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By L. Ashton. Minnesota State University Moorhead. 2018.

Root Palatine tonsil Teeth Vallate Humans and other mammals have heterodont dentition cheap fucidin 10 gm on line. Body The chisel-shaped incisors are adapted for cutting and shearing food buy fucidin 10gm on line. The two pairs of cone-shaped canines (cuspids) are located at the anterior corners of the mouth; they are adapted for hold- Filiform ing and tearing. Incisors and canines are further characterized by papillae a single root on each tooth. The buccal surface of the premolars and molars is adjacent to the cheek. The labial surface Tongue of the incisors and canines is adjacent to the lip. The tongue is a mass of (milk) teeth begin to erupt at about 6 months of age (fig. All of the tongue muscles (those that insert upon the tongue) move the deciduous teeth normally erupt by the age of 2 1/2. Only the anterior two- permanent teeth replace the deciduous teeth in a predictable se- thirds of the tongue lies in the oral cavity; the remaining one- quence. This process begins at about age 6 and continues until third lies in the pharynx (fig. There may not be room in the jaw to accommodate the rior surface of the base of the tongue (fig. The inferior sur- wisdom teeth, however, in which case they may grow sideways face of the tongue is connected along the midline anteriorly to and become impacted, or emerge only partially. If they do erupt the floor of the mouth by the vertically positioned lingual frenu- at all, it is usually between the ages of 17 and 25. The papillae give the tongue a distinct Formula for deciduous dentition: roughened surface that aids the handling of food. As described in I 2/2, C 1/1, DM 2/2 = 10 × 2 = 20 teeth chapter 15, some of them also contain taste buds that respond to sweet, salty, sour, and bitter chemical stimuli. Filiform papillae are sensitive to touch, have tapered tips, and are by far where I = incisor; C = canine; P = premolar; DM = deciduous the most numerous. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 18 Digestive System 643 Canine Medial Second First Second First Lateral incisor Third molar molar molar premolar premolar incisor (wisdom tooth) Upper teeth Creek Lower teeth Third molar (wisdom tooth) Second First Second First molar molar premolar premolar Lateral Medial Canine incisor incisor FIGURE 18. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 644 Unit 6 Maintenance of the Body TABLE 18. An overbite of the upper incisors creates a shearing action as these teeth slide past one another. Masticated food is mixed with saliva, which initiates chemical digestion and aids swallowing. A tooth consists of an exposed crown, which is supported by a neck that is anchored firmly into the jaw by one or more roots (fig. The roots of teeth fit into sockets, called den- tal alveoli, in the alveolar processes of the mandible and maxil- and fasten the tooth in its dental alveolus. Each socket is lined with a connective tissue periosteum, (gum) is the mucous membrane surrounding the alveolar specifically called the periodontal membrane. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 18 Digestive System 645 can be tasted. Saliva also contains starch-digesting enzymes and Enamel lubricating mucus, which aids swallowing. Saliva is secreted con- tinuously, but usually only in sufficient amounts to keep the mu- cous membranes of the oral cavity moist. Dentin Numerous minor salivary glands are located in the mucous membranes of the palatal region of the oral cavity. However, Dental pulp three pairs of salivary glands that lie outside the oral cavity pro- (in pulp cavity) duce most of the saliva, which is transported to the oral cavity via salivary ducts.

