By E. Will. Fullerton College. 2019.
Attempts to increase the survival of grafted neurons have been made by expressing the Bcl-2 gene in cells before transplantation purchase online doxycycline. This concept has been tested with a cell line generated from the substantia nigra buy doxycycline with paypal. In the rodent ﬁmbria-fornix lesion model of cholinergic neuron degeneration order doxycycline 100mg mastercard, neuroprotective effects have been demonstrated by the Bcl-xL gene. Expression of Bcl-xL by lentiviral vectors in this model signiﬁcantly increases cholinergic neuron survival in the septal region subsequent to axotomy of the pathway. Studies of this nature provide evidence that overexpression of antiapototic factors via gene trans- fer in vivo is sufﬁcient to rescue neuronal populations after axotomy. Within a span of approximately 20 years, the transplantation of cells into the brain evolved from the laboratory setting to clinical trials for severe Parkinson’s. Throughout the 1980s and 1990s, tissues were grafted into the brain to study aspects of neural cell development and to identify the function of different brain areas. Now, we are in a new era of establishing the most appropriate cell grafting technologies for application in the clinic. Unfortunately, the dramatic restorative functional changes seen in certain animal models of neurological disease were not seen with the transfer of the grafting techniques to the human situation. Case in point—transplants of fetal substantia nigra neurons stereotaxically injected into the striatum of Parkinson’s patients. The results from the initial clinical trials were partly encouraging in that there were no major side effects from this type of operation. Some of the transplanted cells in the human striatum show extended survival for years, and for some pa- tients there was a therapeutically signiﬁcant reduction in the motor symptoms (rigidity and bradykinesia). The modest to moderate improvement seen in some patients does, however, gradually disappear. To date we cannot predict with certainty that Parkinson’s patients who are ideal candidates for a transplant will beneﬁt from this grafting procedure. One of the primary problems with transplanting neurons into the lab animal and human brain has been the issue of poor graft survival. In humans only about 5% of the fetal dopamine neurons survive using the current transplantation protocols. This raises the issue of just how representative are the animal models of human neurological disorders. Although fetal neurons have shown the greatest potential in terms of graft survival and clinical efﬁcacy for Parkinson’s, there are serious concerns associated with the use of human fetal neurons, namely tissue availability, quality control, and ethics. To circumvent some aspects of these problems, research has examined neural xenografts for Parkinson’s and the use of stem or neuronal cells grown in culture. It is now possible to isolate subpopulations of stem or neuronal progenitor cells from the developing or adult nervous system, expand the cells in culture, and then use the cells for transplanta- tion or as vehicles for gene delivery to selected sites of the nervous system. These cells survive in vitro in media enriched with growth factors and with passage express a neuronal phenotype. A major advantage of using progenitor cells for transplan- tation is that they have not been transformed or immortalized and exist naturally in the brain. Continued collaborative efforts between the basic and the clinical research sectors using stem or progenitor cells for ex vivo transgene delivery will be critical to the progression of effective therapy for Parkinson’s and other neu- rodegenerative conditions. As previously described, a variety of non-neuronal primary cells and cell lines have been used largely as a way to deliver an active substance that promotes survival or growth of neurons. Research centered on cell replacement strategies now focus predominantly on the use of neural stem cells. Stem Cells in the Adult Brain Until just a few years ago, it was generally assumed and believed that the adult brain was incapable of generating new neurons. Research on a number of fronts has estab- lished that the adult mammalian brain contains stem cells that can give rise to the full spectrum of neurons and glial cells. In particular, the subventricular zone, an important layer that forms during development and persists into adulthood retains the capacity to generate both neurons and glial cells (Fig. Stem cells by strict deﬁnition over the lifetime of the animal must be able to proliferate, show self-renewal, produce progeny with multilineage characteristics, and divide when injured. Progenitor cells refer to cells with a more restricted potential than stem cells, and precursor cells refer to cells within a given developmental pathway. The presence of neural stem cells in the adult brain has established the possibility for using the mature brain as a source of precursor cells for transplantation and helps to establish new therapy directions for neurological injury and disease. In fact, as our