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We have had no experience using this regimen except in children with open growth plates purchase malegra dxt 130 mg on line. At 1 year af- ter reconstruction generic malegra dxt 130 mg visa, in spite of these problems malegra dxt 130 mg discount, there is usually good recreation or maintenance of hip joint space on radiographs buy malegra dxt 130mg free shipping. Sudden Pain in Therapy Following hip surgery purchase malegra dxt 130 mg with visa, children who are doing very well with improved range of motion and a decrease in postoperative pain may suddenly develop in- creased pain in physical therapy. When this sudden increased pain occurs, it is very important to do a careful physical examination to ensure that an acute fracture has not occurred. The most common site of an acute fracture fol- lowing hip reconstruction is in the distal metaphysis of the femur or the prox- imal metaphysis of the tibia (Figure 10. These fractures are frequently missed by emergency room doctors and primary care physicians because families and therapists believe the pain is focused on the hip, where it has been throughout this rehabilitation phase. These fractures are especially com- mon in children who have been in spica casts. The fractures themselves are not hard to diagnose if a careful clinical examination is performed, as there is usually obvious swelling and tenderness present in the area surrounding Figure 10. It is very important to do a careful examination of the child, as evidenced by this girl who had prolonged hip pain for 6 months requiring steroid injection. Then, 8 months postoperatively when she had been comfortable for several months, she again presented in severe pain. The parents felt the pain was due to recurrent hip pain. The local doctor obtained hip radiographs that ap- peared unchanged; however, when the severe pain continued for 1 week, she returned for an orthopaedic evaluation. Because of the long experience of hip pain, the resident ordered another hip radiograph that again was unchanged. A physical examination of the child was then performed and a clearly swollen and erythematous knee was noted. A radiograph demonstrated the typical in- sufficiency fracture. However, if radiographs and physical examination do not look at the knee joint, these fractures will not be found. Occasionally, there may also be a fracture surrounding the plate, so doing a good physical ex- amination and making a radiograph of the proximal femoral osteotomy site are also important. Another consideration, especially in the period from 4 to 9 months postoperatively, should be the possibility of a fracture of a thin piece of heterotopic ossification in the sheath of the iliopsoas. These frac- tures usually become painful and then resolve relatively quickly. Evulsion fractures of the lesser trochanter may also occur. Continued or increased pain in the hip following hip reconstruction in children who are noncommunicative can be a real challenge. Caretakers often will feel that the pain is coming from the hip, but a full examination does not seem to demonstrate any evidence of pain. When pain exists in noncommunicative children, other sources of pain need to be considered and the appropriate and typical workup should then proceed. Avascular Necrosis Avascular necrosis has been reported following spastic hip reconstruc- tion56, 119; however, we have never seen a definite case of avascular necro- sis. Both reports of avascular necrosis used cast immobilization, which may explain part of its cause. Abducting spastic hips against the spasticity has been shown to produce avascular necrosis in insensate children. Lateral femoral head collapse may also occur when there is an insuffi- cient capsulotomy and postoperative rehabilitation attempts to stretch the contracted medial capsule. Often, the lateral aspect of the severely sublux- ated femur is very osteoporotic and when high pressure is applied to this osteoporotic femoral head, it may be caused to collapse. This collapse can be prevented with an adequate medial capsulotomy to allow adequate abduc- tion. We initially presumed that 0° of abduction was sufficient intraopera- tively to not require a capsulotomy; however, we now believe that abduction to at least to 20° or 30° in the operating room is possible. This means more medial and more aggressive capsulotomies need to be performed, which has not led to avascular necrosis and has decreased the incidence of finding compression of these osteoporotic lateral femoral heads. It is impossible to ensure that some collapse of the lateral femoral head was not due to avas- cular necrosis; however, this collapse does not have the appearance of a full avascular necrosis as reported. When lateral collapse occurs, it usually creates a flatten- ing of the superolateral border of the femur, limiting abduction similar to the protrusion that becomes present in the hip of Perthes disease with lateral ex- trusion.

