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- Volume 67, 2005
Annual Review of Physiology - Volume 67, 2005
Volume 67, 2005
- Preface
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UNLOCKING THE SECRETS OF CELL SIGNALING
Vol. 67 (2005), pp. 1–21More Less▪ AbstractMy scientific life has been spent trying to understand how cells communicate with each other. This interest in cell signaling began with studies on the control of fluid secretion by an insect salivary gland, and the subsequent quest led to the discovery of inositol trisphosphate (IP3) and its role in calcium signaling, which effectively divided my scientific career into two distinct parts. The first part was primarily experimental and culminated in the discovery of IP3, which set the agenda for the second half during which I have enjoyed exploring the many functions of this remarkably versatile signaling system. It has been particularly exciting to find out how this IP3/Ca2+ signaling pathway has been adapted to control processes as diverse as fertilization, proliferation, cell contraction, secretion, and information processing in neuronal cells.
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PETER HOCHACHKA: Adventures in Biochemical Adaptation
Vol. 67 (2005), pp. 25–37More Less▪ AbstractPeter Hochachka was one of the most creative forces in the field of comparative physiology during the past half-century. His career was truly an exploratory adventure, in both intellectual and geographic senses. His broad comparative studies of metabolism in organisms as diverse as trout, tunas, oysters, squid, turtles, locusts, hummingbirds, seals, and humans revealed the adaptable features of enzymes and metabolic pathways that provide the biochemical bases for diverse lifestyles and environments. In its combined breadth and depth, no other corpus of work better illustrates the principle of “unity in diversity” that marks comparative physiology. Through his publications, his stimulating mentorship, his broad editorial services, and his continuous—and highly infectious—enthusiasm for his field, Peter Hochachka served as one of the most influential leaders in the transformation of comparative physiology.
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CALCIUM, THIN FILAMENTS, AND THE INTEGRATIVE BIOLOGY OF CARDIAC CONTRACTILITY
Vol. 67 (2005), pp. 39–67More Less▪ AbstractAlthough well known as the location of the mechanism by which the cardiac sarcomere is activated by Ca2+ to generate force and shortening, the thin filament is now also recognized as a vital component determining the dynamics of contraction and relaxation. Molecular signaling in the thin filament involves steric, allosteric, and cooperative mechanisms that are modified by protein phosphorylation, sarcomere length and load, the chemical environment, and isoform composition. Approaches employing transgenesis and mutagenesis now permit investigation of these processes at the level of the systems biology of the heart. These studies reveal that the thin filaments are not merely slaves to the levels of Ca2+ determined by membrane channels, transporters and exchangers, but are actively involved in beat to beat control of cardiac function by neural and hormonal factors and by the Frank-Starling mechanism.
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INTRACELLULAR CALCIUM RELEASE AND CARDIAC DISEASE
Vol. 67 (2005), pp. 69–98More Less▪ AbstractIntracellular calcium release channels are present on sarcoplasmic and endoplasmic reticuli (SR, ER) of all cell types. There are two classes of these channels: ryanodine receptors (RyR) and inositol 1,4,5-trisphosphate receptors (IP3R). RyRs are required for excitation-contraction (EC) coupling in striated (cardiac and skeletal) muscles. RyRs are made up of macromolecular signaling complexes that contain large cytoplasmic domains, which serve as scaffolds for proteins that regulate the function of the channel. These regulatory proteins include calstabin1/calstabin2 (FKBP12/FKBP12.6), a 12/12.6 kDa subunit that stabilizes the closed state of the channel and prevents aberrant calcium leak from the SR. Kinases and phosphatases are targeted to RyR2 channels and modulate RyR2 function in response to extracellular signals. In the classic fight or flight stress response, phosphorylation of RyR channels by protein kinase A reduces the affinity for calstabin and activates the channels leading to increased SR calcium release. In heart failure, a cardiac insult causes a mismatch between blood supply and metabolic demands of organs. The chronically activated fight or flight response leads to leaky channels, altered calcium signaling, and contractile dysfunction and cardiac arrhythmias.
