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- Volume 18, 1998
Annual Review of Nutrition - Volume 18, 1998
Volume 18, 1998
- Preface
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- Review Articles
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PERSONAL REFLECTIONS ON A GALVANIZING TRAIL
Vol. 18 (1998), pp. 1–18More Less▪ AbstractThis article encompasses my perception of, and experience in, an exciting segment of the trace element era in nutrition research: the role of zinc in the nutrition of animals and humans. Zinc has been a major player on the stage of trace element research, and it has left a trail that has galvanized the attention of many researchers, including myself. It is ubiquitous in biological systems, and it plays a multitude of physiologic and biochemical functions. A brief historical overview is followed by a discussion of the contributions the work done in my laboratory has made toward understanding the physiological and biochemical functions of zinc. The effort of 40 years has led to the belief that one of zinc's major roles, and perhaps its first limiting role, is to preserve plasma-membrane function as regards ion channels and signal transduction. Although substantial knowledge has been gained relating to the importance of zinc in nutrition, much remains to be discovered.
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BIOAVAILABILITY AND BIOCONVERSION OF CAROTENOIDS
Vol. 18 (1998), pp. 19–38More Less▪ AbstractFactors that influence the bioavailability of carotenoids and their bioconversion to retinol are species of carotenoids, molecular linkage, amount of carotenoids consumed in a meal, matrix in which the carotenoid is incorporated, effectors of absorption and bioconversion, nutrient status of the host, genetic factors, host-related factors, and mathematical interactions. In this paper, current knowledge of these factors is examined. Although data are not sufficiently comparable to allow an extensive systematic comparison of results, a number of conclusions can be drawn from the information available.
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CARNITINE METABOLISM AND ITS REGULATION IN MICROORGANISMS AND MAMMALS
Vol. 18 (1998), pp. 39–61More Less▪ AbstractIn procaryotes, l-carnitine may be used as both a carbon and nitrogen source for aerobic growth, or the carbon chain may be used selectively following cleavage of trimethylamine. Under anaerobic conditions and in the absence of preferred substrates, some bacteria use carnitine, via crotonobetaine, as an electron acceptor. Formation of trimethylamine and γ-butyrobetaine (from reduction of crotonobetaine) from l-carnitine by enteric bacteria has been demonstrated in rats and humans. Carnitine is not degraded by enzymes of eukaryotic origin. In higher organisms, carnitine has specific functions in intermediary metabolism. Concentrations of carnitine and its esters in cells of eukaryotes are rigorously maintained to provide optimal function. Carnitine homeostasis in mammals is preserved by a modest rate of endogenous synthesis, absorption from dietary sources, efficient reabsorption, and mechanisms present in most tissues that establish and maintain substantial concentration gradients between intracellular and extracellular carnitine pools.
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REDEFINING BODY COMPOSITION: Nutrients, Hormones, and Genes in Meat Production1
Vol. 18 (1998), pp. 63–92More Less▪ AbstractGrowth rate and body composition of livestock can be optimized to meet consumer needs for a leaner product and to improve the efficiency of meat-animal production. Optimization strategies have traditionally focused on genetic selection and cost-effective ration formulation to achieve the genetic potential. Advances in understanding the mechanisms of growth and its control have led to additional opportunities for its manipulation. These include nutritional manipulation, the use of growth promotants, and, more recently, the ability to change the genetic potential through genetic engineering. Selection of appropriate candidate genes for manipulation depends on understanding the mechanisms underlying differentiation and growth of embryonic muscle cells. Recent advances in genetic engineering techniques, including gene therapy and germline transgenesis, will likely hasten the genetic progress toward a leaner carcass in domestic livestock. Such strategies may prove to be more beneficial than the controlled enhancement of somatotropin expression.
