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Within each element in the cascade-atherogenesis risk undergoing transition to risk for an active plaque state allergy symptoms images order allegra 180 mg with amex, followed by genetic properties of the thrombotic cascade allergy symptoms lightheaded allegra 180 mg amex, and finally triggering of arrhythmias- genetic influences feed into an integrated pool of characteristics that determine individual probabilities. For example, mining of existing databases can identify risk factors or strong associations. Observations generally are expressed in terms of relative risk statements, which can be derived from low absolute event rates. Low event rates with large relative differences identify effects, but usually with limited individual patient impact. In contrast, randomized clinical trials with large absolute differences in outcomes are able to better define individual patient benefits. Observational studies are limited by their dependence on comparisons between anticipated outcomes that influence study design, rather than actual measures. Cost and risk-benefit uncertainties limit the nature of broad-based interventions and demand a higher resolution of risk identification. With each group-specific escalation of risk, the probability of an event increases, whereas the corresponding absolute number of deaths becomes progressively smaller,1 limiting the population effect of interventions in high-risk subgroups yet magnifying the individual benefit. All studies of group outcomes of therapy for complex pathophysiologic states must consider four factors: (1) relative risk reduction, (2) absolute risk reduction, (3) residual risk, and (4) cumulative benefits of multiple interventions. Relative risk reduction, however, does not quantify the benefit for the individual patient. To do so, a measure of absolute risk reduction is required, such as the absolute numerical difference in risk observed in the test and control groups, or calculations of a number of patients needed to be treated in order to save a life. Other measures of group effects that do not commonly receive attention include residual risk and cumulative benefit. Residual risk refers to the absolute outcome among the treated group or test group in a clinical trial population, which identifies the component of total mortality risk that does not respond to the tested therapy. If residual risk is high, the absolute and relative risk reduction benefits are correspondingly limited. Post hoc subgroup analysis can be used to suggest added benefit of a secondary strategy, but this does not replace stratifying the multiple interventions. Ejection fraction entry criteria were largely in the range of 30% to 40% or less, but enrollment was dominated by lower ranges. American Heart Association: 2001 Heart and Stroke Statistical Update, Dallas, 2000, American Heart Association. Dudas K, Lappas G, Stewart S, et al: Trends in out-of-hospital deaths due to coronary heart disease in Sweden (1991 to 2006). Wisten A, Forsberg H, Krantz P, et al: Sudden cardiac death in 15­35-year olds in Sweden during 1992­99. Mehta D, Curwin J, Gomes A, et al: Sudden death in coronary artery disease: Acute ischemia versus myocardial substrate. Heart Protection Study Collaborative Group: C-reactive protein concentration and the vascular benefits of statin therapy: an analysis of 20 536 patients in the Heart Protection Study. Teodorescu C, Reinier K, Dervan C, et al: Factors associated with pulseless electric activity versus ventricular fibrillation: the Oregon Sudden Unexpected Death Study. Vaillancourt C, Everson-Stewart S, Christenson J, et al; the Resuscitation Outcomes Consortium 31. Investigators: the impact of increased chest compression fraction on return of spontaneous circulation for out-of-hospital cardiac arrest patients not in ventricular fibrillation. Jouven X, Desnos M, Guerot C, et al: Predicting sudden death in the population: the Paris Prospective Study I. Electrophysiologists are asked to evaluate and treat these patients and need to understand the clinical presentations, appropriate therapies, and outcomes in the diseases. Symptoms typically begin before the age of 5 years with proximal muscle weakness that is progressive, leading to a loss of ambulation and later to respiratory failure. Invasive ventilation and spinal surgery has improved outcomes with a median survival of 35 years. Becker muscular dystrophy is less common, has a more variable presentation of skeletal muscle weakness, and has a better prognosis. The majority of patients with Duchenne muscular dystrophy develop a cardiomyopathy, but clinical recognition can be masked by severe skeletal muscle weakness. Predilection for involvement in the posterobasal and posterolateral left ventricle has been observed. Electrocardiograms are abnormal in 90% of patients with Duchenne muscular dystrophy, demonstrating a distinctive pattern of tall R waves and increased R/S amplitude in V1 and deep narrow Q waves in the left precordial leads related to the regional ventricular involvement. Cardiac involvement in Becker muscular dystrophy is more variable, ranging from none or subclinical to severe cardiomyopathy requiring transplant. Electrocardiographic abnormalities similar to that in Duchenne muscular dystrophy are present in up to 75% with echocardiographic abnormalities in 50%. The severity of cardiac involvement does not correlate with the degree of skeletal muscle weakness. ArrhythmiaManifestations Persistent or labile sinus tachycardia is the most common rhythm abnormality observed in Duchenne muscular dystrophy. Atrial arrhythmias including fibrillation and flutter occur in the setting of a dilated cardiomyopathy or as a preterminal rhythm. Ventricular arrhythmias primarily ventricular premature beats are seen on ambulatory monitoring. A primary cardiac etiology for death occurs in approximately one fourth of individual with an equal distribution of death from progressive heart failure and sudden death. The presence of left ventricular systolic dysfunction is a risk factor for all-cause mortality. Arrhythmia manifestations in Becker muscular dystrophy correspond to the degree of associated cardiomyopathy, but are poorly characterized.

