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The traditional AutoCAD method of entering a command and then selecting the object to be edited is sometimes called verb/noun selection. First you tell the software what to do (using a verb such as ERASE) and then you select the object to be acted upon (using a noun such as LINE). When you use grips with editing commands, you are using noun/verb selection. See Fig. 6-7. First you select the object, and then you tell the software what to do with the object. You may nd the grips (noun/verb) method convenient to use, especially if you are familiar with other graphics ERASE + programs that use this technique. However, either method is acceptable. Verb + Object (Noun) The method you choose is a matter of personal preference.
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A Figure 4.21 (A) Pre mini-lift (B) post mini-lift at 6 months
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Extrinsic value can be described as the risk value of the option. The risk value is made up of several components. One of these is time value, which is the length of time that the option writer or seller will assume risk for the sale. A 5-year life insurance policy premium is much cheaper than a 15-year policy premium because the insurance company is exposed to risk for an additional 10 years on the 15-year policy. Options are no different; time has risk, and therefore time has a premium cost to the buyer. Time value can be present in options that are in the money, at the money, or out of the money. Time value is the portion of premium in the options price that is above and beyond the intrinsic value. If an option is at the money or out of the money, then the option would have no intrinsic value and would have time value only. Time value can also be considered the risk value of an option. When you purchase an option, you are compensating the writer for the risk and time of selling the option. Included in the time value of the option is the risk assumed from the volatility of the market. If the market price uctuates wildly, the writer naturally assumes that there is more risk than if a price is very stable, so the time value of the option
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Courtesy of Gary J. Hordemann, Gonzaga University
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duction at the myoneural junction, which is what occurs in myasthenia gravis. H S In large motor and sensory nerves, conH tiguous spread of action potentials along a EP ber is slow and eventually decays over long distances. In these large bers, conduction is H aided by the structure and con guration of the S S myelin sheaths. The sodium channels, which H H generate the action potential, are concentrated EP H M at short exposed segments of the axon, the nodes of Ranvier, lying between longer segments of myelinated axon. The portions of axon that are covered by myelin remain electrically insulated. This creates ux lines that Figure 45-1. Motor end plate showing relationship between various structures in nerve and muscle. converge on the nodes and allows current to Last segment of myelin, with Schwann nucleus (S), terminates abruptly, leaving axis cylinder covered be regenerated at each of these gaps in the by sheaths of Schwann and Henle. End-plate nuclei (EP) of muscle ber lie embedded in sarcoplasm and have same staining reactions as sarcolemmal nuclei (M). Rami cations of axis cylinder (telomyelin. The speed of electrical conduction, dendria) lie in grooves or pouches in granular sarcoplasm, each lined by spiny subneural apparatus which jumps in a saltatory fashion from of Couteaux, which is continuous with membranous sarcolemma and also Schwann membrane. Nunode to node, is many times faster than con- cleus (S) of sheath of Schwann commonly lies near point of branching of axon. Sheath of Henle has duction through an unmyelinated axon. The small nuclei (H) and fuses with endomysial sheath of muscle ber. (Courtesy of Dr. D. Dennylargest-diameter bers, which by reason of Brown.) their size have the fastest conduction times, also have the thickest myelin sheaths and longest internodal distances. about 10,000 molecules, are liberated through an exocytotic proConventional laboratory studies of nerve conduction generally cess by the arrival of axonal action potentials. Arrival of the elecmeasure the speed of these fastest-conducting bers. This depentrical impulse opens calcium channels in the presynaptic memdence of nerve conduction on the myelin sheath explains a number brane, which serve to bind packets of ACh to the membrane and of electrophysiologic abnormalities that are a consequence of mygovern their release. Molecules of ACh diffuse into the synaptic elin destruction. One common nding, as one might predict, is a cleft and attach to receptor sites on the postsynaptic membrane. slowing of nerve conduction due to loss of the impulses contributed Each impulse triggers the release of approximately 200 quanta of by the largest-diameter and fastest-conducting