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Though rivastigmine is an acetylcholinesterase inhibitor buy generic extra super viagra line, which can cause tremors as an adverse effect purchase extra super viagra pills in toronto, its use is not contraindicated in patients with Parkinson disease generic extra super viagra 200mg on line, as this agent is also the only medication approved for dementia associated with Parkinson disease. It should be used with caution, as it may worsen the parkinsonian-related tremors. A risk–benefit discussion should occur with the patient and the caregiver before rivastigmine is used. Which agent may be beneficial to improve walking speed and disability in this patient? Dalfampridine is a potassium channel blocker that exerts its therapeutic effect in multiple sclerosis via potassium channel blockade and has been proven to improve walking speed and disability in patients with multiple sclerosis. Anxiety is an unpleasant state of tension, apprehension, or uneasiness (a fear that arises from either a known or an unknown source). The physical symptoms of severe anxiety are similar to those of fear (such as tachycardia, sweating, trembling, and palpitations) and involve sympathetic activation. Episodes of mild anxiety are common life experiences and do not warrant treatment. However, severe, chronic, debilitating anxiety may be treated with antianxiety drugs (sometimes called anxiolytics) and/or some form of psychotherapy. Because many antianxiety drugs also cause some sedation, they may be used clinically as both anxiolytic and hypnotic (sleep-inducing) agents. Some antidepressants are also indicated for certain anxiety disorders; however, they are discussed with the antidepressants (see Chapter 10). They have largely replaced barbiturates and meprobamate in the treatment of anxiety and insomnia, because benzodiazepines are generally considered to be safer and more effective (ure 9. Though benzodiazepines are commonly used, they are not necessarily the best choice for anxiety or insomnia. For each subunit, many subtypes exist (for example, there are six subtypes of the α subunit). The influx of chloride ions causes hyperpolarization of the neuron and decreases neurotransmission by inhibiting the formation of action potentials. Sedative/hypnotic All benzodiazepines have sedative and calming properties, and some can produce hypnosis (artificially produced sleep) at higher doses. Therapeutic uses the individual benzodiazepines show small differences in their relative anxiolytic, anticonvulsant, and sedative properties. However, pharmacokinetic considerations are often important in choosing one benzodiazepine over another. The benzodiazepines are also useful in treating anxiety related to depression and schizophrenia. These drugs should be reserved for severe anxiety and should not be used to manage the stress of everyday life. Because of their addictive potential, they should only be used for short periods of time. The antianxiety effects of the benzodiazepines are less subject to tolerance than the sedative and hypnotic effects. In the treatment of insomnia, it is important to balance the sedative effect needed at bedtime with the residual sedation (“hangover”) upon awakening. The risk of withdrawal and rebound insomnia is higher with triazolam than with other agents. In general, hypnotics should be used for only a limited time, usually 1 to 3 weeks. Amnesia the shorter-acting agents are often employed as premedication for anxiety-provoking and unpleasant procedures, such as endoscopy, dental procedures, and angioplasty. They cause a form of conscious sedation, allowing the patient to be receptive to instructions during these procedures. Seizures Clonazepam is occasionally used as an adjunctive therapy for certain types of seizures, whereas lorazepam and diazepam are the drugs of choice in terminating status epilepticus (see Chapter 12). Muscular disorders Diazepam is useful in the treatment of skeletal muscle spasms and in treating spasticity from degenerative disorders, such as multiple sclerosis and cerebral palsy. Duration of action the half-lives of the benzodiazepines are important clinically, because the duration of action may determine the therapeutic usefulness. The benzodiazepines can be roughly divided into short-, intermediate-, and long-acting groups (ure 9. However, with some benzodiazepines, the clinical duration of action does not correlate with the actual half-life (otherwise, a dose of diazepam could conceivably be given only every other day, given its long half-life and active metabolites). Fate Most benzodiazepines, including chlordiazepoxide and diazepam, are metabolized by the hepatic microsomal system to compounds that are also active. For these benzodiazepines, the apparent half-life of the drug represents the combined actions of the parent drug and its metabolites. The benzodiazepines are excreted in the urine as glucuronides or oxidized metabolites. Dependence Psychological and physical dependence can develop if high doses of benzodiazepines are given for a prolonged period. Abrupt discontinuation of these agents results in withdrawal symptoms, including confusion, anxiety, agitation, restlessness, insomnia, tension, and (rarely) seizures. Benzodiazepines with a short elimination half-life, such as triazolam, induce more abrupt and severe withdrawal reactions than those seen with drugs that are slowly eliminated such as flurazepam (ure 9. Adverse effects Drowsiness and confusion are the most common adverse effects of the benzodiazepines. Ataxia occurs at high doses and precludes activities that require fine motor coordination, such as driving an automobile. Cognitive impairment (decreased recall and retention of new knowledge) can occur with use of benzodiazepines. Benzodiazepines are, however, considerably less dangerous than the older anxiolytic and hypnotic drugs. As a result, a drug overdose is seldom lethal unless other central depressants, such as alcohol or opioids, are taken concurrently. Frequent administration may be necessary to maintain reversal of a long-acting benzodiazepine. Administration of flumazenil may precipitate withdrawal in dependent patients or cause seizures if a benzodiazepine is used to control seizure activity. Seizures may also result if the patient has a mixed ingestion with tricyclic antidepressants or antipsychotics. Antidepressants Many antidepressants are effective in the treatment of chronic anxiety disorders and should be considered as first- line agents, especially in patients with concerns for addiction or dependence. After 4 to 6 weeks, when the antidepressant begins to produce an anxiolytic effect, the benzodiazepine dose can be tapered. Long-term use of antidepressants and benzodiazepines for anxiety disorders is often required to maintain ongoing benefit and prevent relapse. It has a slow onset of action and is not effective for short-term or “as-needed” treatment of acute anxiety. In addition, buspirone lacks the anticonvulsant and muscle-relaxant properties of the benzodiazepines. The frequency of adverse effects is low, with the most common effects being headache, dizziness, nervousness, nausea, and light-headedness.

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Although the exact mechanism has not been elucidated purchase 200 mg extra super viagra mastercard, risk factors for developing low serum sodium levels include weight gain during the race buy cheap extra super viagra 200 mg online, female sex buy 200mg extra super viagra with amex, racing time, and lower body mass index [7]. Exercise-induced hyponatremia has been described after intense physical activity during marathons, triathlons, and high- intensity competitions. Again, the pathophysiology involves a combination of excessive fluid intake as well as a defect in renal water excretion. This disorder is most often seen in anxious, middle-aged women and in patients with psychiatric illnesses, including those taking medications that can lead to the sensation of dry mouth. This may be manifested clinically by exaggerated weight gain during the day associated with a transient reduction in the plasma sodium concentration. Primary polydipsia can also be induced by hypothalamic lesions that directly affect the thirst center, as may occur with an infiltrative disease such as sarcoidosis. Drug therapy may contribute to the increase in water intake if the medication induces the sensation of a dry mouth. Concurrent thiazide diuretic therapy for systemic hypertension can lead to a marked and symptomatic reduction in the plasma sodium concentration in these patients. An increase in the plasma concentration of proteins (as immunoglobulins in multiple myeloma) or lipids (primarily triglycerides in lipemic plasma) can reduce + the plasma Na concentration. Lipids and proteins displace water from a + given volume of plasma but do not affect the Na concentration in the water phase of plasma. Because the sodium concentration in the aqueous component of plasma is normal, this form of hyponatremia is not of pathophysiologic consequence. The methods of electrolyte determination currently used in many laboratories (ion- selective electrodes) are not affected by plasma lipids or proteins. Some patients absorb 3 L or more of fluid through the exposed mucosal vascular plexus, leading to a dilutional reduction in the plasma sodium concentration that may fall below 100 mEq per L. Several methods have been devised to attempt to monitor the amount of fluid absorbed so that patients at risk for severe hyponatremia can be detected. There are instances in which patients with plasma hyperosmolality may develop hyponatremia (hyperosmolar hyponatremia). This most commonly occurs with severe hyperglycemia or when mannitol is given to patients with renal failure, resulting in an osmotic shift of water from + cells into the extracellular fluid, diluting the plasma Na concentration. In contrast to hypoosmolar hyponatremia, treatment is directed at correcting the high glucose concentration with insulin and free water repletion because cellular dehydration is present. For every 100 mg per + dL rise in the blood sugar, the plasma Na concentration falls by approximately 1. Symptoms of Hypoosmolality the neurologic manifestations of hyponatremia appear to be entirely because of the consequences of plasma hypoosmolality. The resulting increase in cell water, which is of particular importance in the central