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- Volume 48, 1997
Annual Review of Medicine - Volume 48, 1997
Volume 48, 1997
- Review Articles
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THROMBOPOIETIN: UNDERSTANDING AND MANIPULATING PLATELET PRODUCTION
Vol. 48 (1997), pp. 1–11More Less▪ AbstractUntil recently, platelet production was the least understood aspect of blood cell development. This gap in our understanding resulted from the scarcity of megakaryocytes, the marrow precursor of blood platelets, and from confusion surrounding the cytokines and hormones that support their development. The recent cloning and characterization of thrombopoietin (TPO) has profoundly changed our udnerstanding of platelet production. Using in vitro assay systems, several groups have shown that TPO supports the proliferation of megakaryocytic progenitor cells and their differentiation into mature platelet-producing cells. Moreover, and somewhat surprisingly, TPO also acts in synergy with other pluripotent cytokines on the hematopoietic stem cell to augment development of erythroid and myeloid progenitors. These in vitro effects correlate well with the in vivo biology of the hormone. When administered to normal animals, TPO expands the numbers of hematopoietic progenitors of all lineages and greatly accelerates platelet production. Moreover, when TPO or its receptor is genetically eliminated, progenitor cell levels of all lineages are reduced, and platelet production is profoundly impaired. In animals administered cytoreductive therapy, the use of TPO is associated with accelerated hematopoietic recovery, not only of megakaryocytes and platelets, but also of erythrocytes and leukocytes. It, thus, is hoped that TPO may play an important role in reducing the myelosuppressive complications of naturally occurring and iatrogenic states of marrow failure.
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BASIC DETERMINANTS OF MYOCARDIAL HYPERTROPHY: A Review of Molecular Mechanisms1
Vol. 48 (1997), pp. 13–23More Less▪ AbstractThe essential cardiac response to a fixed increase in hemodynamic load is an increase in cardiac mass. If the load increase is neither too severe initially nor indefinitely progressive, cardiac stress is renormalized, and compensated hypertrophy ensues. But hypertrophic compensation is often abrogated by progressively abnormal contractile performance per unit mass of myocardium, even when function at the organ level is maintained by the mass increase itself. That is, even when hypertrophy is appropriate to the load imposed, and in a manner analogous to dystrophic growth of skeletal muscle, specific phenotypic changes occurring during this growth response render compensation imperfect such that congestive heart failure ensues. This fact, and the fact that the presence of deleterious phenotypic changes in hypertrophied myocardium is critically dependent on the type of hemodynamic load imposed, mandates that cardiac hypertrophy be understood on the most basic level as a growth process if early, definitive interventions to prevent congestive heart failure following pathological hemodynamic overloads are to be realized.
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INFECTIVE ENDOCARDITIS CAUSED BY HACEK MICROORGANISMS
Vol. 48 (1997), pp. 25–33More Less▪ AbstractThe HACEK group of fastidious gram-negative organisms is a recognized but unusual cause of infective endocarditis, responsible for approximately 3% of cases. We report our experience with 45 cases of endocarditis caused by HACEK organisms. In Olmsted County, Minnesota, the incidence of HACEK endocarditis was 0.14 per 100,000 person-years. In patients with native valves, 33 cases occurred, and in patients with prosthetic valves, 12 cases occurred. The most common presenting symptoms were fever, splenomegaly, new or changing murmur, and microvascular phenomena. Symptoms were present in the majority of patients anywhere from two weeks to six months prior to diagnosis. Blood cultures became positive in a mean of 3.375 days, and therapy with a beta-lactam alone or as part of a combination was given for anywhere between three and six weeks. Within the first month of diagnosis, surgery was performed for 13 regurgitant valves in 11 patients (24%). Echocardiography was an insensitive predictor of subsequent major arterial embolization (odds ratio, 1.33; 95% confidence interval, 0.31–5.67). The overall survival in our cohort of patients was 87%. These results confirm previous reports that HACEK endocarditis portends a favorable prognosis.