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The condition is known as tic douloureux because of the typical lightning-like jabs of pain that may result in wincing allergy symptoms cough buy 180 mg allegra otc. Orbital lesion Sensory disturbance in the first division only allergy upset stomach buy allegra 120 mg with amex, associated with ophthalmoplegia. Foramen ovale or mandibular lesion Sensory disturbance in the third division only; sometimes only unilateral numbness of the chin. Bilateral trigeminal lesions Motor involvement: more obvious symptoms are usually evident, with weakness and wasting of the temporalis and masseter muscles bilaterally. Investigations these depend on the clinical syndrome and likely location and etiology: Direct examination of the nasopharynx and larynx. It is thought that compression results in partial demyelination and axonal damage, rendering the axons hyperexcitable. Trigger factors include talking, chewing, swallowing, shaving, brushing the teeth, and wind blowing on the face. The pain is described as brief (lasting for seconds) and followed by long pain-free intervals, and as stabbing/ lightning or electric shock-like/penetrating jabs of pain or clusters of stabbing pains. The pattern is episodic: pain may recur several times a day for weeks or months, and then may remit for months or years. Oral hygiene may suffer and weight loss may occur as patients attempt to avoid triggering the pain; depression, dehydration, and even suicide can occur in severely afflicted patients. In a series of 50 patients with trigeminal neuralgia, neurovascular contact was demonstrated on the affected side in 51 of 55 symptomatic nerves studied and on the contralateral side in only 4 of 45 nerves. It may control symptoms by suppressing sodium ion currents in the spinal trigeminal nucleus or in the Gasserian ganglion. A small dose of 50­100 mg nightly is the usual starting dose (to avoid drowsiness), escalating the dose as tolerated until pain relief is achieved (or adverse effects occur). Carbamazepine may also cause hyponatremia, megaloblastic anemia (folate interaction), aplastic anemia, agranulocytosis, and hypersensitivity reactions. Lamotrigine is a potent antiglutamatergic agent which may depress excitatory transmission in the spinal trigeminal nucleus. For patients who fail to respond to medical management, one of several surgical procedures can be undertaken. Decompression Posterior fossa exploration and microvascular decompression (the Jannetta procedure) consists of separating/ removing and decompressing the offending artery or vein from the trigeminal nerve root. The majority of patients have immediate relief after microvascular decompression, although some later have recurrent pain. Despite its risks, microvascular decompression is currently the best first surgical option, especially late in the course of the disease13. Denervation Percutaneous procedures are less invasive than microvascular decompression and are associated with low rates of mortality and morbidity, but they all create trigeminal nerve lesions, occasionally producing anesthesia dolorosa or keratitis. Prognosis Commonly the episodes of pain follow a relapsing and remitting course, with exacerbations lasting weeks to months and spontaneous remissions that become shorter and less frequent over the years. Ten years after microvascular decompression surgery, 70% of patients are free of pain without medication. Recurrence is more likely and occurs sooner after milder damage to the trigeminal nerve, produced either chemically or by compression with a percutaneously positioned balloon. Sensory loss extending beyond the chin and lower lip may indicate a more proximal V3 lesion or leptomeningeal involvement. The motor component of the facial nerve innervates the muscles of facial expression; this component represents about 70% of the facial nerve fibers. The remaining 30% are contained in the nervus intermedius and constitute the somatosensory and secretomotor components of the nerve2. There are five