nervous system, can lead to brain swelling. A variety of symptoms may be found, including lethargy, confusion, nausea, vomiting, and, in severe cases, seizures and coma. Hyponatremic encephalopathy is generally reversible, although permanent neurologic damage or death has been reported, chiefly in premenopausal women [12]. Hyponatremic women may progress rapidly from minimal symptoms (such as headache and nausea) to respiratory arrest. Cerebral edema and herniation have been found in those women who died, suggesting a possible hormonally mediated decrease in the efficiency of the osmotic adaptation. The likelihood that symptoms will develop is related to the level of hyponatremia and the rapidity with which it develops. In comparison, a similar fall in plasma sodium occurring during 1 week or more may not cause any symptoms. This protective response, which begins on the first day and is complete within several days, occurs in two major steps: 1. The initial cerebral edema elevates the interstitial hydraulic pressure, creating a gradient for extracellular fluid movement out of the brain into the cerebrospinal fluid. The brain cells lose solutes, leading to the osmotic movement of water out of the cells and less brain swelling [13]. The volume regulatory response begins with the movement of potassium and sodium salts out of the cells, followed by organic solutes, particularly the amino acids glutamine, glutamate, and taurine, and, to a lesser degree, the carbohydrate inositol. Electrolyte movement occurs quickly because it is mediated by the activation of quiescent cation channels in the cell membrane; organic solute loss occurs later because it requires synthesis of new transporters. The organic solutes (called osmolytes) account for approximately one- third of the cellular solute loss in chronic hyponatremia. Changes in the concentration of these solutes offer the advantage of restoring cell volume without interfering with protein function; in comparison, a potentially deleterious effect on protein function would occur if the volume adaptation was mediated entirely by changes in the cell cation (potassium plus sodium) concentration. The occurrence of symptoms in patients with chronic hyponatremia usually signifies a profoundly low serum sodium concentration of less than 110 to 115 mEq per L. The urinary sodium concentration of patients with hypovolemia is typically less than 20 mEq per L, assuming the patient is not receiving diuretics. As examples, metabolic alkalosis and hypokalemia suggest diuretic use or vomiting; metabolic acidosis and hypokalemia suggest diarrhea or laxative abuse; and metabolic acidosis and hyperkalemia suggest adrenal insufficiency. Although water retention tends to lower these values by dilution, as it does the plasma sodium and chloride concentrations, normal levels are restored by the factors that normally regulate acid–base and potassium balance. These findings are the opposite of what is typically seen in volume depletion and thiazide-induced hyponatremia. Hypouricemia may also be present, which presumably is another manifestation of impaired renal tubular function. Treatment of Hyponatremia Saline or Water Restriction In general, the plasma sodium concentration can be raised by giving patients salt (either as saline or salt tablets) or by restricting their water intake to below the level of excretion. Salt administration, usually as isotonic saline, is appropriate in those with true volume depletion or adrenal insufficiency, in which cortisol replacement is also indicated. Each liter of saline infused raises the plasma sodium by 1 to 2 mEq per L because saline has a higher sodium concentration (154 mEq per L) than plasma. In primary polydipsia, the initiation of water restriction may result in a dramatic rise in the plasma sodium concentration. These patients may be less predisposed to osmotic demyelination because their hyponatremia often is of rapid onset, with less brain cell adaptation apt to occur. In asymptomatic patients, who are more likely to have chronic hyponatremia, the plasma sodium concentration should be raised at a maximum rate of approximately 0. More rapid initial correction is indicated for patients with symptomatic hyponatremia, particularly those presenting with seizures or other severe neurologic manifestations, which primarily result from cerebral edema induced by acute (developing during 2 to 3 days) hyponatremia. This appears to be particularly important in premenopausal women, who may progress from minimal symptoms (headache and nausea) to coma and respiratory arrest; furthermore, irreversible neurologic damage or death is relatively common in younger women with symptomatic hyponatremia, even if the hyponatremia is corrected at an appropriate rate. In comparison, men are at much less risk of symptomatic hyponatremia and of permanent neurologic injury. After the initial 3 to 4 hours of rapid correction, the rate should be slowed down so that the total rise in plasma sodium does not exceed approximately 8 mEq during the initial 24 hours. If the initial aim in an asymptomatic hyponatremic 60-kg woman is to raise the plasma sodium concentration from 110 to 120 mEq per L, then Sodium deficit for initial therapy = 0.