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GENOMIC IMPRINTING: Nature and Clinical Relevance
Vol. 48 (1997), pp. 35–44More Less▪ AbstractMolecular genetic techniques allow investigators to trace chromosomes and genes from parent to child and, in a single individual, from tissue to tissue. These techniques have uncovered a new type of gene control in which the allele from one parent is expressed and the allele from the other parent is not. This differential expression is called genomic imprinting. It may lead to phenotypic differences when inheritance is from the mother versus the father. Genomic imprinting has been observed in a number of disorders having to do with growth, behavior, and abnormal cell growth. It is important to be aware that such a phenomenon exists and to consider it when making diagnoses and determining therapy.
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ACTIVATED PROTEIN C RESISTANCE DUE TO A COMMON FACTOR V GENE MUTATION IS A MAJOR RISK FACTOR FOR VENOUS THROMBOSIS
Vol. 48 (1997), pp. 45–58More Less▪ AbstractInherited resistance to activated protein C (APC) was recently discovered to be a cause of familial thrombophilia and is now known to be the most common genetic risk factor for venous thrombosis. It is caused by a single point mutation in the gene for factor V, which predicts substitution of arginine (R) at position 506 with a glutamine (Q). Accordingly, the activated form of mutated factor V (FVa:Q506) is more slowly degraded by activated protein C than normal FVa (FVa:R506) is, resulting in hypercoagulability and a lifelong 5- to 10-fold increased risk of venous thrombosis. Previously known inherited hypercoagulable states, i.e. deficiencies of the anticoagulant proteins antithrombin III, protein S, and protein C, are found in fewer than 10–15% of thrombosis patients in western countries, whereas inherited APC resistance is present in 20–60% of such patients. The FV mutation is common in populations of Caucasian origin, with prevalences ranging from 1–15%, whereas it is not found in certain other ethnic groups such as Japanese and Chinese. The high prevalence of APC resistance, in combination with the availability of simple laboratory tests, will have a profound influence on the development of therapeutic and prophylactic regimens for thrombosis and will, it is hoped, result in a decreased incidence of thromboembolic events.
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PARVOVIRUS B19 IN HUMAN DISEASE1
Vol. 48 (1997), pp. 59–67More Less▪ AbstractParvovirus B19, the only known human pathogenic parvovirus, is associated with a wide range of disease manifestations. In healthy individuals, the major presentation of B19 infection is erythema infectiosum. In patients with underlying hemolytic disorders, infection is the primary cause of transient aplastic crisis. In immunosuppressed patients, persistent infection may develop that presents as pure red cell aplasia and chronic anemia. In utero infection may result in hydrops fetalis or congenital anemia. Diagnosis is based on examination of bone marrow and virologic studies. Much is known of the pathophysiology of the virus, and studies are in progress to develop a vaccine to prevent this widespread infection.
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CURRENT STATUS OF THE SURGICAL TREATMENT OF PATIENTS WITH CAROTID ARTERY DISEASE: The Surgical Management of Carotid Atherosclerosis
Vol. 48 (1997), pp. 69–77More Less▪ AbstractPatients with carotid atherosclerotic disease present with a history of a neurologic event or with the presence of a bruit on physical examination. Recently, large randomized prospective studies have examined this group of patients to determine the optimal course of medical and surgical management. The data from these studies, together with the natural history of carotid disease and factors associated with stroke risk, are reviewed.
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LOW-MOLECULAR-WEIGHT HEPARIN: Prophylaxis and Treatment of Venous Thromboembolism
Vol. 48 (1997), pp. 79–91More Less▪ AbstractIntravenous heparin followed by warfarin has been the classical anticoagulant therapy of acute venous thromboembolism for the last 30 years. Furthermore, low-dose unfractionated heparin given two to three times daily has been the most popular form of prophylaxis for venous thrombosis. In recent years, a number of low-molecular-weight heparins have become available for clinical trials. These agents have many advantages over unfractionated heparin and are now being used widely internationally for the prevention and treatment of venous thromboembolism. Indeed, low-molecular-weight heparin will undoubtedly replace intravenous unfractionated heparin not only in the treatment of venous thromboembolism, but in other conditions where heparin therapy is indicated. Whether or not the low-molecular-weight heparins can decrease or eliminate some of the complications of unfractionated heparin will depend on the outcome of future clinical trials.