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DIETARY OXIDATIVE STRESS AND THE POTENTIATION OF VIRAL INFECTION1
Vol. 18 (1998), pp. 93–116More Less▪ AbstractOxidative stress is implicated in the pathogenesis of several viral infections, including hepatitis, influenza, and AIDS. Dietary oxidative stress due to either selenium or vitamin E deficiency increases cardiac damage in mice infected with a myocarditic strain of coxsackievirus B3. Such dietary oxidative stress also allows a normally benign (i.e. amyocarditic) coxsackievirus B3 to convert to virulence and cause heart damage. This conversion to virulence is due to a nucleotide sequence change in the genome of the benign virus, which then resembles more closely the nucleotide sequence of virulent strains. Although it has been known for many years that poor nutrition can affect host response to infection, this is the first report of host nutrition affecting the genetic sequence of a pathogen. Further research is needed to determine whether poor host nutrition plays any role in the emergence of new viral diseases via alterations in the genotype of an infectious agent.
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DIETARY FRUCTANS
Vol. 18 (1998), pp. 117–143More Less▪ AbstractFructan is a general term used for any carbohydrate in which one or more fructosyl-fructose link constitutes the majority of osidic bonds. This review focuses on the fate of inulin-type fructans (namely native chicory inulin, oligofructose produced by the partial enzymatic hydrolysis of chicory inulin, and synthetic fructans produced by enzymatic synthesis from sucrose) in the gastrointestinal tract, as well as on their systemic physiological effects on mineral absorption, carbohydrate and lipid metabolism, hormone balance, and nitrogen homeostasis. The scientific evidence for the functional claims of inulin-type fructans is discussed, as well as their potential application in risk reduction of disease, namely constipation, infectious diarrhea, cancer, osteoporosis, atherosclerotic cardiovascular disease, obesity, and non-insulin dependent diabetes.
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NEWLY DISCOVERED REDOX COFACTORS: Possible Nutritional, Medical, and Pharmacological Relevance to Higher Animals
Vol. 18 (1998), pp. 145–177More Less▪ AbstractResearch spurred by the discovery of pyrroloquinoline quinone (PPQ) in 1979 led to the discovery of four additional oxidation-reduction (redox) cofactors, all of which result from transmogrification of amino acyl side chains in respective enzymes. These cofactors are (a) topa quinone in copper-containing amine oxidases, enzymes found in nearly all forms of life, including human; (b) lysyl topa quinone of the copper protein lysyl oxidase, an enzyme required for proper cross-linking of collagen and elastin; (c) tryptophan tryptophylquinone of alkylamine dehydrogenases from gram-negative soil bacteria; and (d) the copper-complexed cysteinyl-tyrosyl radical of fungal galactose oxidase. Originally, PQQ was thought to be a covalently bound cofactor in numerous enzymes from eukaryotes and prokaryotes. Today, PQQ is only found as a noncovalent cofactor in bacterial enzymes. The ubiquity of PQQ in the environment and its ready accessibility in the human diet has raised questions concerning its role as a vitamin, or an essential or helpful nutrient. The relevance to nutrition, medicine, and pharmacology of PQQ, topa quinone, lysyl topa quinone, tryptophan trytophylquinone, the galactose oxidase cofactor, and the enzymes harboring these cofactors are discussed in this review.
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GENETIC DISORDERS OF CARNITINE METABOLISM AND THEIR NUTRITIONAL MANAGEMENT1
Vol. 18 (1998), pp. 179–206More Less▪ AbstractCarnitine functions as a substrate for a family of enzymes, carnitine acyltransferases, involved in acyl-coenzyme A metabolism and as a carrier for long-chain fatty acids into mitochondria. Carnitine biosynthesis and/or dietary carnitine fulfill the body's requirement for carnitine. To date, a genetic disorder of carnitine biosynthesis has not been described. A genetic defect in the high-affinity plasma membrane carnitine-carrierin leads to renal carnitine wasting and primary carnitine deficiency. Myopathic carnitine deficiency could be due to an increase in efflux moderated by the carnitine-carrierout. Defects in the carnitine transport system for fatty acids in mitochondria have been described and are being examined at the molecular and pathophysiological levels. The nutritional management of these disorders includes a high-carbohydrate, low-fat diet and avoidance of those events that promote fatty acid oxidation, such as fasting, prolonged exercise, and cold. Large-dose carnitine treatment is effective in systemic carnitine deficiency.