functional components of the facial nerve (646): Special visceral efferent: innervates the muscles of facial expression, the stapedius, stylohyoid, and posterior belly of the digastric. Motor component Supranuclear control Precentral gyrus: the innervation of the facial muscles begins in the most lateral and inferior aspect of the precentral gyrus, near the Sylvian fissure. The ventral portion innervates the lower two-thirds of the face and receives crossed supranuclear control. The dorsal portion supplies the upper one-third of the face and has bilateral supranuclear control. As a result, a unilateral hemispheric lesion impairs only the lower facial muscles6. Motor root Nervus intermedius Internal auditory meatus Geniculate ganglion Stylomastoid foramen Digastric branch Stylohyoid branch Posterior auricular branch Nerve to stapedius Chorda tympani nerve Lingual nerve Taste fibers To sublingual gland To submandibular gland Temporal Zygomatic Buccal Mandibular Cervical Facial motor branches Nuclear and infranuclear control (647) the facial motor nucleus lies ventral and lateral to the abducens nucleus in the lower pons. From the facial nucleus, all the nerve fibers that innervate the ipsilateral facial muscles ascend posteriorly and medially to hook around the abducens nucleus (genu of the facial nerve) before travelling forward through the pons (just lateral to the corticospinal tract), to emerge from the ventrolateral aspect of the brainstem. The nerve has four segments within the temporal bone: Meatal segment: this segment extends from the porus of the internal auditory canal to the meatal foramen. The nerve proceeds vertically to the stylomastoid foramen where it exits the cranium. Near the exit site at the stylomastoid foramen, the facial nerve gives off the posterior auricular nerve, which supplies auricular muscles and the occipitalis, the digastric branch, and the stylohyoid branch. This division of the facial nerve carries: Sensory fibers that carry taste sensation from the anterior two-thirds of the tongue, afferents from the pharyngeal, nasal, and palatal mucosae, and from the skin of the external auditory canal, lateral ear, and post-auricular region. Somatic afferent fibers from the external auditory canal and post-auricular region end in the spinal nucleus of cranial nerve V. The preganglionic parasympathetic fibers originate in the superior salivatory nucleus at the level of the caudal pons; fibers that control lacrimation arise from the adjacent lacrimal nucleus.

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ArrhythmiaManifestations Approximately 10% of patients with myasthenia gravis have arrhythmia complications not explained by another etiology allergy medicine build up trusted allegra 180 mg. Manifestations included atrial fibrillation allergy testing kirkland wa order generic allegra, atrioventricular block, asystole, and unexplained sudden death. Patients treated with anticholinesterase agents can develop sinus bradycardia and heart block. If anticholinesterase agents cause symptomatic bradycardia, pacing may be required. It is unknown whether immunosuppressive agents or thymectomy improve cardiac disease. Acute Cerebrovascular Disease CardiacPathophysiology Cardiac abnormalities including life-threatening arrhythmias occur in acute cerebrovascular disease including subarachnoid hemorrhage, other stroke syndromes, and head injury. Hypothalamic stimulation reproduces the electrocardiographic changes observed in acute cerebrovascular disease. Electrocardiographic changes associated with hypothalamic stimulation or blood in the subarachnoid space can be prevented with spinal cord transection, stellate ganglion blockade, vagolytics, and adrenergic blockers. In some cases, acute cerebrovascular disease can be associated with the clinical picture of takotsubo cardiomyopathy. Electrocardiographic abnormalities are observed in up to 80% of patients with a higher risk in those with more severe neurologic injury. Bradycardia with sinoatrial block, sinus arrest, and atrioventricular