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USE OF INTRAVENOUS IMMUNOGLOBULIN TO PREVENT OR TREAT INFECTIONS IN PERSONS WITH IMMUNE DEFICIENCY
Vol. 48 (1997), pp. 93–102More Less▪ AbstractIntravenous immunoglobulin (IVIG) concentrates were originally developed as replacement therapy for individuals with primary deficiencies of the immune system. However, in various well-designed, controlled clinical trials, the ability of IVIG to prevent and possibly treat infections in patients with secondary immune deficiencies has also been considered. In this review, we briefly consider these different applications and suggest whether the data are sufficient to employ IVIG in these clinical settings.
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BETA-ADRENERGIC BLOCKING AGENTS IN THE TREATMENT OF CONGESTIVE HEART FAILURE: Mechanisms and Clinical Results
Vol. 48 (1997), pp. 103–114More Less▪ AbstractCongestive heart failure is a major public health problem in Western countries. Despite current treatment including angiotensin converting enzyme inhibitors, mortality and morbidity remain high. The sympathetic nervous system is markedly activated in heart failure, and inhibition of this system with the beta-adrenergic blocking agents may provide further benefit. Several clinical trials involving over 3000 patients have shown that beta-blocker therapy improves left ventricular function in patients with heart failure. However, the effects of such therapy on symptoms and exercise tolerance have been variable. Recent reports have suggested that survival is improved with the beta-blocker carvedilol. Large-scale, long-term clinical trials are required to confirm these findings and to clearly define the role of this promising therapy for patients with heart failure.
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HYPERTENSION IN PREGNANCY: Current Concepts of Preeclampsia
Vol. 48 (1997), pp. 115–127More Less▪ AbstractHypertensive disorders (gestational hypertension, preeclampsia, chronic hypertension, superimposed preeclampsia) are the most common medical complications of pregnancy and constitute a major cause of maternal and perinatal morbidity and mortality. Prediction of those women destined to develop preeclampsia remains elusive. The benefits of calcium supplementation for prevention of preeclampsia are encouraging; however, the definitive study is not yet complete. Aspirin therapy for low-risk women has not been helpful; results of therapy for high-risk women are pending. More experience is being gained with antihypertensive therapy and expectant management in severe preeclampsia. Conservative management of severe preeclampsia, when performed in a tertiary care center, may benefit a select group of women and their fetuses.
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RU486 (MIFEPRISTONE): Mechanisms of Action and Clinical Uses
Vol. 48 (1997), pp. 129–156More Less▪ AbstractRU486 (mifepristone) has proved to be a remarkably active antiprogesterone and antiglucocorticosteroid agent in human beings. The mechanism of action involves the intracellular receptors of the antagonized hormones (progesterone and glucocorticosteroids). At the molecular level, the most important features are high binding affinity to the receptor, interaction of the phenylaminodimethyl group in the 11β-position with a specific region of the receptor binding pocket, and RU486-induced transconformation differences in the ligand-binding domain. These particularities have consequences at different steps of the receptor function as compared with agonists. However, the reasoning cannot be limited to the RU486-receptor interaction, and, for instance, there is the possibility of a switch from antagonistic property to agonist activity, depending on the intervention of other signaling pathways. It would be desirable to have derivatives with only one of the two antagonistic properties (antiprogestin, antiglucocorticosteroid) in spite of similarities between steroid structures, receptors involved, and responsive machineries in target cells. Clinically, the RU486-plus-prostaglandin method is ready to be used on a large scale and is close to being as convenient and safe as any medical method of abortion may be. The early use of RU486 as a contragestive as soon as a woman fears a pregnancy she does not want will help to defuse the abortion issue. Research should now be conducted to define an efficient and convenient contraceptive method with RU486 or other antiprogestins. The usefulness of RU486 for obstetric indications, including facilitation of difficult delivery, has to be assessed rapidly. Gynecologic trials, particularly in leiomyomata, should also be systematically continued. The very preliminary results obtained with tumors, including breast cancers, indicate that further studies are necessary.