If you waste or allow any of this time to pass in the belief (indisputably true) that you don’t have to respond until the end of that 30 days order 10 gm fucidin fast delivery, or that your attorney can probably get an extension of time by which to respond (almost always true) fucidin 10 gm amex, you could lose valu- able opportunities to seize important advantages. The Importance of Time in the Discovery Process To illustrate the importance of time in litigation, consider the proce- dural device of discovery, the means by which parties are to find out from each other what evidence is known to that party or others in support or derogation of the lawsuit. One of these discovery mechanisms is the right to compel a party to appear and answer relevant questions under oath from your lawyer. The answers given to these questions often reveal facts that will determine whether the plaintiff has a viable claim against you or whether you have a defense against liability. Absent a showing to the court of “good cause,” a plain- tiff must normally wait 20 days after serving summons before noticing the defendant’s deposition; however, the defendant need not wait any period of time after being served to notice the plaintiff’s deposition. Hence, it is possible for a defendant to get the jump on the plaintiff and smoke out his or her case early regarding the extent of damage suffered and why the plaintiff believes the defendant is responsible for it. The longer you wait to take the plaintiff’s deposition, the greater the likelihood that “facts” will be revealed or become “known” to the plain- tiff that strengthen his or her case. For this reason, some defense lawyers prefer to wait to take the plaintiff’s deposition until later in the lawsuit, especially because you usually only get one opportunity to take the plaintiff’s deposition, unless there are unusual circumstances involved. However, if you have reason to believe the plaintiff has not put together a case by the time you are served, then it may be possible to get rid of the case early by showing that it is missing one or more elements critical to the liability equation. Time and Summary Judgment or Summary Adjudication Another procedural mechanism that can be combined with the prompt taking of the plaintiff’s deposition is a motion for summary judgment or partial summary adjudication. This motion is a way for the court to look behind the pleadings and determine if the opposing party’s pleadings lack evidentiary support that warrants limiting or terminating the lawsuit. A defendant who does not pay close attention to the passage of time could, through inadvertence, lose the right to invoke summary judgment and end up having to go to trial (perhaps unnecessarily). Chapter 2 / Litigation 31 Therefore, when served with summons, you should immediately notify your medical liability insurer and get a copy of the summons and complaint to the appropriate representative. While doing this, you should also request your insurer to inform you right away of the lawyer who will be defending you. Once you know the identity of your counsel, contact him or her and ask to meet and confer about your case, preferably in person; however, if that cannot be done right away, then make contact by telephone. WHY YOU SHOULD MEET WITH YOUR LAWYER RIGHT AWAY AND WHAT YOU SHOULD SEEK TO ACCOMPLISH The Importance of a Litigation Strategy and Discovery Plan To ensure that the meeting with your lawyer is as productive as possible, you should first read the complaint and try to discern from it what you are accused of having done or not done that supposedly makes you liable. If the complaint is what is known as a form com- plaint, this generally will be more difficult than if it is written by the plaintiff’s counsel and sets forth some specific facts. However, in read- ing the complaint, you will at least be able to learn the identity of the plaintiff and when the event that allegedly resulted in injury occurred, even if it is a general form. Check your own records to see what they reveal about the plaintiff and to help refresh your memory. Make cop- ies of these records so that you can review them without getting marks on your originals that could be misconstrued as attempts to alter the records. You will want to have reviewed whatever information you can quickly assemble before you meet with your attorney so that you can share all you recall about your role in treating the plaintiff. If there were others involved in the incident of treatment about which plaintiff com- plains, make some notes as to who they were, what role they played in that treatment, and how you know that they were involved or witnessed the treatment. What legal theories, other than negligence, is the plaintiff relying on? What are the necessary elements to those theories and how does your lawyer think the plaintiff will try to satisfy them? Are the theories asserted in the complaint’s various causes of action supported in law? Now, there are two things any good malpractice defense attorney will do to best represent a client: put together a discovery plan and a 32 Hiestand litigation strategy. The two go hand-in-hand, and although not all attorneys put them in writing, you will want a commitment from your attorney to do so for you. These are privileged documents, so your opponent will not be able to force you to disclose them. To be sure, both the initial discovery plan and litigation strategy will change as new information is learned and as there are rulings on motions filed by the parties that affect the course of the litigation.