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TRANSGENIC MICE IN THE ANALYSIS OF METABOLIC REGULATION
Vol. 18 (1998), pp. 207–232More Less▪ AbstractIn normal animals, the extracellular concentration of glucose is maintained within a very narrow range by the matching of glucose flux into and out of the extracellular space through the tightly coordinated secretion of insulin and glucagon. Functional alterations in β-cells, liver, or skeletal muscle and adipose tissue may disrupt glucose homeostasis and lead to the development of non–insulin-dependent diabetes mellitus (type 2 diabetes). This review outlines the contribution of these organs and tissues to the control of glucose homeostasis. We discuss new insights obtained through studies of transgenic mice that overexpress or show decreased expression of putative key genes in the regulation of pancreatic β-cell function, in the control of hepatic glucose uptake and output, and in the regulation of glucose uptake and utilization by skeletal muscle and adipose tissue.
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THE GENETICS OF OSTEOPOROSIS: Vitamin D Receptor Polymorphisms
Vol. 18 (1998), pp. 233–258More Less▪ AbstractOsteoporosis is a metabolic bone disease characterized by low bone mass and deterioration of bone tissue that leads to bone fragility and an increase in fracture risk. It is a disease with a complex etiology that includes genetic and environmental contributors. Environmental factors that influence bone density include dietary factors—such as intakes of calcium, alcohol, and caffeine—and lifestyle factors—such as exercise and smoking. Ethnic differences in the propensity to nontraumatic bone fracture suggest that genetic factors are important. Recently, common allelic variations in the vitamin D receptor gene have been found to be associated with bone mineral density in racially diverse population groups, as well as in prepubertal girls, young adult and postmenopausal women, and men. However, many studies have not been able to find this association. Additional approaches, such as sib-pair analysis, will probably be necessary in the future to identify the important genetic determinants of osteoporosis.
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LIPASES AND CARBOXYLESTERASES: Possible Roles in the Hepatic Metabolism of Retinol
Vol. 18 (1998), pp. 259–276More Less▪ AbstractThe formation and hydrolysis of retinyl esters are key processes in the metabolism of the fat-soluble micronutrient vitamin A. Long-chain acyl esters of retinol are the major chemical form of vitamin A (retinoid) stored in the body. Retinyl esters are found in a variety of tissues and cell types, but most of the total body retinoid is accounted for by the retinyl esters stored in the liver. Thus, these esters represent the major endogenous source of retinoid that can be delivered to peripheral tissues for conversion to biologically active forms. This review summarizes current knowledge about the identity, function, and regulation of the hepatic enzymes potentially involved in catalyzing the hydrolysis of retinyl esters. These enzymes include several known and characterized lipases and carboxylesterases. Although there is accumulating evidence that these enzymes function as retinyl ester hydrolases in vitro, it is not clear which play important physiological roles in hepatic retinyl ester metabolism.
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NUTRITIONAL PROPERTIES AND SIGNIFICANCE OF VITAMIN GLYCOSIDES
Vol. 18 (1998), pp. 277–296More Less▪ AbstractGlycosylated forms of pyridoxine, vitamin D, niacin, pantothenate, and riboflavin exist in nature, whereas glycosides of retinol and ascorbic acid are products of in vitro transglycosidation. β-Glucosides of pyridoxine (a) are prevalent in plant-derived foods, (b) contribute to human nutrition as partially available sources of vitamin B6, (c) undergo partial hydrolysis by a novel mammalian cytosolic β-glucosidase, and (d) exert a weak antagonistic effect on the utilization of free pyridoxine. Niacin exists in grains as complexed forms with low bioavailability, whereas vitamin D glycosides are toxic components of certain calcinogenic plants of importance in animal health. Glycosides of pantothenate and riboflavin appear to be minor products of mammalian metabolism. Glycosylation of retinol or other hydrophobic alcohols may facilitate glycolipid turnover, whereas a stable ascorbyl glucoside may have nutritional applications. Glycosylation of vitamins exerts widely ranging chemical and biological effects, with great nutritional and metabolic significance.