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They should be able to recognize the most frequent side effects and know how to manage them generic extra super viagra 200mg line. Pillboxes are popular; these contain all the drugs taken during 1 week in separate compartments extra super viagra 200 mg on line. The establishment of a detailed written schedule cheap extra super viagra express, showing how and when to take prescribed drugs in relation to meals and drinks, is recommended. More elaborate and expensive procedures involve use of electronic pillboxes, involving a device that records each time a bottle cap is unscrewed; the information can be downloaded into a computer and discussed with the patient. Directly observed therapy is possible with once-daily regimens; this approach may be particularly appropriate in combination with methadone maintenance. Above approximately 50 copies per cubic millimeter, the nadir of viral load reached through treatment predicts duration of viral suppression. Time to optimal viral suppression depends on the initial viral load and the sensitivity of the viral load test. Combination treatment must produce a rapid fall in viral load, which should drop to fewer than 400 copies per cubic millimeter after 12 weeks and to fewer than 50 copies after 24 weeks. The presence of resistance genotypes and phenotypes can be detected using commercially available methods. Studies show that these tests are useful mainly for excluding drugs to which the virus is resistant; they are less helpful for finding drugs to which the virus is sensitive. Resistance tests should be ordered before treatment commences in patients who are likely to have been infected in 1997 or later. They are recommended in cases of unexpected toxicity, suspected problems with compliance that cannot be otherwise investigated, or when multiple medications may produce unforeseeable pharmacokinetic interactions. Treatment Modification and Simplification Once-a-day treatment with one pill has become the standard for initial treatment. Despite the common suggestion to “never change a winning team,” there is no objection to simplification, provided that there is no evidence for pretreatment resistance to the new drug combination. Procedures in Case of Failure Treatment must often be changed because of intolerance, drug interactions, or side effects. If viremia is below 50 copies per cubic millimeter, a single offending drug can be replaced. Virologic failure—that is, viremia—that does not decline to fewer than 50 copies per cubic millimeter after 6 months (9 months if the initial viremia exceeded 1 million copies per cubic millimeter) or that rises to more than 200 copies requires a different approach. In this situation, a new combination should be chosen, containing (if possible) a drug from a class that had not already been used. At least one additional drug should also be replaced by another to which the patient is unlikely to be resistant, given personal medication history and resistance tests. A new combination should be chosen, containing (if possible) a drug from a class that has not already been used. At least one additional drug should also be replaced by another to which the patient is unlikely to be resistant. Start and End of Prophylaxis for Opportunistic Infections Efficacious antiretroviral treatment—provided that it is started in time— prevents immune deficiency and obviates the need for prophylaxis of opportunistic infections. Chances for success are best in the previously untreated; therefore, every effort must be made to optimize the first treatment given. A specialist should be consulted when starting or changing antiretroviral treatment. Compliance remains essential for treatment success; drugs must be taken as prescribed. Patients often ask whether there is hope for a “cure,” that is, discontinuation of drugs without relapse of viremia. This is a hot topic for scientific meetings, but unfortunately without any solid leads at the present time. Indefinite maintenance treatment, using drugs that are well tolerated and that remain effective, is a more realistic outlook. Two weeks earlier, he had been seen by his local doctor for the same complaints and had been given an oral antibiotic at that time. An epidemiologic history noted that the patient reported multiple episodes of unprotected homosexual intercourse 3 years earlier, but several months’ abstinence recently. The patient denied intravenous drug use and said that he had never smoked cigarettes. No lymphadenopathy was evident, but white plaques consistent with thrush were seen on the posterior pharynx. No organomegaly was evident on abdominal exam, and the genitalia was within normal limits. Chest X-ray revealed2 3 bilateral, interstitial, diffuse, fluffy infiltrates forming a butterfly pattern. Chest radiograph shows symmetric infiltrates of the lower lobes similar in appearance to pulmonary edema. Sample of bronchoalveolar lavage stained with toluene blue, showing multiple organisms. The patient was started