block can occur. Ventricular tachycardia including torsades de pointes and ventricular fibrillation have been reported. Stroke syndromes other than subarachnoid hemorrhage are associated with abnormal electrocardiograms, but it is unclear whether these are related to the stroke syndrome or underlying cardiac disease. Bradycardias are less common in stroke syndromes other than subarachnoid hemorrhage. TreatmentandPrognosis Life-threatening arrhythmias occur primarily in the first 24 hours following a neurologic event. Monitoring of potassium levels especially in patients with subarachnoid hemorrhage is warranted. Stellate ganglion blockade has been reported to control refractory ventricular arrhythmias effectively. Patients with epilepsy are at an increased risk of sudden death of unknown cause that has been termed sudden unexpected death in epilepsy. Sudden unexpected death is a frequent cause of premature mortality in epilepsy with, an incidence varying from 0. Central or obstructive apnea, excessive respiratory secretions, acute pulmonary edema, and arrhythmias could all be involved. ArrhythmiaManifestations Sinus arrest and asystole during the periictal period was observed in 21% of patients with poorly controlled epilepsy who were undergoing long-term rhythm monitoring with an insertable loop recorder. Risk factors for sudden unexpected death in epilepsy include a higher seizure frequency, earlier onset, and longer duration of epilepsy, and the need for three or more antiepileptic drugs. TreatmentandPrognosis Primary arrhythmia disorders should be considered in the differential diagnosis of epilepsy. Patients with poorly controlled epilepsy require treatment in a tertiary epilepsy center. Nighttime supervision of the epileptic patient can decrease the risk of sudden death. Permanent pacing should be considered in the epileptic patient with documented peri-ictal bradycardia. Rau F, Freyermuth F, Fugier C, et al: Misregulation of miR-1 processing is associated with heart defects in myotonic dystrophy. Nigro V, Aurino S, Piluso G: Limb girdle muscular dystrophies: update on genetic diagnosis and therapeutic approaches. Weidemann F, Rummey C, Bijnens B, et al: the heart in Friedreich ataxia: definition of cardiomyopathy, disease severity, and correlation with neurologic symptoms. Wahbi K, Larue S, Jardel C, et al: Cardiac involvement is frequent in patients with the m. Das M, Gonsalves S, Saha A, et al: Acute subarachnoid haemorrhage as a precipitant for takotsubo cardiomyopathy: a case report and discussion. Major causes of proarrhythmia include direct pharmacologic effects on ion channels of the heart. In addition, certain drugs can cause a cardiomyopathy that ultimately leads to ventricular tachyarrhythmias-specifically, ventricular tachycardia. The proportion of patients with proarrhythmia that initially manifests as sudden death, and the extent to which proarrhythmia contributes to the overall problem of sudden death, are unknown. General treatment guidelines focus on avoidance of drug treatment in high-risk patients, recognition of the syndromes of drug-induced proarrhythmia, and withdrawal of the culprit agents. The latter most commonly occurs when the culprit drug is eliminated by a single metabolizing pathway. If this pathway is susceptible to inhibition by the administration of a second drug, inhibited by coadministration of other drugs or by genetic factors, marked elevation of drug concentrations and electrophysiological toxicity can result. A subset of the population absolutely lacks catalytic activity, so that plasma concentrations of substrate drugs are much higher in such "poor metabolizer" patients. Genetic Predisposition Administration of a drug can unmask a subclinical (forme fruste) monogenic arrhythmia syndrome. In these monogenic syndromes, penetrance of the electrocardiographic phenotype can be highly variable, an effect often attributed to unidentified modifier genes. In addition, genetic polymorphisms can increase the risk for drug-induced sudden cardiac death.