understanding of stem cell neurobiology grows, it may be possible to control the proliferation and migration of such cells into areas of the nervous system affected by the diseases discussed in this chapter. The notion of self-repair in the brain is now visible at the basic research level. The potential growth factors governing the commitment and differentiation of the neuronal lineage are indicated. More- over, these newly generated neurons had also made connections to their appropri- ate target. Multipotent stem cell proliferation and differentiation can be regulated by neu- rotrophic factors. When growth factors are added in sequence to neural stem cells, they regulate whether the cells will acquire neuronal or glial characteristics. One sector of gene therapy research focuses on a neural-stem-cell-based strat- egy. With the capability of differentiating along multiple cell lineages, stem cells may be very effective for the delivery of therapeutic gene prod- ucts throughout the brain or spinal cord. The enzyme deﬁciency in this mouse model causes lysosomal accumulations of undegraded glycosominoglycans in the brain and other tissues that results in fatal degenerative changes. Similar therapeutic paradigms are also being evaluated for other inherited neurogenetic diseases that are characterized by an absence of discrete gene products. Engineered cells and progenitors are also being grafted into mouse models of hexosaminadase deﬁciencies causing Tay-Sachs and Sandhoff disease. Clones of stem cells or prog- enitor cells are used extensively to study aspects of differentiation along neuronal and glial lineages. These types of progenitor cell lines have been useful in the iden- tiﬁcation of molecules and neurotrophic factors that initiate and modulate differ- entiation at speciﬁc developmental time points. The myc family of protooncogenes consist of a number of well-characterized members including c-myc,N-myc, and L-myc. This retrovirus induces a number of carcinomas in addition to the leukemic disorder myelocytomatosis (myc) in birds and can transform primary cells in tissue culture. The transformation of cells from the developing nervous system with a retrovirus expressing v-myc have revealed extraordinary characteristics. In culture, progenitor cells immortalized with the v-myc oncogene divide continuously. However, when removed from the culture environment and transplanted back into the nervous system of laboratory animals, these v-myc-immortalized cells withdraw from the cell cycle and undergo terminal differentiation. In addition, certain neural progenitor cells generated with v-myc not only stop dividing in the animals’ brain, but the cells also undergo site-speciﬁc differentiation.
In this case buy cheap doxycycline online, giardia could not be documented and the bird responded to a change in diet discount doxycycline 200 mg with mastercard. The tail feathers were replace the normally elastic patagial tissue with scar transected to reduce the pressure on the postventer skin generic 200 mg doxycycline visa. The tissue, which may make the bird more susceptible to lesions were cleansed daily with chlorhexidine solution and were future lesions. This lesion is common in mal- occur in heavy-bodied birds (African Grey and Mealy nourished birds and may begin when a bird with an Amazon Parrots) that have had improper wing trims. The A bird that attempts to fly from a high perch and has impact of the tail with the ground causes a hyperex- no lift may land on its sternum, resulting in a bruise tension of the rectrices and places excessive pressure or open wound over the cranial portion of the keel. The skin wounds should be treated as discussed Disorders Affecting the Feet and Legs under general therapy for integumentary lesions, Skin on the legs may be damaged by bands (rings) or, and several of the clipped primary and secondary in the case of falconers’ birds, by badly fitted leather feathers from each wing should be removed to stimu- jesses. These new feathers can occur and impair healing, particularly when a will provide the bird with the necessary lift to pre- foreign object is constantly in contact with the vent further injury. Supportive dressing (see Chapter 16) will keep the wound clean care is successful in most minor cases and the lesions 8 and moist and permit regular visual inspection. Pox lesions on the feet and legs are characterized by Birds with chronic ulcerative dermatitis in the cau- dry, brown plaques. Other viral infections appear to dal aspect of the postventer region may be presented be rare, but a herpesvirus has been implicated in skin with a history of blood-tinged excrement. The another collection were introduced to the wounds were debrided and flushed repeat- nursery. The fact that part of the distal edly with copious amounts of sterile saline feather is normal indicates that there was solution. Burns on the legs and feet of a goose were cleaned and treated with silvadene cream Color 24. This photograph, taken two weeks af- Feather cysts are common in canaries, par- ter the initial burns, shows a healthy bed of ticularly the Norwich, Crested, Crest-bred