on intravenous methylprednisolone and trimethoprim–sulfamethoxazole. His shortness of breath gradually improved over the next 3 days, and he was discharged on oral trimethoprimsulfamethoxazole. Opportunistic infections typically represent reactivation of latent infection or acquisition of a new infection, often caused by microorganisms of intrinsically low virulence. Once immune deficiency is profound, these microorganisms may start to proliferate. Progressively, however, organ damage and symptoms occur—for example, stomatitis and symptomatic esophagitis from Candida albicans. In advanced stages of immune suppression, agents that are usually nonpathogenic can have devastating consequences. Several infections can be present at the same time, greatly complicating diagnosis and treatment. After treatment of active infections, secondary prophylaxis is often necessary to prevent relapse. Therefore, as long as the underlying immune deficiency is not corrected, secondary prevention is necessary. Empiric treatment should start with amoxicillin–clavulanate, a cephalosporin, or one of the quinolones with activity against gram-positive bacteria. The chest X-ray pattern is helpful in narrowing the diagnostic possibilities (see Table 16. However, in all patients, whatever their degree of immune suppression, a definitive diagnosis usually requires bronchoalveolar lavage. Symptoms originate in the respiratory tract (dry cough, dyspnea) and are accompanied by fever (always), weight loss, and fatigue. Initially, patients experience shortness of breath with exercise, but do not complain of shortness of breath at rest. Alveolar fluid accumulation associated with Pneumocystis infection interferes with oxygen exchange, and patients quickly outstrip the ability of their lungs to supply arterial oxygen.

In a patient with a full stomach order extra super viagra with american express, compressing the cricoid cartilage posteriorly against the vertebral body can reduce the diameter of the hypopharynx purchase 200mg extra super viagra overnight delivery. This technique discount extra super viagra online mastercard, known as Sellick maneuver, may prevent passive regurgitation of stomach contents into the trachea during intubation. Moreover, cricoid pressure increased the incidence of an unopposed esophagus by 50% and caused airway compression of greater than 1 mm in 81% of the volunteers [31]. Consequently, compression of the alimentary tract was demonstrated with midline and lateral displacement of the cricoid cartilage relative to the underlying vertebral body [32]. Cadaver studies have demonstrated the efficacy of cricoid pressure [33], and clinical studies have shown that gastric insufflation with gas during mask ventilation is reduced when cricoid pressure is applied [34]. In aggregate, these data suggest that it is prudent to continue to use cricoid pressure in patients suspected of having full stomachs. In addition, placing the patient in the partial recumbent or reverse Trendelenburg position may reduce the risk of regurgitation and aspiration. The laryngoscope handle is grasped in the left hand whereas the patient’s mouth is opened with the gloved right hand. Often, when the head is extended in the unconscious patient, the mouth opens; if not, the thumb and index finger of the right hand are placed on the lower and upper incisors, respectively, and moved past each other in a scissor-like motion. The laryngoscope blade is inserted on the right side of the mouth and advanced to the base of the tongue, pushing it toward the left. With the blade in place, the operator should lift forward in a plane 45 degrees from the horizontal to expose the vocal cords (s. This motion decreases the risk of the blade striking the upper incisors and either chipping or dislodging teeth. The cuff is inflated with enough air to prevent a leak during positive-pressure ventilation with a bag valve device. The view of the glottis is usually very good, but intubation can sometimes be problematic because the proprietary stylets are rigid and cannot be molded to the optimal curvature. Complications can include mucosal damage or perforation of the palatoglossal arch, palatopharyngeal arch, or the retromolar trigone. A classification grading the view of the laryngeal aperture during direct laryngoscopy has been described [35] and is depicted in ure 8. This tube has a nylon cord running the length of the tube attached to a ring at the proximal end, which allows the operator to direct the tip of the tube anteriorly. If the attempt to intubate is still unsuccessful, the algorithm should be followed (see “Management of the Difficult Airway” section of this chapter). If the tube has been advanced too far, it will lodge in one of the main bronchi (particularly the right bronchus), and only one lung will be ventilated. A useful rule of thumb for tube placement in adults of average size is that the incisors should be at the 23-cm mark in men and the 21-cm mark in women. Alternatively, proper depth (5 cm above the carina) can be