Syndromes

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The host immune response causes inflammation allergy medicine without antihistamine generic allegra 120 mg without prescription, with a neutrophil and cytokine response allergy testing geelong buy generic allegra 120 mg on-line. Acute inflammation of the leptomeninges with purulent exudates is seen grossly (423) and on microscopic examination of tissue specimens (424). Only 40­50% of patients present with all of the classic signs, but 95% display at least two and almost all have at least one4. Other signs include cranial nerve palsies and sensorineural deafness, particularly later in the course of disease. Therefore, delirium, confusion, and focal deficits are common early in the course of disease. While the presence of rash is nonspecific, it occurs in 10­60% of patients with invasive N. Nuchal rigidity can usually be elicited with a simple chin-to-chest maneuver, with the patient displaying resistance to passive flexion of the neck. However, imaging studies should not delay initiation of empiric antibiotic therapy. If there is an indication to continue therapy, a trough should be measured prior to the third or fourth dose, with the goal of 15­20 µg/ml. If there is an indication to continue therapy, a trough should be measured prior to the third or fourth dose, with the goal of 15 to 20 µg/ml. Empiric therapy generally consists of ampicillin plus gentamicin, which also treats Listeria spp; however, enteric Gram-negatives such as Escherichia coli are frequently resistant to ampicillin. Many experts include cefotaxime in the initial empiric regimen, particularly if the onset of meningitis occurs after the first week of life. A total of 14­21 days of therapy should be completed, depending upon the pathogen, and infectious diseases consultation is recommended. Supportive care should be provided with antipyretics, aggressive intravenous fluid management, maintaining a patent airway, and antiepileptics if seizures occur. Risk factors include head and neck infections, trauma, neurosurgery, immunocompromise, and bacteremia from any source. It is not a reportable infectious disease, so the incidence is difficult to quantify. Depending upon the epidemiologic setting, other protozoa, helminths, and mycobacteria must be kept in mind. Despite the fact that Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, and Listeria monocytogenes are common pathogens seen in bacterial meningitis, they are uncommon causes of brain abscess. Prognosis Risk factors for death include: age 60 years old, hypotension, altered mental status, leukopenia, thrombocytopenia, or seizures within the first 24 hours. Other neurologic sequelae include seizures, focal neurologic deficits, and cerebrovascular abnormalities. Infections of the central nervous system 427 Multiple abscesses in the watershed vascular areas of the brain are more typically the result of septic emboli from hematogenous spread. Clinical features Most of the presenting clinical features of brain abscess result from the space-occupying lesion itself, and the specific signs and symptoms are a manifestation of the size and location of the abscess as well as the virulence of the pathogen(s) involved. Pathology Histologic findings depend upon whether the infection is acute or chronic. However, liquefaction occurs over the first 2­3 weeks, followed by organization inside a fibrotic capsule. Gram stains, acid-fast, and modified acid-fast smears, fungal staining, and cultures often reveal a pathogen when abscess material is sent to the microbiology laboratory. E It is appropriate, therefore, to presumptively treat a patient presenting with this clinical syndrome for toxoplasmic encephalitis. Infections of the central nervous system 429 Treatment Adequate, curative therapy often involves a combination of surgical drainage and antibiotic therapy. Stereotactic aspiration or open resection is often necessary for diagnosis and also may be therapeutic. Stereotactic needle aspiration through a burr hole is safer and therefore may be the prudent choice over open surgical excision18. However, the annual incidence of syphilis began increasing in the year 2001 and reached 7. After direct contact with abraded skin or an intact mucous membrane, spirochetes enter the local lymphatics and bloodstream, disseminating to multiple organ systems. After approximately 3 weeks, a primary chancre develops, which contains many spirochetes. The clinician should consider whether the patient has early (first year) or late (after 1 year) syphilis. Primary the patient develops a painless papule at the site of inoculation, which develops into a chancre with a smooth base and raised, firm borders. A chancre does not develop in every case, and may go unnoticed due to its painless nature. Like other spirochete syndromes, syphilis is divided into discrete clinical stages with characteristic manifestations; however, neurosyphilis can occur during any phase of illness. The lesions are bilaterally symmetric, pale red/ pink, nonpruritic, discrete, round macules, about 5­10 mm (0. Secondary Disseminated infection develops 6­12 weeks after inoculation, although it can occur earlier, with the primary chancre still present25. This stage is characterized by a diffuse rash consisting of nonpruritic macules, papules, or pustules, often involving the palms and soles (428­431), and mucocutaneous lesions. Symptoms of meningitis, such as headache, nuchal rigidity, and photophobia, are common. Meningeal inflamation can be either diffuse (leptomeningitis) or can present as more focal inflammatory areas called syphilitic gummas.