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PARANEOPLASTIC SYNDROMES AFFECTING THE CENTRAL NERVOUS SYSTEM
Vol. 48 (1997), pp. 157–166More Less▪ AbstractParaneoplastic syndromes affecting the nervous system are rare neurologic syndromes caused by cancer but not ascribable to metastases. Any portion of the nervous system may be involved in a paraneoplastic syndrome. The pathogenesis of these disorders appears to be an immune reaction against antigens shared by the cancer and the nervous system. Some disorders, such as the Lambert-Eaton myasthenic syndrome, are effectively treated by removal of autoantibodies directed against the presynaptic cholinergic synapse. In other disorders, such as paraneoplastic cerebellar degeneration or paraneoplastic sensory neuronopathy, neither removal of the autoantibody nor treatment of the cancer is effective.
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BONE DISEASE IN MODERATE RENAL FAILURE: Cause, Nature, and Prevention
Vol. 48 (1997), pp. 167–176More Less▪ AbstractThere are two primary types of bone disorders observed in patients with end-stage renal disease: a high-turnover osteodystrophy characterized by osteitis fibrosa, and a low-turnover osteodystrophy characterized initially by osteomalacia and, more recently, by adynamic or aplastic bone disease. This article reviews the clinical presentation, pathogenesis, and laboratory findings of patients with these two disorders. It discusses the important roles of phosphorus binding, vitamin D administration, and correction of acidosis in prevention and treatment of bone disease in patients with moderate renal insufficiency.
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MANAGEMENT OF BENIGN PROSTATIC HYPERPLASIA
Vol. 48 (1997), pp. 177–189More Less▪ AbstractBenign prostatic hyperplasia (BPH) is a common cause of morbidity among older men. Primary care physicians need to develop expertise in its management. The causes of BPH are unknown; aging and the presence of male androgens are the dominant risk factors. Obtaining a medical history is a key step in assessing whether lower urinary tract symptoms are due to BPH or to some other process. A reliable and valid seven-item questionnaire has been developed to objectively assess symptom severity. A focused physical examination including a digital rectal exam should be performed, as well as a urinalysis and serum creatinine. Optional tests include uroflowmetry, post-void residual urine, and prostate-specific antigen measurements. BPH is treated primarily to improve the quality, rather than increase the quantity, of life. Optimal decisions about treatment are best made by a clinician and an informed patient working together.
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ADJUVANT TREATMENT OF COLORECTAL CANCER
Vol. 48 (1997), pp. 191–202More Less▪ AbstractThe adjuvant therapy of colorectal cancer has seen many important advances in recent years. Chemotherapy improves long-term disease-free survival rates in high-risk patients with resected colon cancer. Combined modality therapy, using surgery, radiation therapy, and chemotherapy, improves both local control and survival in patients with stage II and III rectal cancer. We examine in detail the data on which current recommendations for adjuvant treatments are based. We also review some of the more promising experimental approaches currently under investigation.
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TOWARD CYSTIC FIBROSIS GENE THERAPY
Vol. 48 (1997), pp. 203–216More Less▪ AbstractCystic fibrosis (CF) is a common genetic disorder characterized by defective epithelial chloride transport and progressive lung disease. Although great strides have been made in the treatment of CF, it remains lethal, often by early adulthood. CF is one of the most extensively researched genetic diseases as a target for gene therapy development. It may also serve as an important model for gene therapy of other diseases. Preclinical and clinical research has lead to the rapid development of a variety of vectors designed to correct the basic defect in CF, including adenovirus, adeno-associated virus, and liposomes. Clinical studies have identified the host immune response and low vector efficiency as key impediments to effective CF gene therapy. Further research promises to refine vector technology and bring CF gene therapy to the bedside.
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NEUROPSYCHIATRIC CONSEQUENCES OF STROKE
Vol. 48 (1997), pp. 217–229More Less▪ AbstractNumerous emotional and behavioral disorders occur following cerebrovascular lesions. Depression is the most common of these, affecting up to 40% of patients. Clinical correlates of post-stroke depression include severity of physical and cognitive impairment as well as location of brain injury. Perhaps the most compelling reason to identify post-stroke depression, however, is its substantial impact on recovery in activities of daily living, cognitive function, and survival. Antidepressant medication has been shown to effectively treat depression, although its administration may require careful clinical monitoring. Other post-stroke emotional/behavioral disorders include mania, bipolar disorder, anxiety disorder, apathy, and pathological crying. Controlled studies have not documented the effect of these disorders on long-term recovery, but the potential impact of syndromes such as mania and apathy on rehabilitation efforts or pathological crying on social functioning are evident. With the exception of pathological crying, which has been shown to respond to antidepressant drug therapy, the other post-stroke emotional/behavioral disorders need to be evaluated in controlled treatment trials for response to therapy.