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CHEMICAL PHYSIOLOGY OF BLOOD FLOW REGULATION BY RED BLOOD CELLS:
Vol. 67 (2005), pp. 99–145More Less▪ AbstractBlood flow in the microcirculation is regulated by physiological oxygen (O2) gradients that are coupled to vasoconstriction or vasodilation, the domain of nitric oxide (NO) bioactivity. The mechanism by which the O2 content of blood elicits NO signaling to regulate blood flow, however, is a major unanswered question in vascular biology. While the hemoglobin in red blood cells (RBCs) would appear to be an ideal sensor, conventional wisdom about its chemistry with NO poses a problem for understanding how it could elicit vasodilation. Experiments from several laboratories have, nevertheless, very recently established that RBCs provide a novel NO vasodilator activity in which hemoglobin acts as an O2 sensor and O2-responsive NO signal transducer, thereby regulating both peripheral and pulmonary vascular tone. This article reviews these studies, together with biochemical studies, that illuminate the complexity and adaptive responsiveness of NO reactions with hemoglobin. Evidence for the pivotal role of S-nitroso (SNO) hemoglobin in mediating this response is discussed. Collectively, the reviewed work sets the stage for a new understanding of RBC-derived relaxing activity in auto-regulation of blood flow and O2 delivery and of RBC dysfunction in disorders characterized by tissue O2 deficits, such as sickle cell disease, sepsis, diabetes, and heart failure.
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RNAI AS AN EXPERIMENTAL AND THERAPEUTIC TOOL TO STUDY AND REGULATE PHYSIOLOGICAL AND DISEASE PROCESSES
Vol. 67 (2005), pp. 147–173More Less▪ AbstractOver the past four years RNA interference (RNAi) has exploded onto the research scene as a new approach to manipulate gene expression in mammalian systems. More recently, RNAi has garnered much interest as a potential therapeutic strategy. In this review, we briefly summarize the current understanding of RNAi biology and examine how RNAi has been used to study the genetic basis of physiological and disease processes in mammalian systems. We also explore some of the new developments in the use of RNAi for disease therapy and highlight the key challenges that currently limit its application in the laboratory, as well as in the clinical setting.
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BIOPHYSICS, PHYSIOLOGICAL ECOLOGY, AND CLIMATE CHANGE: Does Mechanism Matter?
Vol. 67 (2005), pp. 177–201More Less▪ AbstractRecent meta-analyses have shown that the effects of climate change are detectable and significant in their magnitude, but these studies have emphasized the utility of looking for large-scale patterns without necessarily understanding the mechanisms underlying these changes. Using a series of case studies, we explore the potential pitfalls when one fails to incorporate aspects of physiological performance when predicting the consequences of climate change on biotic communities. We argue that by considering the mechanistic details of physiological performance within the context of biophysical ecology (engineering methods of heat, mass and momentum exchange applied to biological systems), such approaches will be better poised to predict where and when the impacts of climate change will most likely occur.
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COMPARATIVE DEVELOPMENTAL PHYSIOLOGY:An Interdisciplinary Convergence
Vol. 67 (2005), pp. 203–223More Less▪ AbstractComparative developmental physiology spans genomics to physiological ecology and evolution. Although not a new discipline, comparative developmental physiology's position at the convergence of development, physiology and evolution gives it prominent new significance. The contributions of this discipline may be particularly influential as physiologists expand beyond genomics to a true systems synthesis, integrating molecular through organ function in multiple organ systems. This review considers how developing physiological systems are directed by genes yet respond to environment and how these characteristics both constrain and enable evolution of physiological characters. Experimental approaches and methodologies of comparative developmental physiology include studying event sequences (heterochrony and heterokairy), describing the onset and progression of physiological regulation, exploiting scaling, expanding the list of animal models, using genetic engineering, and capitalizing on new miniaturized technologies for physiological investigation down to the embryonic level. A synthesis of these approaches is likely to generate a more complete understanding of how physiological systems and, indeed, whole animals develop and how populations evolve.