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Males usually exhibit a rise of serum uric acid levels from puberty allergy testing logan utah generic allegra 180 mg fast delivery, a reason for higher preponderance in males allergy symptoms after running cheap allegra 180 mg overnight delivery. Females exhibit little change in serum uric acid concentrations until menopause, when uric acid levels rise and reach values equal to that of men. Diet rich in meat and sea food carries high-risk of gout whereas intake of dairy foods lower the serum urate levels. Drugs causing gout by increasing urate levels are diuretics, intravenous heparin, cyclosporine. The basic pattern of clinical gout begins with acute attacks of intensely painful arthritis. The first attack is usually monoarticular and associated with few constitutional symptoms. Attacks occurring later are associated with polyarticular, long lasting, slow and incomplete resolution. Acute attacks rarely affects shoulders, hips, spine, sacroiliac joints, sternoclavicular joints or temporomandibular joints. Acute gout affecting up to three sites occurs in one-third of cases and occurrence of four or more sites simultaneously is a rarity. Within a few hours, the affected becomes dusky red, hot, swollen and extremely tender. The term "intercritical gout" has been applied to the periods between gouty attacks. Radiological changes may occur in intercritical period also even though there are no signs of tophi. Aspiration of synovial fluid is a useful adjunct to diagnose gout in intercritical period. Later attacks are less explosive in onset, polyarticular, more severe and lasts longer, resolve more slowly progressing into a chronic and crippling phase of arthritis. After a series of acute gouty attacks with intercritical period, individual enters the chronic phase, which is characterized by polyarticular presentation, increased symptom tolerance and absence of pain free intercritical period. Ten years after the first attack, about half are free of tophi with the other half having minimal tophi. Twenty years after first attack, 28% are free of tophi and 2% have severe crippling disease. A chronic inability to eliminate hyperuricemia leads to expanding urate pool, deposition of urate crystals in cartilage, synovium, tendons, soft tissues and elsewhere. They are more likely in gout secondary to myeloproliferative diseases, juvenile gout occurring in metabolic diseases like glycogen storage diseases. Tophi can occur in a variety of locations producing irregular, asymmetric, moderately discrete tumescence of involved joint. Tophi also involve cartilage (anthelix of pinna), bursae (olecranon bursa), tendons (Achilles tendon). Tophi themselves are painless but acute inflammation around them causes pain and eventual destruction causing bizarre deformities. Radiographic changes, particularly erosions with sclerotic margins and overhanging edges of bone occur with development of tophi. According to American College of Rheumatology, criteria used for a presumptive diagnosis include a triad of acute monoarticular arthritis, hyperuricemia, dramatic response to colchicine therapy. The presence of hyperuricemia in the absence of typical clinical picture of gout is not always an indication for antihyperuricemic therapy. Rather, the presence of asymptomatic hyperuricemia indicates the presence of a previously unsuspected disorder which should be investigated and treated like metabolic syndrome. Thus, the common practice is not to treat asymptomatic hyperuricemia until symptoms develop. The only indication to treat asymptomatic hyperuricemia is uric acid more than 10 mg/dL or in a patient who is receiving chemotherapy. The attack of acute gout can be successfully terminated by early initiation of treatment. The doses can be increased to 50 to 75 mg initial dose followed by 50 mg every 6 to 8 hours with a maximum dose of 200 mg in the first 24 hours. The drugs include naproxen, fenoprofen, ibuprofen, piroxicam, ketoprofen, and ketorolac. Prophylaxis is used until there are no attacks for 3 to 6 months and serum urate levels are well in normal limits. However, almost invariably this is preceded by a period of recurrent monoarthritis in the past. There was no positional variation and the symptoms were progressively getting bad and he was unable to sleep. Decreased levels Primarypolycythemia Anemias secondary to inflammation, rheumatoid arthritis and neoplasms Renalfailure. It is a clonal disorder which results in increase in red cell production independent of stimulation by erythropoietin. Up to 50% patients have non-specific complaints like weight loss, sweating, headache, visual complaints, fatigue related to low blood Ringing in Ears in Young Man 131 flow due to increased velocity. Phlebotomy should be considered in all patients with target hematocrit less than 45%. Usually 500 mL of blood is removed every 1 to 2 days till hematocrit is less than 45%. Hydroxyurea should be given to high risk polycythemia vera (age > 65 years, prior thrombosis). Patient should be instructed to stop smoking, control hypertension and diabetes which are also risk for thrombosis. Physiopathology, Etiologic Factors, Diagnosis, and Course of Polycythemia Vera as Related to Therapy According to William Dameshek, 1940-1950.

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