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- Volume 59, 1997
Annual Review of Physiology - Volume 59, 1997
Volume 59, 1997
- Preface
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- Review Articles
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LUNG SURFACTANT: A Personal Perspective
Vol. 59 (1997), pp. 1–21More Less▪ AbstractThis perspective tells the story of the discovery, characterization, and understanding of the surfactant system of the lung; of how investigators from many disciplines studied the system, stimulated by the demonstration of surfactant deficiency in respiratory distress syndrome of the newborn; and of how the resulting knowledge formed a basis for highly successful surfactant substitution treatment for this syndrome. The chapter includes personal reminiscences and reflections of the author and ends with a few thoughts about the present status and future prospects of this field of research.
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O2-Sensing Mechanisms in Excitable Cells: Role of Plasma Membrane K+ Channels
Vol. 59 (1997), pp. 23–42More LessAlthough carotid chemosensitive glomus cells have been the most extensively studied from the vantage point of how cells sense the lack of O2, it is clear that all tissues sense O2 deprivation. In addition, all mammalian cells can trigger a cascade of events that, depending on the severity and duration of hypoxia-induced stress, can lead to permanent injury and death or to adaptation and survival. Crucial in this cascade, we believe, how the cascade is initiated, how O2 lack is detected by cells, and how these initial steps can activate further processes. In this chapter, we focus on the initial steps of O2 sensing in tissues most commonly studied, i.e. carotid glomus cells, central neurons, smooth muscle cells, and neuro-epithelial bodies of the airways.
Recently it has become clear that plasma membranes of various tissues can sense the lack of O2, not only indirectly via alterations in the intracellular milieu (such as pH, Ca, ATP, etc), but also directly through an unknown mechanism that involves plasma-membrane K channels and possibly other membrane proteins. This latter mechanism is suspected to be totally independent of cytosolic changes because excised patches from plasma membranes were used in these experiments from carotid cells and neurons.
There are a number of questions in this exciting area of research that pertain to the role of this plasma-membrane O2-sensing mechanism in the overall cell response, identification of all the important steps in O2 sensing, differences between O2-tolerant and O2-susceptible cells, and differences between acute and chronic cell responses to lack of O2.
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THE PULMONARY LIPOFIBROBLAST (LIPID INTERSTITIAL CELL) AND ITS CONTRIBUTIONS TO ALVEOLAR DEVELOPMENT1
Vol. 59 (1997), pp. 43–62More Less▪ AbstractThe pulmonary lipofibroblast is located in the alveolar interstitium and is recognizable by its characteristic lipid droplets. During alveolar development it participates in the synthesis of extracellular matrix structural proteins, such as collagen and elastin, and as an accessory cell to the type II pneumocyte, in the synthesis of surfactant. The lipofibroblast contains cortical contractile filaments and is thereby related to the contractile interstitial cells that are normally found at the alveolar septal tips and after lung injury. The morphologic, immunologic, and biochemical characteristics of the lipofibroblast and its probable physiologic functions are reviewed. The retinoid and lipid metabolism of the lipofibroblast is compared with that of the hepatic lipocyte and the adipocyte. Although the functions of the lipofibroblast remain incompletely characterized, this cell type is emerging as an important contributor to pulmonary alveolar septal development.
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EMERGING ROLES FOR CYSTEINE PROTEASES IN HUMAN BIOLOGY
Vol. 59 (1997), pp. 63–88More Less▪ AbstractCysteine proteases have traditionally been viewed as lysosomal mediators of terminal protein degradation. However, recent findings refute this limited view and suggest a more expanded role for cysteine proteases in human biology. Several newly discovered members of this enzyme class are regulated proteases with limited tissue expression, which implies specific roles in cellular physiology. These roles appear to include apoptosis, MHC class II immune responses, prohormone processing, and extracellular matrix remodeling important to bone development. The ability of macrophages and other cells to mobilize elastolytic cysteine proteases to their surfaces under specialized conditions may also lead to accelerated collagen and elastin degradation at sites of inflammation in diseases such as atherosclerosis and emphysema. The development of inhibitors of specific cysteine proteases promises to provide new drugs for modifying immunity, osteoporosis, and chronic inflammation.