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The synaptic action of a NTmay also be increased by drugs that have an allosteric action on the receptor to increase its affinity or response to the endogenous NT generic 10gm fucidin otc, e order fucidin 10gm free shipping. Approaches (1)±(3) clearly depend on there being some residual neuronal function and NTrelease. Its value depends on all, or at least one stage, of the synthesis being sufficiently specific to the NTinvolved so that only its synthesis is affected. A good example would be choline acetyltransferase in the synthesis of ACh or glutamic acid decarboxylase in the synthesis of GABA. By contrast, inhibiting amino acid decarboxylase could reduce NA, DA and 5-HTsynthesis. It may be possible to reduce the neuronal uptake of a precursor if this requires a specific transport mechanism. Thus the synthesis of ACh can be reduced by blocking the uptake of precursor choline with hemicholinium. This is most likely to be achieved by stimulating inhibitory pre- synaptic autoreceptors (2a). Some drugs may reduce storage (2b) and hence release, although it is unlikely that this can be targeted at just one NT. As with agonists, these have the advantage that they can be designed to have a long half-life and act specifically on one type of receptor. Currently it is not possible to increase the rate of removal (uptake) or metabolism of a NT. RELATING NT MANIPULATION TO THE CAUSE OF THE DISORDER To what extent the above approaches can provide successful therapy will depend on both the cause of the disorder and the manner in which the NTis used in normal neuronal function. Thus the disorder could be due to: NEUROTRANSMITTER FUNCTION IN HUMANS 297 (1) An actual degeneration of a NTpathway or (2) No actual degeneration but a biochemical abnormality or some circuitry failure, leading to inadequate or excessive activity of the NT. The requirement in respect of NT function may be: (a) That it must be released physiologically from its nerve terminals by appropriate synaptic activity in order to produce the desired effect or (b) That it is sufficient merely to provide the NT at the synapse, without the need for it to be released physiologically. Clearly a disorder combining (1) with (a) would mean that little improvement could be expected by manipulating the lost NT, since the nerves are no longer there to release it physiologically. The main hope then would be to try to replenish the neurons with transplants (regeneration may be possible one day) and hope they become appro- priately innervated, or modify the action of some other NTwhich has become exaggerated (or reduced), as a result of the primary NTloss. By contrast it is easier to treat a disorder, whether characterised by neuronal degeneration ((1) above) or not (2), if it is sufficient just to provide NT(b), as appears to be the case in Parkinsonism. Of course, the effectiveness and specificity of any of the above manipulations will depend on how widely the NTis distributed and used and whether the malfunction applies only to one area or activity. Thus trying to increase (or decrease) the activity of a NTin only one area will be difficult if it has actions elsewhere which have not been affected by the disorder. The nervous system also has remarkable adaptive powers so the synaptic loss (or increase) of a NTis generally followed by a local compensating increase (decrease) in postsynaptic receptor number. This can be a useful response initially but it will be negated by the therapeutic provision of more (less) NT. Also a change in the activity of one NTcan lead to desirable compensating changes in the function of other NTs either working in conjunction with it or normally controlled by it. It must also be remembered that some NTs, like ACh, NA and 5-HT, have important peripheral as well as central roles and any attempt to modify them centrally will affect those peripheral effects as well. Thus if attempts made to increase the central action of a NT result in peripheral effects, these may be counteracted by using an appropriate antagonist that does not cross the blood±brain barrier. It is less easy to overcome peripheral side-effects caused by using a drug that antagonises the action of a NT, although in theory drugs that mimic or augment its action and do not cross the blood±brain barrier could be used. In fact this approach has proved valuable in treating the peripheral neuro- muscular disorder of myasthenia gravis which presents as a muscle weakness caused by insufficient cholinergic activity at skeletal neuromuscular junctions. The function of ACh can be increased and the symptoms alleviated, without central side-effects, by reducing the destruction of ACh by giving the anticholinesterase drug neostigmine, which does not cross the blood±brain barrier. Of course, nothing is perfect and anti- muscarinic drugs may be needed to overcome the accompanying increased peripheral parasympathomimetic effects of ACh. Despite all these problems there has been considerable progress in the treatment of disease states through NTmanipulation. Before the advent of levodopa therapy in Parkinsonism the treatment of neurological and psychiatric disorders had little 298 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION scientific basis but the initial and striking success with levodopa in Parkinsonism perhaps raised false expectations. In respect of drug therapy, Parkinsonism presented with a number of advantageous features that are unlikely to be repeated in other conditions.