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PLASMA LIPID TRANSFER PROTEINS, HIGH-DENSITY LIPOPROTEINS, AND REVERSE CHOLESTEROL TRANSPORT
Vol. 18 (1998), pp. 297–330More Less▪ AbstractCholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP) are members of the lipid transfer/lipopolysaccharide binding protein gene family. Recently, the crystal structure of one of the members of the gene family, bactericidal permeability increasing protein, was solved, providing potential insights into the mechanisms of action of CETP and PLTP. These molecules contain intrinsic lipid binding sites and appear to act as carrier proteins that shuttle between lipoproteins to redistribute lipids. The phenotype of human CETP genetic deficiency states and CETP transgenic mice indicates that CETP plays a major role in the catabolism of high-density lipoprotein (HDL) cholesteryl esters and thereby influences the concentration, apolipoprotein content, and size of HDL particles in plasma. PLTP also appears to have an important role in determining HDL levels and speciation. Recent data indicate that genetic CETP deficiency is associated with an excess of coronary heart disease in humans, despite increased HDL levels. Also, CETP expression is anti-atherogenic in many mouse models, even while lowering HDL. These data tend to support the reverse cholesterol transport hypothesis, i.e. that anti-atherogenic properties of HDL are related to its role in reverse cholesterol transport. Recently, another key molecule involved in this pathway was identified, scavenger receptor BI; this mediates the selective uptake of HDL cholesteryl esters in the liver and thus constitutes a pathway of reverse cholesterol transport parallel to that mediated by CETP. Reflecting its role in reverse cholesterol transport, the CETP gene is up-regulated in peripheral tissues and liver in response to dietary or endogenous hypercholesterolemia. An analysis of the CETP proximal promoter indicates that it contains sterol regulatory elements highly homologous to those present in 3-hydroxy-3-methylglutaryl-coenzyme A reductase; the CETP gene is transactivated by the binding of SREBP-1 to these elements. A challenge for the future will be the manipulation of components of the reverse cholesterol transport pathway, such as CETP, PLTP, or scavenger receptor BI for therapeutic benefit.
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NUTRITIONAL AND HORMONAL REGULATION OF ENZYMES IN FAT SYNTHESIS: Studies of Fatty Acid Synthase and Mitochondrial Glycerol-3-Phosphate Acyltransferase Gene Transcription
Hei Sook Sul, and Dong WangVol. 18 (1998), pp. 331–351More Less▪ AbstractThe activities of critical enzymes in fatty acid and triacylglycerol biosynthesis are tightly controlled by different nutritional, hormonal, and developmental conditions. Feeding previously fasted animals high-carbohydrate, low-fat diets causes a dramatic induction of enzymes—such as fatty acid synthase (FAS) and mitochondrial glycerol-3-phosphate acyltransferase (GPAT)—involved in fatty acid and triacylglycerol synthesis. During fasting and refeeding, transcription of these two enzymes is coordinately regulated by nutrients and hormones, such as glucose, insulin, glucagon, glucocorticoids, and thyroid hormone. Insulin stimulates transcription of the FAS and mitochondrial GPAT genes, and glucagon antagonizes the insulin effect through the cis-acting elements within the promoters and their bound trans-acting factors. This review discusses advances made in the understanding of the transcriptional regulation of FAS and mitochondrial GPAT genes, with emphasis on elucidation of the mechanisms by which multiple nutrients and hormones achieve their effects.