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CELLULAR AND MOLECULAR MECHANISMS OF PULMONARY VASCULAR REMODELING
Vol. 59 (1997), pp. 89–144More Less▪ AbstractIn many organs and tissues, the cellular response to injury is associated with a reiteration of specific developmental processes. Studies have shown that, in response to injury, vascular wall cells in adult organisms express genes or gene products characteristic of earlier developmental states. Other genes, expressed preferentially in adult cells in vivo, are down-regulated following injurious stimuli. Complicating matters, however, are recent observations demonstrating that the vascular wall is comprised of phenotypically heterogeneous subpopulations of endothelial cells, smooth muscle cells, and fibroblasts. It is unclear how specific subsets of cells respond to injury and thus contribute to the vascular remodeling that characterizes chronic pulmonary hypertension. This review discusses vascular development in the lung and the cellular responses occurring in pulmonary hypertension; special attention is given to heterogeneity of responses within cell populations and reiteration of developmental processes.
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ION CHANNELS IN VASCULAR ENDOTHELIUM
Vol. 59 (1997), pp. 145–170More Less▪ AbstractThe functional impact of ion channels in vascular endothelial cells (ECs) is still a matter of controversy. This review describes different types of ion channels in ECs and their role in electrogenesis, Ca2+ signaling, vessel permeability, cell-cell communication, mechano-sensor functions, and pH and volume regulation. One major function of ion channels in ECs is the control of Ca2+ influx either by a direct modulation of the Ca2+ influx pathway or by indirect modulation of K+ and Cl− channels, thereby clamping the membrane at a sufficiently negative potential to provide the necessary driving force for a sustained Ca2+ influx. We discuss various mechanisms of Ca2+ influx stimulation: those that activate nonselective, Ca2+-permeable cation channels or those that activate Ca2+-selective channels, exclusively or partially operated by the filling state of intracellular Ca2+ stores. We also describe the role of various Ca2+- and shear stress-activated K+ channels and different types of Cl− channels for the regulation of the membrane potential.
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INWARD RECTIFIER POTASSIUM CHANNELS
Vol. 59 (1997), pp. 171–191More Less▪ AbstractThe past three years have seen remarkable progress in research on the molecular basis of inward rectification, with significant implications for basic understanding and pharmacological manipulation of cellular excitability. Expression cloning of the first inward rectifier K channel (Kir) genes provided the necessary breakthrough that has led to isolation of a family of related clones encoding channels with the essential functional properties of classical inward rectifiers, ATP-sensitive K channels, and muscarinic receptor-activated K channels. High-level expression of cloned channels led to the discovery that classical inward so-called anomalous rectification is caused by voltage-dependent block of the channel by polyamines and Mg2+ ions, and it is now clear that a similar mechanism results in inward rectification of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-kainate receptor channels. Knowledge of the primary structures of Kir channels and the ability to mutate them also has led to the determination of many of the structural requirements of inward rectification.
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CYTOPLASMIC ATP-DEPENDENT REGULATION OF ION TRANSPORTERS AND CHANNELS: Mechanisms and Messengers
Vol. 59 (1997), pp. 193–220More Less▪ AbstractMany ion transporters and channels appear to be regulated by ATP-dependent mechanisms when studied in planar bilayers, excised membrane patches, or with whole-cell patch clamp.Protein kinases are obvious candidates to mediate ATP effects, but other mechanisms are also implicated. They include lipid kinases with the generation of phosphatidylinositol phosphates as second messengers, allosteric effects of ATP binding, changes of actin cytoskeleton, and ATP-dependent phospholipases. Phosphatidylinositol-4,5-bisphosphate (PIP2) is a possible membrane-delimited messenger that activates cardiac sodium-calcium exchange, KATP potassium channels, and other inward rectifier potassium channels. Regulation of PIP2 by phospholipase C, lipid phosphatases, and lipid kinases would thus tie surface membrane transport to phosphatidylinositol signaling. Sodium-hydrogen exchange is activated by ATP through a phosphorylation-independent mechanism, whereas ion cotransporters are activated by several protein kinase mechanisms. Ion transport in epithelium may be particularly sensitive to changes of cytoskeleton that are regulated by ATP-dependent cell signaling mechanisms.
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CHOLECYSTOKININ CELLS
Vol. 59 (1997), pp. 221–242More Less▪ AbstractCholecystokinin (CCK) is an important hormonal regulator of the digestive process. CCK cells are concentrated in the proximal small intestine, and hormone is secreted into the blood upon the ingestion of food. The physiological actions of CCK include stimulation of pancreatic secretion and gallbladder contraction, regulation of gastric emptying, and induction of satiety. Therefore, in a highly coordinated manner, CCK regulates the ingestion, digestion, and absorption of nutrients. CCK is produced by two separate cell types: endocrine cells of the small intestine and various neurons in the gastrointestinal tract and central nervous system. Accordingly, CCK can function as either a hormone or a neuropeptide. This review focuses on the physiology of the CCK cell in the intestine and, in particular, on how the CCK cell is regulated to secrete its hormone product. The effects of ingested nutrients on the CCK cell and the intracellular messenger systems involved in controlling secretion are reviewed. A summary is provided of recent studies examining the electrophysiological properties of CCK cells and newly discovered proteins that act as releasing factors for CCK, which mediate feedback pathways critical for regulated secretion in the intact organism.