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MOLECULAR AND EVOLUTIONARY BASIS OF THE CELLULAR STRESS RESPONSE
Vol. 67 (2005), pp. 225–257More Less▪ AbstractThe cellular stress response is a universal mechanism of extraordinary physiological/pathophysiological significance. It represents a defense reaction of cells to damage that environmental forces inflict on macromolecules. Many aspects of the cellular stress response are not stressor specific because cells monitor stress based on macromolecular damage without regard to the type of stress that causes such damage. Cellular mechanisms activated by DNA damage and protein damage are interconnected and share common elements. Other cellular responses directed at re-establishing homeostasis are stressor specific and often activated in parallel to the cellular stress response. All organisms have stress proteins, and universally conserved stress proteins can be regarded as the minimal stress proteome. Functional analysis of the minimal stress proteome yields information about key aspects of the cellular stress response, including physiological mechanisms of sensing membrane lipid, protein, and DNA damage; redox sensing and regulation; cell cycle control; macromolecular stabilization/repair; and control of energy metabolism. In addition, cells can quantify stress and activate a death program (apoptosis) when tolerance limits are exceeded.
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ENDOCRINOLOGY OF THE STRESS RESPONSE1
Vol. 67 (2005), pp. 259–284More Less▪ AbstractThe stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRH); arginine vasopressin; the proopiomelanocortin-derived peptides α-melanocyte-stimulating hormone and β-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors.
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LESSONS IN ESTROGEN BIOLOGY FROM KNOCKOUT AND TRANSGENIC ANIMALS
Vol. 67 (2005), pp. 285–308More Less▪ AbstractTremendous progress has been made in elucidating numerous critical aspects of estrogen signaling. New tools and techniques have enabled detailed molecular analysis of components that direct estrogen responses. At the other end of the spectrum, generation of a multiplicity of transgenic animals has allowed analysis of the physiological roles of the estrogen-signaling components in biologically relevant models. Here, we review the ever-increasing body of knowledge in the field of estrogen biology, especially as applied to the female reproductive processes.
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LIGAND CONTROL OF COREGULATOR RECRUITMENT TO NUCLEAR RECEPTORS
Vol. 67 (2005), pp. 309–333More Less▪ AbstractNuclear receptors modulate transcription through ligand-mediated recruitment of transcriptional coregulator proteins. The structural connection between ligand and coregulator is mediated by a molecular switch, made up of the most carboxy-terminal helix in the ligand-binding domain, helix 12. The dynamics of this switch are thought to underlie ligand specificity of nuclear receptor signaling, but the details of this control mechanism have remained elusive. This review highlights recent structural work on how the ligand controls this molecular switch and the modulation of this signaling pathway by receptor subtype and dimer partner.
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REGULATION OF SIGNAL TRANSDUCTION PATHWAYS BY ESTROGEN AND PROGESTERONE
Vol. 67 (2005), pp. 335–376More Less▪ AbstractThe female sex steroid hormones 17β-estradiol and progesterone mediate their biological effects on development, differentiation, and maintenance of reproductive tract and other target tissues through gene regulation by nuclear steroid receptors that function as ligand-dependent transcription factors. However, not all effects of 17β-estradiol and progesterone are mediated by direct control of gene expression. These hormones also have rapid stimulatory effects on the activities of a variety of signal transduction molecules and pathways and, in many cases, these effects appear to be initiated from the plasma cell membrane. There is growing evidence that a subpopulation of the conventional nuclear steroid receptor localized at the cell membrane mediates many of the rapid signaling actions of steroid hormones; however, novel membrane receptors unrelated to conventional steroid receptors have also been implicated. This chapter reviews the nature of the receptors that mediate rapid signaling actions of estrogen and progesterone and describes the signaling molecules and pathways involved, the mechanisms by which receptors couple with components of signaling complexes and trigger responses, and the target tissues and cell functions regulated by this mode of steroid hormone action.