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CYCLIC AMP SIGNALING AND GENE REGULATION
Vol. 18 (1998), pp. 353–383More Less▪ AbstractCyclic adenosine monophosphate (cAMP) is a ubiquitous second messenger produced in cells in response to hormones and nutrients. The production of cAMP is dependent upon the actions of many different proteins that affect its synthesis and degradation. An important function of cAMP is to activate the phosphorylating enzyme, protein kinase A. The key roles of cAMP and protein kinase A in the phosphorylation and regulation of enzyme substrates involved in intermediary metabolism are well known. A newly discovered role for protein kinase A is in the phosphorylation and activation of transcription factors that are critical for the control of the transcription of genes in response to elevated levels of cAMP.
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NITROGEN CYCLING IN THE GUT
Vol. 18 (1998), pp. 385–411More Less▪ AbstractThis review examines the involvement of the gastrointestinal tract in the utilization of nitrogen, the identities of the nitrogenous substances entering and leaving the gut, and the significance of this recycling in the overall nitrogen economy of the body. It is concerned with nonruminant mammals, including man.
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DIET, NUTRITION, AND PROSTATE CANCER
Vol. 18 (1998), pp. 413–440More Less▪ AbstractCancer of the prostate gland is one of the most common malignancies in affluent nations, in part due to the application of new screening and diagnostic tools. The development of life-threatening prostate cancer is the culmination of a complex series of initiation and promotional events over a period of decades and under the influence of many interacting genetic and environmental factors. A rapidly accumulating scientific literature provides compelling evidence for the hypothesis that diet and nutrition are important factors modifying risk of prostate cancer. Additional resources devoted to interactive research efforts by laboratory scientists and epidemiologists will provide further enlightenment and continued refinement of our assessment of risks and benefits for specific nutrients and dietary patterns. These studies provide hope that evidence-based dietary interventions will significantly impact the risk of prostate cancer and enhance the efficacy of therapeutic interventions.
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THE MOLECULAR BIOLOGY OF METAL ION TRANSPORT IN SACCHAROMYCES CEREVISIAE
Vol. 18 (1998), pp. 441–469More Less▪ AbstractTransition metals such as iron, copper, manganese, and zinc are essential nutrients. The yeast Saccharomyces cerevisiae is an ideal organism for deciphering the mechanism and regulation of metal ion transport. Recent studies of yeast have shown that accumulation of any single metal ion is mediated by two or more substrate-specific transport systems. High-affinity systems are active in metal-limited cells, whereas low-affinity systems play the predominant roles when the substrate is more abundant. Metal ion uptake systems of cells are tightly controlled, and both transcriptional and posttranscriptional regulatory mechanisms have been identified. Most importantly, studies of S. cerevisiae have identified a large number of genes that function in metal ion transport and have illuminated the existence and importance of gene families that play related roles in these processes in mammals.
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Previous Volumes
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Volume 44 (2024)
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Volume 43 (2023)
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Volume 42 (2022)
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Volume 41 (2021)
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Volume 40 (2020)
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Volume 39 (2019)
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Volume 38 (2018)
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Volume 37 (2017)
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Volume 36 (2016)
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Volume 35 (2015)
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Volume 34 (2014)
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Volume 33 (2013)
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Volume 32 (2012)
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Volume 31 (2011)
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Volume 30 (2010)
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Volume 29 (2009)
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Volume 28 (2008)
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Volume 27 (2007)
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Volume 26 (2006)
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Volume 25 (2005)
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Volume 24 (2004)
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Volume 23 (2003)
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Volume 22 (2002)
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Volume 21 (2001)
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Volume 20 (2000)
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Volume 19 (1999)
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Volume 18 (1998)
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Volume 17 (1997)
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Volume 16 (1996)
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Volume 15 (1995)
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Volume 14 (1994)
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Volume 13 (1993)
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Volume 12 (1992)
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Volume 11 (1991)
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Volume 10 (1990)
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Volume 9 (1989)
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Volume 8 (1988)
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Volume 7 (1987)
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Volume 6 (1986)
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Volume 5 (1985)
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Volume 4 (1984)
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Volume 3 (1983)
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Volume 2 (1982)
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Volume 1 (1981)
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Volume 0 (1932)