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With the publication of Terminologia Anatomica (Thieme order 10gm fucidin visa, rable to the line drawing and corresponding stained section discount fucidin 10 gm with amex. This ap- New York, 1998), a new official international list of anatomical terms proach retains the inherent strengths of the full-page, colorized line for neuroanatomy is available. This new publication, having been v vi Preface to the Sixth Edition adopted by the International Federation of Associations of Anatomists, References: supersedes all previous terminology lists. Every effort has been made Council of Biology Editions Style Manual Committee. Scientific Style and to incorporate any applicable new or modified terms into this book. The number of changes is modest and related primarily to directional Cambridge: Cambridge University Press, 1994. Terminologia Ana- previous term appears in parentheses following the official term, i. American Medical Association Manual of Style—A Guide have eluded detection; these will be caught in subsequent printings. Last, but certainly not least, the sixth edition is a few pages McKusick, VA. On the naming of clinical disorders, with particular ref- longer than was the fifth edition. Mendelian Inheritance in Man, A Catalog of Human Genes clinical information, including more clinical examples (text and il- and Genetic Disorders. Baltimore: The Johns Hopkins Uni- lustrations), and the inclusion of Study/Review and USMLE style versity Press, 1998. Preface to the First Edition his atlas is a reflection of, and a response to, suggestions from pro- dents in the laboratory and greatly enhances their ability to grasp and Tfessional and graduate students over the years I have taught human retain information on CNS connections. Admittedly, some personal philosophy, as regards tempt to teach clinical concepts, a chapter correlating selected views teaching, has crept into all parts of the work. These examples formation, in the form of photographs and drawings, so that the initial illustrate that a clear understanding of normal morphological relation- learning experience will be pleasant, logical, and fruitful, and the re- ships, as seen in the laboratory, can be directly transposed to clinical view process effective and beneficial to longterm professional goals. First, the entire This atlas was not conceived with a particular audience in mind. It anatomy of the central nervous system (CNS), external and internal, was designed to impart a clear and comprehensive understanding of has been covered in appropriate detail. Second, a conscientious effort CNS morphology to its readers, whoever they may be. It is most obvi- has been made to generate photographs and drawings of the highest ously appropriate for human neurobiology courses as taught to med- quality: illustrations that clearly relay information to the reader. In addition, students in nursing, complementary information always appears on facing page. This may physical therapy, and other allied health curricula, and psychology as take the form of two views of related structures such as brainstem or well, may also find its contents helpful and applicable to their needs. Fourth, illustrations of blood supply have been in- ternal, and the summary pathway drawings may be useful to the indi- cluded and integrated into their appropriate chapters. When gross vidual requiring a succinct, yet comprehensive review before taking anatomy of the brain is shown, the patterns of blood vessels and rela- board exams in the neurological, neurosurgical, and psychiatric spe- tionships of sinuses appear on facing pages. If one is to err, it seems more judi- ternal vascular patterns represents a distinct departure from what is cious to err on the side of greater detail than on the side of inadequate available in most atlases, and illustrations of internal vessel distribution detail. If the student is confronted with more information on a partic- are unique to this atlas. In the chapter containing cross- learning is completed, the additional information will be there to en- sections, special effort has been made to provide figures that are accu- hance the review process. If students have inadequate information in rate, clear, and allow considerable flexibility in how they can be used front of them it may be difficult, or even impossible, to fill in missing for both teaching and learning. The use of illustrations that are one-half points that may not be part of their repertoire of knowledge. In this atlas, tion, information may be inserted out of context, and, thereby, hinder however, the sections are large, clearly labeled, and the drawing side the learning experience. One section of the atlas is de- A work such as this is bound to be subject to oversights, and for such voted to summaries of a variety of major pathways. I welcome comments, suggestions, and terial in a laboratory atlas represents a distinct departure from the stan- corrections from my colleagues and from students.

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