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PHYSIOLOGY OF ISOLATED GASTRIC ENDOCRINE CELLS
Vol. 59 (1997), pp. 243–256More Less▪ AbstractThe regulation of gastric acid secretion is achieved in the periphery by interplay between three major gastric endocrine cells: the enterochromaffin-like (ECL) cell, the gastrin or G cell, and the somatostatin or D cell. Regulation of these cells is via stimulatory or inhibitory paracrine, endocrine, and neural pathways. Upregulation of ECL function is determined by activation of CCK-B receptors, by gastrin, and by activation of β-adrenergic receptors, as well as by acetylcholine in some (10–29%) of the cells. Gastrin and acetylcholine produce typical biphasic calcium signals. Inhibition of ECL cell histamine release and calcium signaling is produced by somatostatin acting at a type 2 receptor, histamine acting at a histamine-3 receptor, and by peptide PYY. Stimulation of ECL cells results in activation of chloride channels, and there is evidence that voltage-dependent calcium channels, along with the receptor-operated calcium channels, also are responsible for elevation of [Ca]i. Depolarization-activated K+ channels presumably restore the potential after depolarization by activation of the chloride channel. The D cell is activated by either gastrin or CCK and appears to be inhibited by acetylcholine and somatostatin. The G cell is activated by acetylcholine and gastrin-releasing peptide (GRP) and is inhibited by somatostatin. The functional integration of these three cell types is the primary determinant of the degree of stimulation of the parietal cell.
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ENTEROGLUCAGON
Vol. 59 (1997), pp. 257–271More Less▪ AbstractThe gene encoding proglucagon, the biosynthetic precursor of glucagon, is expressed not only in the pancreatic islets but also in endocrine cells of the gastrointestinal mucosa. The proglucagon (PG)-derived peptides from the gut include glicentin (corresponding to PG 1–69); smaller amounts of oxyntomodulin (PG 33–69) and glicentin-related pancreatic polypeptide (GRPP, PG 1–30); glucagon-like peptide-1 (GLP-1, PG 78–107 amide); intervening peptide-2 (IP-2, PG 111–122 amide); and glucagon-like peptide-2 (GLP-2, PG 126–158). All are secreted into the blood in response to ingestion of carbohydrates and lipids. Only oxyntomodulin and GLP-1 have proven biological activity; oxyntomodulin possibly because it interacts (but with lower potency) with GLP-1 and glucagon receptors. GLP-1 is the most potent insulinotropic hormone known and functions as an incretin hormone. It also inhibits glucagon secretion and, therefore, lowers blood glucose. This effect is preserved in patients with non-insulin-dependent diabetes mellitus, in whom infusions of GLP-1 may completely normalize blood glucose. However, GLP-1 also potently inhibits gastrointestinal secretion and motility, and its physiological functions include mediation of the “ileal-brake” effect, i.e. the inhibition of upper gastrointestinal functions elicited by the presence of unabsorbed nutrients in the ileum. As such it may serve to regulate food intake.
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The G Cell
Vol. 59 (1997), pp. 273–298More Less▪ AbstractThe study of gastrin continues to serve as an excellent model for gastrointestinal regulatory processes. This review highlights some recent advances in the field by outlining gastrin biosynthesis, summarizing current understanding of gastrin receptors, describing the regulation of gastrin release, and discussing the clinical implications of gastrin in the pathogenesis of peptic ulcer disease. Emphasis is on three emerging areas of gastrin research: the novel finding that one of gastrin's posttranslational processing intermediates has biological activity distinct from that of the mature peptide; elucidation of gastrin's signal transduction mechanisms that mediate the trophic effects of the peptide; and the role of gastrin in peptic ulcer disease pathogenesis secondary to Helicobacter pylori infection.
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EVOLUTION AND REGULATION OF UREA SYNTHESIS AND UREOTELY IN (BATRACHOIDID) FISHES
Vol. 59 (1997), pp. 299–323More Less▪ AbstractSelected teleostean (bony) fish species of the family Batrachoididae (toadfishes and midshipmen) possess high titers of all enzymes of the ornithine-urea cycle in their livers. These species have proven valuable in understanding the short-term regulation of urea synthesis, urea permeability, and transport across epithelial tissues, and how urea synthesis and excretion have evolved among vertebrates. One species in particular, the gulf toadfish (Opsanus be), has been shown to rapidly switch from ammonia excretion to urea synthesis and excretion during a variety of stress conditions (including confinement). The transition is accompanied by an upregulation of hepatic glutamine synthetase activity, and a switch to pulsatile urea excretion from the anterior end of the fish. In fact, a single day's excretion can be voided in a period of <3 h. Hypotheses on the environmental significance of these patterns of urea synthesis and excretion are discussed.