granulation tissue over the burns, and the and new color canaries that have “double- bird healed with no complications. A mature, male budgerigar with dermatitis was presented for progressive shivering Color 24. The bird had been treated Split section of a feather cyst showing the with an over-the-counter, oil-based antibi- accumulation of cellular debris in multiple otic. Sev- liferative yellowish-colored lesions on the eral areas of self-mutilation were present foot of a canary. The bird was presented including both feet and legs and the cervical with a shifting leg lameness. The feathers returned to normal color Brown hypertrophy of the cere in a male with subsequent molts. This syndrome is believed to be caused by imbalances in the ratio of sex Color 24. Ulcerative lesions were present with an acute onset of picking at the feet on the cranial edge of both propatagial and legs. The cause of this bird’s problem chronic ulcerative dermatitis (and wing could not be determined, but it responded splinting), but many of the feather follicles to general dermatologic therapy. Necrotic digits in adult passerine birds are One pad was ulcerated, and a thick, green- commonly caused by fibers that wrap ish-yellow discharge was present in the around the toe. The necrotic material examining the proximal edge of the affected was surgically removed from both feet and digit under a dissecting or operating micro- the wounds were packed with antibiotic- scope. In these latter birds, the lesions may spon- volving cracking of the feet that is responsive to high taneously resolve when the clients stop smoking or doses of biotin has been documented in flamingos, wash their hands before handling the birds. Other ratites and waders (see Color 48) (Greenwood A, cases will respond to a change in diet, frequent expo- unpublished). Topical steroids should be ap- Keratomas that appear clinically as digit-like projec- plied with caution to prevent toxicity. These callus-like growths Atarax and oral antibiotics were found to be effective may predispose a bird to bumblefoot (see Chapter in some cases. Virus-induced papillomas are common on the may be prevented by the oral administration of pred- feet of finches in Europe. Initially, the bandage may re- formes, waders, penguins and many Psittaciformes quire daily changing. In Psittaciformes and Passeriformes, changes can be reduced as the wound becomes less most lesions are believed to be the result of malnutri- exudative. Once granulation tissue forms at the edge tion, which causes the skin of the foot to become dry of the ulcers, scabs should be removed and the lesions and hyperkeratotic. Hepatic dysfunction may also be should be kept clean to facilitate healing (see Chap- involved in some cases. The in the treated birds and the indiscriminate admini- fibrous band can be surgically excised to correct the stration of thyroxine, can cause fatal toxicity (see problem (see Chapter 41). Pruritic, ulcerative lesions have been described on Diseases of the Feathers the feet and legs of Amazon parrots (particularly Yellow-naped and Double Yellow-headed Amazon Parrots). The lesions start with a bird chewing at the feet and legs followed by the formation of hyperemic The appearance of malformed, broken, bent, dirty, lesions, sometimes within minutes of the initial stained or unusually colored feathers should be con- pruritic episode. Feather conditions can be divided the bird continues to chew on the feet and legs (Color into two main groups: those affecting normal feath- 24. Characteristic histopathologic findings asso- ers and those in which abnormality of the feather is ciated with this syndrome include ulcerative derma- the primary feature. A simple method to determine if titis that may contain coccoid bacteria and fungi. The a feather problem occurs during or after development role that the bacteria or fungi play in the pathogene- is to remove an affected feather (it should be exam- sis of this syndrome is undetermined. Immune-medi- ined cytologically, microscopically and possibly his- ated and allergic reactions with secondary involve- tologically) and evaluate the growth of the new ment of autochthonous skin flora have been proposed feather over the next one to three weeks. Some common epidermis descriptive terms that may be needed by the clinician Ballooning Intracellular accumulation of fluid (edema) to interpret the results of pathology reports arelisted degeneration in Table 24. The results of 213 feather biopsies from Depigmentation Loss of (melanin) pigmentation a group of Psittaciformes are listed in Table 24. Hyperkeratosis Increased thickness of the stratum corneum (hyperkeratinization) These abnormalities represent segmental dysplasia Hyperplasia Thickening of the epidermis that occurred in the developing barbs and barbules Hypopigmentation Reduced (melanin) pigmentation and represent a brief period of dysfunction in the Melanosis Dark appearance due to increased epidermal collar (Figure 24. These marks can be melanocyte activity and deposition of induced by the administration of exogenous corticos- melanin teroids, suggesting that they are truly “stress” Parakeratosis Retention of pyknotic nuclei in the cells of marks. Restraint, illness, a brief period of food depri- the stratum corneum, usually associated with defective keratinization vation or exposure to environmental extremes should Spongiosis Extracellular accumulation (edema) causing be expected to induce these lesions. Deficiencies of separation of epithelial cells arginine (curled wing feathers), riboflavin (clubbed Telangiectasis Persistent vasodilation: skin does not blanch down feathers) and pantothenic acid, niacin and se- when compressed with a microscope slide lenium (poor feathering) are nutritional causes of poor feather structure in poultry. These birds Inactive feather follicle - no lesion 22 should be taught to preen the feathers by gently Epidermal atrophy 6 breaking the sheaths while encouraging the bird to Staphylococcus dermatitis 3 pick at an area with its beak. Over-preening Suspected bacterial pulpitis 9 (feather picking) occurs when what is a normal part Dermatomycosis 3 of feather maintenance becomes a pathologic condi- Sarcoptic mange 1 tion (see Chapter 4).
You want your mental pictures to approximate actual experience as much as pos- sible cheap 100 mg doxycycline with amex. The way to do this is pay attention to small details buy generic doxycycline 100 mg on line, sights order doxycycline online now, sounds, objects, in your imagined environment. And if the imagination is vivid enough and detailed enough, your imagination practice is equiva- lent to an actual experience, insofar as your nervous system is concerned. The next important thing to remember is that during this 30 minutes you see yourself acting and reacting appro- priately, successfully, ideally. If you have been shy and timid, see yourself moving among people with ease and poise—and feeling good because of it. If you have been fearful and anxious in certain situations—see yourself act- ing calmly and deliberately, acting with confidence and courage—and feeling expansive and confident because you are. This exercise builds new "memories" or stored data into your mid-brain and central nervous system. After practicing it for a time, you will be surprised to find yourself "acting differently," more or less automatically and spontaneously—"without trying. You do not need to "take thought" or "try" or make an effort now in order to feel ineffective and act inadequately. Your present inadequate feeling and doing is automatic and spontaneous, because of the memories, real and imagined, you have built into your automatic mechanism. You will find it will work just as automatically upon positive thoughts and experiences as upon negative ones. Alfred Adler had an experience when a young boy which illustrates just how powerful belief can be upon behavior and ability. He got off to a bad start in arithmetic and his teacher became convinced that he was "dumb in mathematics. One day, however, he had a sudden flash of insight and thought he saw how to work a problem the teacher had put on the board, and which none of the other pupils could work. Whereupon, he became in- dignant, strode to the blackboard, and worked the prob- lem much to their amazement. He felt a new con- fidence in his ability, and went on to become a good math student. What held him back was his belief that he could not make a good talk, and that he would fail to impress his audience, simply because he did not have an imposing appearance... He mistakenly concluded that, if he could have an operation to improve his appearance, he would then gain the confidence he needed. He succeeded in replacing the negative belief with a positive belief that he had a message of extreme impor- tance that he alone could deliver, no matter what he looked like. Now the point I want to make is this: Adler had been hypnotized by a false belief about himself. Remember that we said in the last chapter that the power of hypnosis is the power of belief. In Chapter One we told of how Prescott Lecky had brought about almost miracu- lous improvement in the grades of school children by showing them how to change their self-image. With such self-definitions, the student had to make poor grades in order to be true to himself. It would be as "wrong," from his own viewpoint, for him to make good grades, as it would be to steal if he defines himself as an honest person. The Case of the Hypnotized Salesman In the book, Secrets of Successful Selling, John D. A certain salesman always managed to make almost exactly $5,000 per year, regard- less of the territory they assigned to him or the commis- sion he was paid. The following year the company increased the commission paid to all salesmen, but this salesman still managed to make only $5,000. When he was assigned a good territory, he found all sorts of excuses to coast when the $5,000 was in sight. Once, when the goal had been reached, he got sick and was unable to work any more that year, although doctors could find nothing wrong with him and he miraculously recovered by the first of the next year. Russell" aged 20 years almost overnight because of a false idea, then re- gained his youth almost as quickly