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The rate of the chemical reaction in the absence of chymotrypsin is slow because there are too few OH called proteases best malegra dxt 130 mg. CHAPTER 8 / ENZYMES AS CATALYSTS 121 molecules in H2O with enough energy to form the transition state complex and too Poly- few OH molecules colliding with the substrate at the right orientation malegra dxt 130 mg. Catalytic Strategies in the Reaction Catalyzed R1 OH– + H+ R2 by Chymotrypsin H2O In the reaction catalyzed by chymotrypsin buy cheap malegra dxt 130 mg, the same oxyanion intermediate is chymotrypsin formed by using the hydoxyl group of a serine residue for the attack instead of a O H free hydroxyl anion cheap malegra dxt 130mg with visa. The rate of the chymotrypsin-catalyzed reaction is faster CH C OH + N CH because functional groups in the enzyme active site activate the attacking hydroxyl H group buy malegra dxt 130mg low price, stabilize the oxyanion transition state complexes, form a covalent intermedi- R1 R2 ate, and destabilize the leaving group. Chymotrypsin hydrolyzes certain cleavage of the peptide bond in the denatured substrate protein and formation of a peptide bonds in proteins. The scissile bond is covalent acyl-enzyme intermediate (Fig. The carbonyl carbon, which acyl-enzyme intermediate to release the remaining portion of the substrate protein carries a partial positive charge, is attacked by (Fig. The names of the catalytic strategies employed in the various a hydroxyl group from water. An unstable steps are in italics in the following paragraphs. SPECIFICITY OF BINDING TO CHYMOTRYPSIN electrons return to the carbonyl carbon, it becomes a carboxylic acid, and the remaining Chymotrypsin hydrolyzes the peptide bond on the carbonyl side of a phenylalanine, proton from water adds to the leaving group to tyrosine, or tryptophan in a denatured protein. The substrate recognition site consists form an amine. The substrate protein must be denatured to fit into the pocket and be held rigidly in place by glycines in the enzyme peptide backbone. Scissile bond specificity is also provided by the sub- sequent steps of the reaction, such as moving serine 195 into attacking position (proximity and orientation). FORMATION OF THE ACYL-ENZYME INTERMEDIATE In the stomach, gastric acid IN CHYMOTRYPSIN decreases the pH to 1 to 2 to dena- ture proteins through disruption of In the first stage of the reaction, the peptide bond of the denatured protein substrate hydrogen bonding. The protease in the stom- is cleaved as an active site serine hydroxyl group attacks the carbonyl carbon of the ach, pepsin, is a member of the aspartate pro- scissile bond (nucleophilic catalysis-a nucleophile is a chemical group that is tease superfamily, enzymes that use two attracted to the positively charged nucleus) (Fig. Aspartate and histi- aspartate residues in the active site for acid- dine cooperate in converting this hydroxyl group (with a partial negative charge on base catalysis of the peptide bond. Why can the oxygen) into a better nucleophilic attacking group by giving it a more negative they not use histidine like chymotrypsin? An active site histidine acts as a base and abstracts a proton from the serine hydroxyl (acid-base catalysis). The protonated histidine is stabilized by the nega- tive charge of a nearby aspartate. Serine proteases in blood coagula- The aspartate-histidine-serine combination, referred to as the catalytic triad, is an tion. The use of an active site ser- example of cooperative interactions between amino acid residues in the active site. Blood clots are formed from fibrin, a protein In the next step of the reaction sequence, an oxyanion tetrahedral transition state present in the blood as the inactive precur- complex is formed that is stabilized by hydrogen bonds with –NH groups in the sor, fibrinogen. The serine protease throm- bin cleaves a peptide bond in fibrinogen to peptide backbone (Fig. The original view of the way enzymes form form active fibrin. Thrombin has the same transition state complexes was that they stretched the bonds or distorted the bond aspartate-histidine-serine catalytic triad angles of the reacting substrates. However, most transition state complexes, such as found in chymotrypsin and works in essen- the oxyanion tetrahedral complex, are better described as showing “electronic tially the same way. Thrombin is also pres- strain,” an electrostatic surface that would be highly improbable if it were not sta- ent as an inactive precursor, prothrombin, bilized by bonds with functional groups on the enzyme. Stabilization of the transi- which is itself activated through proteolytic tion state complex lowers its energy level and increases the number of molecules cleavage by another blood coagulation ser- that reach this energy level. The covalent acyl–enzyme intermediate 195 195 Asp His Ser Asp His Ser C Gly C Gly CH2 N CH2 N – • N – • N O HN N• HN N• O H H H H O O O OO O N C H CC C C C H C C CH N NH2 CH2 N HO H NH2 H R R Tyr Tyr 2.