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THE CHLORIDE CELL:Structure and Function in the Gills of Freshwater Fishes
Vol. 59 (1997), pp. 325–347More Less▪ AbstractThis review focuses on the structure and function of the branchial chloride cell in freshwater fishes. The mitochondria-rich chloride cell is believed to be the principal site of trans-epithelial Ca2+ and Cl− influxes. Though currently debated, there is accruing evidence that the pavement cell is the site of Na+ uptake via channels linked electrically to an apical membrane vacuolar H+-ATPase (proton pump).
Chloride cells perform an integral role in acid-base regulation. During conditions of alkalosis, the surface area of exposed chloride cells is increased, which serves to enhance base equivalent excretion as the rate of Cl−/HCO3− exchange is increased. Conversely, during acidosis, the chloride cell surface area is diminished by an expansion of the adjacent pavement cells. This response reduces the number of functional Cl−/HCO3− exchangers.
Under certain conditions that challenge ion regulation, chloride cells proliferate on the lamellae. This response, while optimizing the Ca2+ and Cl− transport capacity of the gill, causes a thickening of the blood-to-water diffusion barrier and thus impedes respiratory gas transfer.
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REGULATION OF OVARIAN FOLLICLE ATRESIA
Vol. 59 (1997), pp. 349–363More Less▪ AbstractThe majority of ovarian follicles undergo atresia, a hormonally controlled apoptotic process. Monitoring apoptotic DNA fragmentation provides a quantitative and sensitive endpoint to study the hormonal regulation of atresia in ovarian follicles. During follicle development, gonadotropins, together with local ovarian growth factors (IGF-I, EGF/TGF-α, basic FGF) and cytokine (interleukin-1β), as well as estrogens, activate different intracellular pathways to rescue follicles from apoptotic demise. In contrast, TNF-α, Fas ligand, presumably acting through receptors with a death domain, and androgens are atretogenic factors. These diverse hormonal signals probably converge on selective intracellular pathways (including genes of the bcl-2 and ICE families) to regulate apoptosis. With a constant loss of follicles from the original stockpile, the ovary provides a unique model for studying the hormonal regulation of apoptosis.
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SPECIFIC, NONGENOMIC ACTIONS OF STEROID HORMONES
Vol. 59 (1997), pp. 365–393More Less▪ AbstractTraditionally, steroid hormone action has been described as the modulation of nuclear transcription, thus triggering genomic events that are responsible for physiological effects. Despite early observations of rapid steroid effects that were incompatible with this theory, nongenomic steroid action has been widely recognized only recently. Evidence for these rapid effects is available for steroids of all clones and for a multitude of species and tissues. Examples of nongenomic steroid action include rapid aldosterone effects in lymphocytes and vascular smooth muscle cells, vitamin D3 effects in epithelial cells, progesterone action in human sperm, neurosteroid effects on neuronal function, and vascular effects of estrogens. Mechanisms of action are being studied with regard to signal perception and transduction, and researchers have developed a patchy sketch of a membrane receptor-second messenger cascade similar to those involved in catecholamine and peptide hormone action. Many of these effects appear to involve phospholipase C, phosphoinositide turnover, intracellular pH and calcium, protein kinase C, and tyrosine kinases. The physiological and pathophysiological relevance of these effects is unclear, but rapid steroid effects on cardiovascular, central nervous, and reproductive functions may occur in vivo. The cloning of the cDNA for the first membrane receptor for steroids should be achieved in the near future, and the physiological and clinical relevance of these rapid steroid effects can then be established.
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BIOLOGICAL FUNCTIONS OF ANGIOTENSIN AND ITS RECEPTORS
T. Matsusaka, and I. IchikawaVol. 59 (1997), pp. 395–412More Less▪ AbstractAngiotensin receptors are present in a number of organs and systems including heart, kidney, gonad, and placenta; pituitary and adrenal glands; the peripheral vessels, and the central nervous system. This octapeptide exerts diverse effects that include induction of cell hypertrophy and/or hyperplasia and a stimulation of hormone synthesis and ion transport in the heart, kidney, and adrenal, primarily through type 1 (AT1) receptors. In the kidney, several heterogeneous cell populations—endothelial, epithelial, and vascular—carry AT1 receptors. Some studies suggest that AT2 receptors are also functional, but the cell type carrying this receptor and the nature of its specific function have not been fully elucidated. Although studies indicate that AT1 receptors are affected in response to physiological and pathophysiological manipulations, the functional significance of these modulations remains largely uncertain. Nevertheless, recent human genetic studies indicate that polymorphisms in AT1 receptors, as well as in other angiotensin-related genes, have significant impact on organ remodeling processes of the heart and the kidney.