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GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance
Vol. 48 (1997), pp. 231–240More Less▪ AbstractMineralocorticoid and glucocorticoid receptors act as homodimers via canonical pentadecamer hormone response elements to regulate transcription. Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown also to modulate AP-1- and NFκB-induced transcription by direct protein-protein interactions. The role of 11β-hydroxysteroid dehydrogenase in conferring aldosterone specificity on epithelial mineralocorticoid receptors has been proven by the demonstration of sequence mutations in all cases of apparent mineralocorticoid excess examined to date. The autosomal form of aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect loss-of-function mutations in epithelial sodium channel subunit sequence. (Patho)physiological roles for aldosterone and glucocorticoid membrane receptors, and for the recently described nuclear receptors for 11–ketosteroids in 11β–hydroxysteroid dehydrogenase–protected epithelia, remain to be established.
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PERIPHERAL BLOOD STEM CELLS FOR AUTOGRAFTING
Vol. 48 (1997), pp. 241–251More Less▪ AbstractHigh-dose therapy with autologous hematopoietic progenitor cell support is effective treatment for patients with a variety of high-risk malignancies. Accelerating of marrow recovery from near-lethal or lethal toxicity with hematopoietic cell support improves the safety and cost effectiveness of the high-dose regimens. Peripheral blood progenitor cells will soon replace marrow as the major source of hematopoietic support. This chapter reviews the techniques of peripheral blood progenitor cell collection, mobilization, purification (for tumor removal), and ex vivo expansion.
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Previous Volumes
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Volume 76 (2025)
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Volume 75 (2024)
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Volume 74 (2023)
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Volume 73 (2022)
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Volume 72 (2021)
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Volume 71 (2020)
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Volume 70 (2019)
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Volume 69 (2018)
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Volume 68 (2017)
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Volume 67 (2016)
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Volume 66 (2015)
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Volume 65 (2014)
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Volume 64 (2013)
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Volume 63 (2012)
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Volume 62 (2011)
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Volume 61 (2010)
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Volume 60 (2009)
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Volume 59 (2008)
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Volume 58 (2007)
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Volume 57 (2006)
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Volume 56 (2005)
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Volume 55 (2004)
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Volume 54 (2003)
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Volume 53 (2002)
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Volume 52 (2001)
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Volume 51 (2000)
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Volume 50 (1999)
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Volume 49 (1998)
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Volume 48 (1997)
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Volume 47 (1996)
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Volume 46 (1995)
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Volume 45 (1994)
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Volume 44 (1993)
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Volume 43 (1992)
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Volume 42 (1991)
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Volume 41 (1990)
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Volume 40 (1989)
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Volume 39 (1988)
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Volume 38 (1987)
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Volume 37 (1986)
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Volume 36 (1985)
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Volume 35 (1984)
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Volume 34 (1983)
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Volume 33 (1982)
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Volume 32 (1981)
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Volume 31 (1980)
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Volume 30 (1979)
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Volume 29 (1978)
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Volume 28 (1977)
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Volume 27 (1976)
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Volume 26 (1975)
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Volume 25 (1974)
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Volume 24 (1973)
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Volume 23 (1972)
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Volume 22 (1971)
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Volume 21 (1970)
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Volume 20 (1969)
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Volume 19 (1968)
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Volume 18 (1967)
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Volume 17 (1966)
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Volume 16 (1965)
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Volume 15 (1964)
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Volume 14 (1963)
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Volume 13 (1962)
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Volume 12 (1961)
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Volume 11 (1960)
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Volume 10 (1959)
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Volume 9 (1958)
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Volume 8 (1957)
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Volume 7 (1956)
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Volume 6 (1955)
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Volume 5 (1954)
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Volume 4 (1953)
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Volume 3 (1952)
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Volume 2 (1951)
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Volume 1 (1950)
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Volume 0 (1932)