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MECHANISMS OF BICARBONATE SECRETION IN THE PANCREATIC DUCT
Vol. 67 (2005), pp. 377–409More Less▪ AbstractIn many species the pancreatic duct epithelium secretes HCO3− ions at a concentration of around 140 mM by a mechanism that is only partially understood. We know that HCO3− uptake at the basolateral membrane is achieved by Na+-HCO3− cotransport and also by a H+-ATPase and Na+/H+ exchanger operating together with carbonic anhydrase. At the apical membrane, the secretion of moderate concentrations of HCO3− can be explained by the parallel activity of a Cl−/HCO3− exchanger and a Cl− conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca2+-activated Cl− channel (CaCC). However, the sustained secretion of HCO3− into a HCO3−-rich luminal fluid cannot be explained by conventional Cl−/HCO3− exchange. HCO3− efflux across the apical membrane is an electrogenic process that is facilitated by the depletion of intracellular Cl−, but it remains to be seen whether it is mediated predominantly by CFTR or by an electrogenic SLC26 anion exchanger.
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MOLECULAR PHYSIOLOGY OF INTESTINAL N+/H+ EXCHANGE
Vol. 67 (2005), pp. 411–443More Less▪ AbstractThe sodium/hydrogen exchange (NHE) gene family plays an integral role in neutral sodium absorption in the mammalian intestine. The NHE gene family is comprised of nine members that are categorized by cellular localization (i.e., plasma membrane or intracellular). In the gastrointestinal (GI) tract of multiple species, there are resident plasma membrane isoforms including NHE1 (basolateral) and NHE2 (apical), recycling isoforms (NHE3), as well as intracellular isoforms (NHE6, 7, 9). NHE3 recycles between the endosomal compartment and the apical plasma membrane and functions in both locations. NHE3 regulation occurs during normal digestive processes and is often inhibited in diarrheal diseases. The C terminus of NHE3 binds multiple regulatory proteins to form large protein complexes that are involved in regulation of NHE3 trafficking to and from the plasma membrane, turnover number, and protein phosphorylation. NHE1 and NHE2 are not regulated by trafficking. NHE1 interacts with multiple regulatory proteins that affect phosphorylation; however, whether NHE1 exists in large multi-protein complexes is unknown. Although intestinal and colonic sodium absorption appear to involve at least NHE2 and NHE3, future studies are necessary to more accurately define their relative contributions to sodium absorption during human digestion and in pathophysiological conditions.
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REGULATION OF FLUID AND ELECTROLYTE SECRETION IN SALIVARY GLAND ACINAR CELLS
Vol. 67 (2005), pp. 445–469More Less▪ AbstractThe secretion of fluid and electrolytes by salivary gland acinar cells requires the coordinated regulation of multiple water and ion transporter and channel proteins. Notably, all the key transporter and channel proteins in this process appear to be activated, or are up-regulated, by an increase in the intracellular Ca2+ concentration ([Ca2+]i). Consequently, salivation occurs in response to agonists that generate an increase in [Ca2+]i. The mechanisms that act to modulate these increases in [Ca2+]i obviously influence the secretion of salivary fluid. Such modulation may involve effects on mechanisms of both Ca2+ release and Ca2+ entry and the resulting spatial and temporal aspects of the [Ca2+]i signal, as well as interactions with other signaling pathways in the cells. The molecular cloning of many of the transporter and regulatory molecules involved in fluid and electrolyte secretion has yielded a better understanding of this process at the cellular level. The subsequent characterization of mice with null mutations in many of these genes has demonstrated the physiological roles of individual proteins. This review focuses on recent developments in determining the molecular identification of the proteins that regulate the fluid secretion process.
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SECRETION AND ABSORPTION BY COLONIC CRYPTS
Vol. 67 (2005), pp. 471–490More Less▪ AbstractThe intestines play an important role in the absorption and secretion of nutrients. The colon is the final area for recapturing electrolytes and water prior to excretion, and in order to maintain this electrolyte homeostasis, a complex interaction between secretory and absorptive processes is necessary. Until recently it was thought that secretion and absorption were two distinct processes associated with either crypts or surface cells, respectively. Recently it was demonstrated that both the surface and crypt cells can perform secretory and absorptive functions and that, in fact, these functions can be going on simultaneously. This issue is important in the complexities associated with secretory diarrhea and also in attempting to develop treatment strategies for intestinal disorders. Here, we update the model of colonic secretion and absorption, discuss new issues of transporter activation, and identify some important new receptor pathways that are important modulators of the secretory and absorptive functions of the colon.
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Previous Volumes
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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)