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RENAL K+ CHANNELS: Structure and Function
Vol. 59 (1997), pp. 413–436More Less▪ AbstractThe activity of potassium (K+) channels is intimately linked to several important transport functions in renal tubules. We review recent progress concerning the properties, site along the nephron, and physiological regulation of native K+ channels, and compare their characteristics with those of recently cloned K+ channels. We do not fully cover work on K+ channels in amphibian tubules, cell cultures, and single tubule cells and do not review K+ channels in mesangial cells.
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REGULATION OF GENE EXPRESSION BY HYPERTONICITY1
Vol. 59 (1997), pp. 437–455More Less▪ AbstractAdaptation of cells to hypertonicity often involves changes in gene expression. Since the concentration of salt in the interstitial fluid surrounding renal inner medullary cells varies with operation of the renal concentrating mechanism and generally is very high, the adaptive mechanisms of these cells are of special interest. Renal medullary cells compensate for hypertonicity by accumulating variable amounts of compatible organic osmolytes, including sorbitol, myo-inositol, glycine betaine, and taurine. In this review we consider how these solutes help relieve the stress of hypertonicity and the nature of transporters and enzymes responsible for their variable accumulation. We emphasize recent developments concerning the molecular basis for osmotic regulation of these genes, including identification and characterization of osmotic response elements. Although osmotic stresses are much smaller in other parts of the body than in the renal medulla, similar mechanisms operate throughout, yielding important physiological and pathophysiological consequences.
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Previous Volumes
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Volume 87 (2025)
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Volume 86 (2024)
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Volume 85 (2023)
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Volume 84 (2022)
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Volume 83 (2021)
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Volume 82 (2020)
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Volume 81 (2019)
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Volume 80 (2018)
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Volume 79 (2017)
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Volume 78 (2016)
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Volume 77 (2015)
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Volume 76 (2014)
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Volume 75 (2013)
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Volume 74 (2012)
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Volume 73 (2011)
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Volume 72 (2010)
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Volume 71 (2009)
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Volume 70 (2008)
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Volume 69 (2007)
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Volume 68 (2006)
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Volume 67 (2005)
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Volume 66 (2004)
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Volume 65 (2003)
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Volume 64 (2002)
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Volume 63 (2001)
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Volume 62 (2000)
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Volume 61 (1999)
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Volume 60 (1998)
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Volume 59 (1997)
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Volume 58 (1996)
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Volume 57 (1995)
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Volume 56 (1994)
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Volume 55 (1993)
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Volume 54 (1992)
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Volume 53 (1991)
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Volume 52 (1990)
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Volume 51 (1989)
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Volume 50 (1988)
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Volume 49 (1987)
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Volume 48 (1986)
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Volume 47 (1985)
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Volume 46 (1984)
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Volume 45 (1983)
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Volume 44 (1982)
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Volume 43 (1981)
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Volume 42 (1980)
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Volume 41 (1979)
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Volume 40 (1978)
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Volume 39 (1977)
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Volume 38 (1976)
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Volume 37 (1975)
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Volume 36 (1974)
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Volume 35 (1973)
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Volume 34 (1972)
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Volume 33 (1971)
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Volume 32 (1970)
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Volume 31 (1969)
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Volume 30 (1968)
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Volume 29 (1967)
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Volume 28 (1966)
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Volume 27 (1965)
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Volume 26 (1964)
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Volume 25 (1963)
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Volume 24 (1962)
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Volume 23 (1961)
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Volume 22 (1960)
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Volume 21 (1959)
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Volume 20 (1958)
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Volume 19 (1957)
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Volume 18 (1956)
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Volume 17 (1955)
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Volume 16 (1954)
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Volume 15 (1953)
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Volume 14 (1952)
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Volume 13 (1951)
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Volume 12 (1950)
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Volume 11 (1949)
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Volume 10 (1948)
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Volume 9 (1947)
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Volume 8 (1946)
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Volume 7 (1945)
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Volume 6 (1944)
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Volume 5 (1943)
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Volume 4 (1942)
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Volume 3 (1941)
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Volume 2 (1940)
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Volume 1 (1939)
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Volume 0 (1932)