estimated using the following formula: (height in cm/5) − 13 [37]. Palpation of the anterior trachea in the neck may detect cuff inflation because air is injected into the pilot tube and can serve as a means to ascertain correct tube position. Measurement of end-tidal carbon dioxide by standard capnography if available or by means of a calorimetric chemical detector of end-tidal carbon dioxide (e. If the tube is in the trachea, the bulb reexpands, and if the tube is in the esophagus, the bulb remains collapsed. After estimating proper tube placement clinically, it should be confirmed by chest radiograph or bronchoscopy because the tube may be malpositioned. It must be remembered that flexion or extension of the head can advance or withdraw the tube 2 to 5 cm, respectively. Nasotracheal Intubation Many of the considerations concerning patient preparation and positioning outlined for orotracheal intubation apply to nasal intubation as well. Blind nasal intubation is more difficult to perform than oral intubation because the tube cannot be observed directly as it passes between the vocal cords. Nasal intubation should not be attempted in patients with abnormal bleeding parameters, nasal polyps, extensive facial trauma, cerebrospinal rhinorrhea, sinusitis, or any anatomic abnormality that would inhibit atraumatic passage of the tube. As previously discussed in “Airway Adjuncts” section, after the operator has alternately occluded each nostril to ascertain that both are patent, a topical vasoconstrictor and anesthetic are applied to the nostril that will be intubated. The patient should be monitored with a pulse oximeter, and supplemental oxygen should be given as necessary. Here the tube operator must continually monitor for the presence of air movement through the tube by listening for breath sounds with the ear near the open end of the tube. The tube must never be forced or pushed forward if breath sounds are lost, because damage to the retropharyngeal mucosa can result. If resistance is met, the tube should be withdrawn 1 to 2 cm and the patient’s head repositioned (extended further or turned to either side). Once positioned in the oropharynx, the tube is advanced to the glottis while listening for breath sounds through the tube. If breath sounds cease, the tube is withdrawn several centimeters until breath sounds resume, and the plane of entry is adjusted slightly. In this case, after adequate topical anesthesia, laryngoscopy can be used to visualize the vocal cords directly and Magill forceps used to grasp the distal end of the tube and guide it through the vocal cords. Assistance in pushing the tube forward is essential during this maneuver so that the operator merely guides the tube. Management of the Difficult Airway A difficult airway may be recognized (anticipated) or unrecognized at the time of the initial preintubation airway evaluation. Difficulty managing the airway may be the result of abnormalities such as congenital hypoplasia, hyperplasia of the mandible or maxilla, or prominent incisors; injuries to the face or neck; acromegaly; tumors; and previous head and neck surgery. Difficulties ventilating the patient with a mask can be anticipated if two of the following factors are present: older than 2 55 years of age, body mass index greater than 26 kg per m, beard, lack of teeth, and a history of snoring [38]. When a difficult airway is recognized before the patient is anesthetized, an awake tracheal intubation is usually the best option. It may be particularly useful when the upper airway anatomy has been distorted by tumors, trauma, endocrinopathies, or congenital anomalies. This technique is sometimes valuable in accident victims in whom a question of cervical spine injury exists and the patient’s neck cannot be manipulated. An analogous situation exists in patients with severe degenerative disk disease of the neck or rheumatoid arthritis with markedly impaired neck mobility. After adequate topical anesthesia is obtained (discussed in “Anesthesia before Intubation” section), the bronchoscope can be used to intubate the trachea via either the nasal or oral route. If mask ventilation cannot be maintained, a cannot ventilate–cannot intubate situation exists and immediate lifesaving rescue maneuvers are required. When properly inserted, it fits over the laryngeal inlet and allows positive-pressure ventilation of the lungs. When air is aspirated, the needle is in the airway, and the catheter is passed over the needle into the trachea. Management of the Airway in Patients with Suspected Cervical Spine Injury Any patient with multiple trauma who requires intubation should be treated as if cervical spine injury was present. In the absence of severe maxillofacial trauma or cerebrospinal rhinorrhea, nasal intubation can be considered. If oral intubation is required, an assistant should maintain the neck in the neutral position by ensuring axial stabilization of the head and neck because the patient is intubated.

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