the contracting volume rate process are closely similar [409]. 

Figure 49-8. Diagram of the relationships among the sarcolemma (plasma membrane), a T tubule, and two cisternae of the sarcoplasmic reticulum of skeletal muscle (not to scale). The T tubule extends inward from the sarcolemma. A wave of depolarization, initiated by a nerve impulse, is transmitted from the sarcolemma down the T tubule. It is then conveyed to the Ca release channel (ryanodine receptor), perhaps by interaction between it and the dihydropyridine receptor (slow Ca voltage channel), which are shown in close proximity. Release of Ca from the Ca release channel into the cytosol initiates contraction. Subsequently, Ca is pumped back into the cisternae of the sarcoplasmic reticulum by the Ca ATPase (Ca pump) and stored there, in part bound to calsequestrin.

Fedida, D., Noble, D., Rankin, A.C. and Spindler, A.J. (1987). The arrhythmogenic transient inward current iTI and related contraction in isolated guinea-pig ventricular myocytes. J. Physiol. 392, 523-542. 

During exercise or voluntary hyperventilation, expiration becomes an active process. Under these conditions, a larger volume of air must be exhaled more rapidly. Therefore, two muscle groups are recruited to facilitate this process. The most important muscles of expiration are the muscles of the abdominal wall. Contraction of these muscles pushes inward on the abdominal contents and increases abdominal pressure. As a result, the diaphragm is pushed upward more rapidly and more forcefully toward its preinspiration... 

The simplest and most common device for measuring flow rate in a pipe is the orifice meter, illustrated in Fig. 10-7. This is an obstruction meter that consists of a plate with a hole in it that is inserted into the pipe, and the pressure drop across the plate is measured. The major difference between this device and the venturi and nozzle meters is the fact that the fluid stream leaving the orifice hole contracts to an area considerably smaller than that of the orifice hole itself. This is called the vena contracta, and it occurs because the fluid has considerable inward radial momentum as it converges into the orifice hole, which causes it to continue to flow inward for a distance downstream of the orifice before it starts to expand to fill the pipe. If the pipe diameter is D, the orifice diameter is d, and the diameter of the vena contracta is d2, the contraction ratio for the vena contracta is defined as Cc = A2/A0 = (d2/d)2. For highly turbulent flow, Cc 0.6. 

Kotlikoff I would agree, although we don t know what the functional effect of the release is, whether it is relaxation or contraction. One difference here is the prominent presence of inward currents that are depolarizing. 

In addition to modification of calcium influx/efflux, other mechanisms like inhibition of slow inward current [363] and nickel-calcium exchange [364] have been suggested to explain the positive inotropic effects of nickel. Moreover, these inotropic effects might be mediated by an action of nickel on the outside surface of the cardiac cell membrane, where nickel inhibits the ATP-dependent component of the calcium extrusion, thereby causing contraction-enhancement [364, 365],... 

Phase separation controlled by diffusion exchange often results in a skin which is composed of a micellar assembly of nodules, as will be discussed below. When extremely hydrophobic polymers (e.g., modifled-PPO) are cast from dioxane into water (pg = p = p ) a dense polymer layer is formed at the solution s interface that somewhat resembles the type of layer formed by Interfacial polymerization. There is almost no inward contraction of the interfacial skin, and the coagulation process is controlled by diffusion through the dense, interfacial thin film. These result in an anisotropic membrane with a very fine "coral" structure (Figures 9 and 10). 

Relationship Between Nodular and Rejecting Layers. Nodular formation was conceived by Maler and Scheuerman (14) and was shown to exist in the skin structure of anisotropic cellulose acetate membranes by Schultz and Asunmaa ( ), who ion etched the skin to discover an assembly of close-packed, 188 A in diameter spheres. Resting (15) has identified this kind of micellar structure in dry cellulose ester reverse osmosis membranes, and Panar, et al. (16) has identified their existence in the polyamide derivatives. Our work has shown that nodules exist in most polymeric membranes cast into a nonsolvent bath, where gelation at the interface is caused by initial depletion of solvent, as shown in Case B, which follows restricted Inward contraction of the interfacial zone. This leads to a dispersed phase of micelles within a continuous phase (designated as "polymer-poor phase") composed of a mixture of solvents, coagulant, and a dissolved fraction of the polymer. The formation of such a skin is delineated in the scheme shown in Figure 11. 

Figure II. Initial mechanisms of phase inversion (I) polymer solution interface at zero time (II) initial depletion of solvent, inward contraction, and formation of the nodular layer (III) end of contraction and establishment of the nodular layer.

On the other hand, if a chemical is somewhat less similar to acetylcholine, it may interact with the receptor but be unable to induce the exact molecular change necessary to allow the inward movement of sodium. In this instance the chemical does not cause contraction, but because it occupies the receptor site, it prevents the interaction of acetylcholine with its receptor. Such a drug is termed an antagonist. An example of such a compound is d-tubocurarine, an antagonist of acetylcholine at the end-plate receptors. Since it competes with acetylcholine for its receptor and prevents acetylcholine from producing its characteristic effects, administration of d-tubocurarine results in muscle relaxation by interfering with acetylcholine s ability to induce and maintain the contractile state of the muscle cells. 

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