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CLINICAL COMMENTS The two most serious complications of acute viral hepatitis found in patients such as Percy Veere are massive hepatic necrosis leading to ful- minant liver failure and the eventual development of chronic hepatitis purchase 130 mg malegra dxt amex. Both complications are rare in acute viral hepatitis type A cheap malegra dxt 130 mg mastercard, however order malegra dxt 130mg online, suggesting that acetaminophen toxicity may have contributed to Percy’s otherwise unexpectedly severe hepatocellular dysfunction and early hepatic encephalopathy purchase 130mg malegra dxt visa. Fortunately buy cheap malegra dxt 130mg on-line, bed rest, rehydration, parenteral nutrition, and therapy directed at decreasing the production of toxins that result from bacterial degradation of nitrogenous substrates in the gut lumen (e. As with most patients who survive an episode of fulminant hepatic failure, recovery to his previous state of health occurred over the next 3 months. Percy’s liver function studies returned to normal, and a follow-up liver biopsy showed no histologic abnormalities. BIOCHEMICAL COMMENTS Disorders of the urea cycle are dangerous because of the accumulation of ammonia in the circulation. Ammonia is toxic to the nervous system, and its concentration in the body must be carefully controlled. Under normal conditions, free ammonia is rapidly fixed into either -ketoglutarate (by glutamate dehydrogenase, to form glutamate) or glutamate (by glutamine synthease, to form glutamine). The glutamine can be used by many tissues, including the liver; the glu- tamate donates nitrogens to pyruvate to form alanine, which travels to the liver. Within the liver, as the nitrogens are removed from their carriers, carbamoyl phos- phate synthetase I fixes the ammonia into carbamoyl phosphate to initiate the urea CHAPTER 38 / FATE OF AMINO ACID NITROGEN: UREA CYCLE 709 cycle. However, when a urea cycle enzyme is defective, the cycle is interrupted, which leads to an accumulation of urea cycle intermediates before the block. Because of the block in the urea cycle, glutamine levels increase in the circulation, and because -ketoglutarate is no longer being regenerated by removal of nitrogen from glutamine, the -ketoglutarate levels are too low to fix more free ammonia, leading to elevated ammonia levels in the blood. So how does one reduce ammonia and glutamine levels in such patients? The key to treating patients with urea cycle defects is to diagnose the disease early and then aggressively treat with compounds that can aid in nitrogen removal −SCoA A ATP AMP + PPi C (activation) C O O − SCoA O H −O C C H (Glycine) NH + 3 −SCoA C O C O Hippuric acid SCoA NH (excreted) CH2 C O − B O O CH2CH2CH2 C CH2 C O− O− β-oxidation Phenylbutyrate Phenylacetate O CoAS− CH2 C ATP SCoA O AMP + PPi C NH2 CH2 CH2 H C + HSCoA 3 C O − O O (Glutamine) H CH2 CH2CH2 C NH2 C O − Phenylacetylglutamine (excreted) Fig. The metabolism of benzoic acid (A) and phenylbutyrate (B), two agents used to reduce nitrogen levels in patients with urea cycle defects. Low-protein diets are essential to reduce the potential for exces- sive amino acid degradation. If the enzyme defect in the urea cycle comes after the synthesis of argininosuccinate, massive arginine supplementation has proved bene- ficial. Once argininosuccinate has been synthesized, the two nitrogen molecules destined for excretion have been incorporated into the substrate; the problem is that ornithine cannot be regenerated. If ornithine could be replenished to allow the cycle to continue, argininosuccinate could be used as the carrier for nitrogen excretion from the body. Thus, ingesting large levels of arginine leads to ornithine production by the arginase reaction, and nitrogen excretion via argininosuccinate in the urine can be enhanced. Arginine therapy will not work for enzyme defects that exist in steps before the synthesis of argininosuccinate. For these disorders, drugs are used that form conju- gates with amino acids. The conjugated amino acids are excreted, and the body then has to use its nitrogen to resynthesize the excreted amino acid. The two compounds most frequently used are benzoic acid and phenylbutyrate (the active component of pheylbutyrate is pheylacetate, its oxidation product. Phenylacetate has a bad odor, which makes it difficult to take orally). As