when he accepted the truth. His girl friend had no objection to his spending money on her, and she insisted that she loved him, but explained she could never marry him because of his too- large lower lip. However, when he told her this and proudly exhibited his new lower lip, her reaction was just as I had expected, but not as Mr. In her anger and disgust she also announced that she was placing a "Voodoo curse" upon him. Russell and his girl friend had been born on an island in the West Indies where Voodoo was prac- ticed by the ignorant and superstitious. Yet, when in the heat of anger, his girl friend "cursed" him, he felt vaguely uncomfortable but did not think too much about it. However, he remembered and wondered when a short time later he felt a strange small hard "bump" on the in- side of his lip. Smith," who promptly assured him that the bump inside his mouth was the feared "Afri- can Bug," which would slowly eat away all his vitality and strength. Russell" who had first called upon me had been a very impressive individual, slightly too-large lip and all. He stood about six feet four, a large man with the physique of an athlete and the bearing and manner that bespoke of an inner dignity and gave him a magnetic personality. The bump which had caused all the trouble was merely a small bit of scar tissue from his operation. He gave a sigh of relief, and it seemed as if there was an almost immediate change in his posture and ex- pression. The truth had not only set him free of fear and restored his confidence— but had actually reversed the "aging process. Russell as I did, both "be- fore" and "after," you would never again entertain any doubts about the power of belief, or that an idea accepted as true from any source, can be every bit as powerful as hypnosis. It is no exaggeration to say that every human being is hypnotized to some extent, either by ideas he has uncriti- cally accepted from others, or ideas he has repeated to himself or convinced himself are true. These negative ideas have exactly the same effect upon our behavior as the negative ideas implanted into the mind of a hypnotized subject by a professional hypnotist. He strains and struggles until the muscles of his arm and shoulder stand out like cords. And although normally he can hoist a 400 pound weight overhead, he now actually cannot lift the pencil. On the one hand they "try" to lift their hand, or the pencil, by voluntary effort, and actually con- tract the proper lifting muscles.
Paracellin-1 is also Gitelman’s syndrome is a variant of Bartter syn- known as claudin-16; both names are used in the litera- drome characterized by potassium and magnesium ture that can be confusing cheap 200mg doxycycline amex. Paracellin-1 gene expression is also shown patients and present after the age of 6 years with in cornea and retinal epithelium in animals explaining metabolic abnormalities including mild hypokalemic the link with ocular abnormalities observed in some metabolic alkalosis buy genuine doxycycline online, hypomagnesemia cheap 200 mg doxycycline mastercard, and hypocal- patients [34, 39, 42]. Some patients can be asymptomatic and oth- Autosomal dominant hypocalcemia results from ers complain of transient episodes of weakness, tetany, activating mutation of calcium-sensing receptor. Normal values of urine mag- nesium to creatinine ratio in different age groups are 5. In contrast to other electrolytes, the plasma magnesium concentration Monitoring of magnesium status becomes a routine is not always a routine screening blood test. It is reason- nutrition should contain magnesium; otherwise, these able to perform serum magnesium screening in most patients are prone to develop hypomagnesemia. Hypomagnesemia is defined most patients, hypomagnesemia can be prevented as a decrease in serum Mg2+ concentration to levels less by sufficient daily magnesium supplementation than 1. Can the for example, due to low intake and increased gastroin- etiologic factor(s) be withdrawn or ameliorated? Is the patient symptomatic with regard to magne- remains unclear, the differential diagnosis between renal sium depletion? Furthermore, since plasma magnesium 1–10 years 150–250 mg concentration is the major regulator of magnesium 11–18 years 300–400 mg renal handling, acute rise in magnesium concentration >18 years 300–400 mg results in hypermagnesuria with loss of up to 50% of infused magnesium . Therefore, slow continuous Pregnant/lactating +150 mg intravenous infusion over 24 h is effective and safe. The dose may be repeated or adjusted to maintain serum Mg2+ concentration above 1–1. Thus, once started magnesium reple- entiate if these electrolyte abnormalities result from tion should be continued for 3–7 days despite normal magnesium deficit or independent of magnesium renal blood magnesium concentration [1, 34]. For example, hypokalemia is often associated adverse effects of fast magnesium repletion are due to with hypomagnesemia and can result from the tubu- development of hypermagnesemia. Thus, in some cases dif- of deep tendon reflexes can be used in nonparalyzed ferentiation may be practically impossible. In