bers. When myelin ACh and produces a depolarization of suf cient size to initiate an destruction is severe or a circulating factor impedes the channels action potential in the muscle through the same mechanism of a that regenerate a sodium current, there is a total block of electrical regenerative sodium current described earlier. Botulinum toxin and conduction. An intermediate state of partial demyelination slows a high concentration of Mg ions interfere with the entry of calcium and desynchronizes the electrical volley, leading to temporal dison the presynaptic side and raise the threshold for quantal release. persion of the action potentials that reach the muscle. The cumuThere is also a nonquantal release of ACh through continuous leaklative effect of these changes is to reduce the number of nerve bers age. This appears to play a role in the trophic in uence of nerve that are capable of conducting an electrical volley, leading to a on muscle. graduated reduction in the amplitude of the muscle action potential The ACh molecule binds to the postsynaptic ACh receptor, a over longer segments of nerve. This reduction in amplitude of the complex of ve proteins that constitute the postsynaptic ion chancompound motor action potential (CMAP) as the stimulating elecnel. Binding of Ach by this receptor causes a conformational trode is moved proximally is termed conduction block (discussed change in the Ach receptor that leads to a local increase in the under Studies of Nerve Conduction, later). Blocked conduction of conductance of Na and K and other small ions. This produces a this nature is the most reliable marker of an acquired demyelinating depolarization known as the end-plate potential. Small (miniature) neuropathy; of all the electromyographic changes, it corresponds end-plate potentials (MEPPs) are continuously formed and regenmost closely to the degree of muscle weakness (see further on). erated as the membranes repolarize, much as in the process of pasIn contrast to these effects of demyelination of peripheral sive decay previously described. These potentials are too small to nerve, the result of loss of axon bers is a reduction in the summed be recorded by routine EMG testing, although fortuitous needle electrical activity of the attached muscle and an atrophic denervaplacement adjacent to a synapse may detect them. The bound ACh tion as described further on. is hydrolyzed by cholinesterase, a glycoprotein enzyme that exists in free form in the cleft. Its main function is to terminate the action potential and permit the sequential activation of muscle. The postTHE NEUROMUSCULAR synaptic membrane, once depolarized, is refractory to another acJUNCTION (MOTOR END PLATE) tion potential until it is repolarized. The calcium that entered the presynaptic nerve terminal is This is the interface between the nely branched nerve ber and sequestered and then extruded and the choline from the hydrolyzed the muscle ber, where the electrical activity of the motor nerve is ACh enters the nerve terminal, where it is resynthesized to ACh translated into muscle action (Fig. 45-1). The nerve ber contacts near the release sites. the muscle membrane in a trough-like junctional space of 50 mm The analysis of a rapid series of electrically elicited muscle the synaptic cleft between the axolemma and sarcolemma (see contractions is used speci cally to analyze the function of the neuFig. 53-1). Within the nerve terminal, a relatively xed number of romuscular junction. In general, a decrement in the amplitude of packets, or quanta, of acetylcholine (ACh), each packet containing
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which creates a more compact breast that will be less likely to contribute to the return of ptosis.54 The short-scar mammaplasty is more commonly used for breast reduction but can be adapted for a mastopexy by taking the tissue that would be normally resected and folding it inward onto itself to provide superior pole fullness. This technique described by Chiari55 is best for patients with moderate ptosis but ample breast volume where a loose skin envelope requires resection. The nal scar does not have a medial inframammary component and the technique itself confers the ability to achieve a good nal shape with adequate breast projection without distorting the areola. The preoperative markings can be dif cult at rst, making this one of the biggest drawbacks to this approach. The combination of mastopexy with augmentation is useful for patients with de cient glandular tissue with skin envelope excess. This combined procedure is also useful in cases of breast asymmetry with de cient glandular volume. The addition of an implant will help ll the skin envelope but creates a larger risk for incision breakdown because of increased tension on the suture lines. Any mastopexy technique that requires undermining of skin aps should not be combined with subglandular augmentation because this can contribute to glandular necrosis.
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