glycine is synthesized from serine, the body now uses nitrogens to synthesize ser- ine, so more glycine can be produced. This conjugate removes two nitrogens per molecule and requires the body to resynthesize glutamine from glucose, thereby using another two nitrogen molecules. Urea cycle defects are excellent candidates for treatment by gene therapy. This is because the defect only has to be repaired in one cell type (in this case, the hepa- tocyte), which makes it easier to target the vector carrying the replacement gene. Preliminary gene therapy experiments had been carried out on individuals with ornithine transcarbamolyase deficiency (the most common inherited defect in the urea cycle), but the experiments came to a halt when one of the patients died of a severe immunologic reaction to the vector used to deliver the gene. This incident has placed gene replacement therapy in the United States “on hold” for the fore- seeable future. The Metabolic and Molecular Bases of Inherited Disease, vol II, 8th Ed.

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Effects of early and vigorous exercise on recovery from infectious hepatitis purchase 130 mg malegra dxt with mastercard. Joint Position Statement: human immunodeficiency virus and other blood borne pathogens in sports cheap malegra dxt 130 mg on line. Principles and Practice of Primary Care Sports Medicine generic malegra dxt 130 mg line. Philadelphia: Lipincott discount 130 mg malegra dxt, Williams and Wilkins 2001 purchase malegra dxt 130mg without prescription;239–246. Epstein-Barr virus infections, including infectious mononucleosis. Aerobic capacity after contracting infectious mononucleosis. Infectious mononucleosis: relation of bed rest and activity to prognosis. When to resume sports after infectious mononucleosis. Spontaneous rupture of the spleen in patients with infectious mononucleosis. Hepatosplenomegaly in infectious mononucleosis, assessed by ultrasononic scanning. Infectious mononucleosis: recognizing the condition, “reactivating” the patient. Rupture of the pathologic spleen: is there a role for nonoperative therapy? IAN SHRIER Introduction Over the past 30 years, sport medicine professionals have promoted stretching as a way to decrease the risk of injury. These changes in muscle stiffness would allow for an increased range of motion (ROM) around a joint (i. Despite these claims, new research has challenged some of these concepts. First, stretching must be differentiated from range of motion. There are many individuals who have excellent range of motion but never stretch, and many individuals who stretch but continue to have limited range of motion. Therefore, different injury rates in people with different ranges of motion may not be related to the effect of stretching but rather occur because of underlying variations in tissue properties (for example strength), anatomy, etc. To understand the specific effect of stretching, then one should limit the review to studies that directly look at that intervention. Second, stretching immediately before exercise may have different effects than stretching at other times. These should be considered separate interventions, and completely different from studies on flexibility. Whereas there is a considerable amount of clinical data on stretching immediately before exercise, there is much less data on stretching at other times. However, the reader should realise that “flexibility” has other meanings in other domains, and is often used as a synonym for compliance, i. Mathematically, compliance is the reciprocal of stiffness, and is equal to change in length produced by a given force. Stretching may decrease the stress applied to a tissue both locally (i. One example of a distant effect is that stretching the hamstring muscles may decrease the stress on the low back during toe touching. This is because toe touching is achieved through both hip and lumbar flexion. If hip flexion is limited because of stiff hamstrings, then more motion must come from, and more stress must be applied to the lumbar spine to achieve the same range of motion. In this chapter, I will first review new findings that have changed our understanding of what stretching actually does to muscle. This will include changes at the level of the whole muscle (for example compliance) and at the level of the myofiber.

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