addition, intravenous administration Obviously, symptomatic magnesium depletion needs of magnesium sulfate results in decrease in plasma repletion. The importance of treating asymptomatic Ca2+ concentration due to binding of Ca2+ and sulfate hypomagnesemia remains controversial. Therefore, in case of concurrent hypocalcemia recommend to replete any hypomagnesemic patient calcium replacement should precede the magnesium with significant underlying cardiac disease, convulsive repletion. Another disadvantage of magnesium sulfate disorder, or concurrent hypokalemia or hypocalcemia. Multiple oral Mg2+ salts are avail- ing patient should be given magnesium intravenously able. Bioavailability of oral magnesium preparations is (2–5 mg kg–1 of elemental magnesium) over 8–24 h. Patients on magnesium replacement therapy should be monitored for magnesium, potassium, cal- 5. Mild to moderate hypermagnesemia can be occasionally observed in patients with familial hypocalciuric hyper- 5. Spontaneous return to normal values occurs regulated mainly by magnesium serum concentration. Whether hypermagnesemia plays a patho- Increased magnesium load results in decreased Mg 2+ physiological role in asphyxic child remains unknown. This mechanism is so efficient that hypermag- nesemia usually is not seen in the presence of normal from magnesium-treated eclamptic mothers . In clinical practice, hypermagnesemia slow the normalization of serum magnesium level. Mild hypermagnesemia is usually asymptomatic, whereas In chronic renal failure, the remaining nephrons adapt severe hypermagnesemia can potentially be a fatal to the decreased filtered magnesium load by increas- condition. Initial manifestations are seen when magne- ing their fractional excretion of magnesium. This –1 sium concentration exceeds 4–5 mg dL and include adaptive mechanism preserves normal magnesium nausea, vomiting, flushing, headache, drowsiness, and serum concentration even in the presence of advanced diminished deep tendon reflexes. In patients with creatinine clearance –1 –1 concentrations between 7 and 12 mg dL are often below 15 mL min mild hypermagnesemia can be associated with somnolence, hypocalcemia, absent observed. Hypermagnesemia can be seen in patients with nor- mal kidney function when magnesium intake exceeds 5. It is rarely observed in children, but is a well-appreciated complication of Hypotension usually appears when magnesium con- large magnesium infusions in pregnant women with centration exceeds 5–6 mg dL–1 and is thought to be the preeclampsia. Mg2+ is an effective described in children with Epsom salt (contain- calcium-channel blocker both intracellular and extracel- ing Mg2+ sulfate) poisoning, in laxative abusers, or lular; it also modulates the function of K+ channels in in patients receiving magnesium as a cathartic [8, cardiac muscle and aortic smooth muscle cells . Hypermagnesemia from oral magnesium salts changes are common with magnesium concentrations is more common in patients with bowel inflam- above 8 mg dL–1 but nonspecific. Complete heart block and cardiac arrest may occur Dead Sea water poisoning, since the ingested water at plasma concentrations above 18 mg dL–1. The typical dialysate for hemodialysis contains Increased concentrations of extracellular Mg pro- –1 2+ 0. Clinical manifestations progress from hyporeflexia to flaccid muscle paralysis, respiratory depression, smooth muscle paralysis with urinary retention, and ileus. Central nervous system Take-Home Pearls depression manifests with somnolence, lethargy, and › About 70% of serum magnesium (not protein bound) is coma in severe hypermagnesemia . Resulting mild hypocalcemia is usually asymp- filtered magnesium is reabsorbed in the distal tubule via tomatic and thought not to be clinically important. The next step of treatment is treatment with loop diuretics, amphotericin, calcineurin inhibitors, and cisplatin. In cases of severe symptoms, especially cardiac nesemia, familial hypomagnesemia with hypercalciuria toxicity, intravenous calcium is given as a magnesium and nephrocalcinosis as well as autosomal dominant antagonist. Both hemo- › 7–10 day course of magnesium supplementation is neces- dialysis and peritoneal dialysis have been successfully sary to correct a symptomatic hypomagnesemia. Hemodialysis provides higher Chapter 5 Abnormalities in Magnesium Metabolism 83 References 23. Annu Rev Physiol 53:299–307 Magnesium metabolism studies in children with chronic 3. Citterio F (2004) Evolution of the therapeutic drug monitoring salt-losing tubulopathies. Nat Genet 31(2):171–4 on the Scientific Evaluation of Dietary Reference Intakes, 46. Over the last 2 health and has been followed since infancy for sup- months, he has developed increasing dysphagia and ravalvular aortic stenosis and is status post a patch has been treated for gastroesophageal reflux and ero- repair of his ascending aorta. He has residual aortic coarctation and has also been found had significant decrease in oral intake because of S. Goldstein his dysphagia, and his mother estimates that he has from mild, where effects on outcome are still unclear, gone down from taking in 1.