SRBR 2008 Program Book

Total Page:16

File Type:pdf, Size:1020Kb

SRBR 2008 Program Book 20th Anniversary Meeting Society for Research on Biological Rhythms Program and Abstracts SRBR May 17–21, 2008 Sandestin Golf and Beach Resort Destin, Florida SOCIETY FOR RESEARCH ON BIOLOGICAL RHYTHMS I Executive Committee Animal Issues Committee Trainee Professional Development Day Martha Gillette, Ph.D., President Larry Morin, Ph.D., Chair Organizing Committee University of Illinois at Stony Brook University Urbana-Champaign Eric Bittman, Ph.D. Kenneth P. Wright Jr., Joseph Takahashi, Ph.D., President-elect University of Massachusetts Ph.D., Chair University of Colorado at Boulder Northwestern University Lance Kriegsfeld, Ph.D. Amita Sehgal, Ph.D., Treasurer University of California–Berkeley Nicolas Cermakian, Ph.D. McGill University University of Pennsylvania Laura Smale, Ph.D. David Weaver, Ph.D., Secretary Michigan State University Marian Comas University of Massachusetts Medical University of Groningen ChronoHistory Committee School Stephanie Crowley Members-at-Large Anna Wirz-Justice, Ph.D., Chair Brown University University of Basel Elizabeth B. Klerman, M.D., Ph.D. Charlotte Helfrich-Foerster, Ph.D. Josephine Arendt, Ph.D. Harvard Medical School University of Regensburg University of Surrey Luciano Marpegan, Ph.D. Martha Merrow, Ph.D. Eric Bittman, Ph.D. Washington University University of Groningen University of Massachusetts Michael J. Muskus Ignacio Provencio, Ph.D. Serge Daan, Ph.D. University of Missouri– University of Virginia University of Groningen Kansas City Ex-Officio Members Patricia DeCoursey, Ph.D. Ozgur Tataroglu University of South Carolina Heidelberg University Lawrence Morin, Ph.D., Comptroller Stony Brook University Jeffrey Hall, Ph.D. David Weaver, Ph.D. Brandeis University University of Massachusetts Medical William J. Schwartz, M.D., School Past President J. Woodland Hastings, Ph.D. University of Massachusetts Medical Harvard University Trainee Research Awards School Elizabeth Klerman, M.D., Ph.D. Committee Martin Zatz, Ph.D., M.D., Editor Brigham & Women’s Hospital Kenneth Wright Jr., Journal of Biological Rhythms and Harvard Medical School Ph.D., Chair Program Committee Michael Menaker, Ph.D. University of Colorado at Boulder University of Virginia Michael Antle, Ph.D. Ravi Allada, M.D., Marty Zatz, M.D., Ph.D. University of Calgary Program Chair Editor, Journal of Biological Rhythms Northwestern University Justin Blau, Ph.D. Communications Committee New York University Russel Van Gelder, M.D., Ph.D. Nicolas Cermakian, Ph.D. University of Washington Frank AJL Scheer, Ph.D., McGill University Carla Green, Ph.D. Program Chair University of Virginia Brigham and Women's Hospital, Deborah Bell-Pedersen, Ph.D. Harvard Medical School Texas A&M University Charalambos Kyriacou, Ph.D. University of Leicester Janis Anderson, Ph.D. Susan Doyle, Ph.D. Brigham and Women's Hospital, University of Virginia Michael Nitabach, J.D., Ph.D. Harvard Medical School Yale University Samer Hattar, Ph.D. Ralph Mistlberger, Ph.D. Johns Hopkins University Shantha Rajaratnam, Ph.D. Simon Fraser University Monash University David Welsh, Ph.D. Shelley A. Tischkau, Ph.D. University of California– Fred Turek, Ph.D. Southern Illinois University School of San Diego Northwestern University Medicine Erik Herzog, Ph.D. Hiroki Ueda, M.D., Ph.D. Washington University RIKEN Nominating Committee Ralph Mistlberger, Ph.D. Phyllis Zee, M.D., Ph.D. Rae Silver, Ph.D., Chair Simon Fraser University Northwestern University Barnard College and Columbia University Shelley Tischkau, Ph.D. Facilities Chair Southern Illinois University School of Justin Blau, Ph.D. Medicine Shelley Tischkau, Ph.D. New York University Southern Illinois University Elizabeth Klerman, M.D., Ph.D. Elizabeth Klerman, M.D., Ph.D. School of Medicine Harvard Medical School Brigham & Women’s Hospital and Harvard Medical School II SRBR 2008 PROGRAM AND ABSTRACTS Horacio de la Iglesia, Ph.D. Advisory Board Laura Smale University of Washington Timothy J. Bartness Michigan State University Naomi Rogers, Ph.D. Georgia State University Joseph S. Takahashi University of Sydney Domien G.M. Beersma Northwestern University David Weaver, Ph.D. University of Groningen David K. Welsh University of Massachusetts Medical Eric Bittman University of California– School University of Massachusetts–Amherst San Diego Phyllis Zee, M.D., Ph.D. Vincent M. Cassone Russell N. Van Gelder Northwestern University Texas A&M University University of Washington School of Medicine Horacio O. de la Iglesia David R. Weaver Projectionists University of Washington University of Massachusetts Medical School Norman Atkins, Jr Marie Dumont University of Illinois at Urbana- University of Montreal Conference Arrangements Champaign Charmane Eastman Ethan Buhr Rush Medical Center Northwestern University Isaac Edery Erin Evans Rutgers University Brigham and Women's Hospital/ Russell Foster 302 East John St., Suite 202 University of Surrey University of Oxford Champaign, IL 61820 Phone: 217-333-2880 Rhiannon Mear Jaga Giebultowicz E-mail: [email protected] Simon Fraser University Oregon State University www.srbr.org Roxanne Sterniczuk Martha Gillette University of Calgary University of Illinois at Ian Webb Urbana-Champaign University of Western Ontario Michael Gorman Journal of Biological University of California–San Diego Rhythms Carla Green University of Virginia Martin Zatz, Ph.D., M.D., Editor Erik Herzog Associate Editors Washington University Josephine Arendt John Hogenesch University of Surrey University of Pennsylvania School of Medicine Paul Hardin Texas A&M Helena Illnerova Czech Academy of Sciences Michael Hastings MRC, Cambridge Carl Hirschie Johnson Vanderbilt University Sato Honma Hokkaido University David Kennaway School of Medicine University of Adelaide Medical School William J. Schwartz Charalambos P. Kyriacou University Massachesetts Medical University of Leicester School Jennifer Loros Editorial Board Dartmouth Medical School Ralph E. Mistlberger Serge Daan Simon Fraser University University of Groningen Larry Morin Bruce Goldman Stony Brook University University of Connecticut Hitoshi Okamura Terry Page Kyoto University Vanderbilt University Till Roenneberg Ueli Schibler Ludwig Maximilian University University of Geneva Rae Silver Michael Terman Columbia University Columbia University SOCIETY FOR RESEARCH ON BIOLOGICAL RHYTHMS III Society for Research on Biological Rhythms Gratefully Thanks Our Sponsors Supported in part by a grant from IV SRBR 2008 PROGRAM AND ABSTRACTS Table of Contents General Information. 2 Headquarters SRBR Information Desk and Message Center Messages Hotel Check-in Posters The Village of Baytowne Wharf Special Events Meeting at a Glance . 4 Trainee Professional Development Day . 6 Aaron Lerner Memorial Symposium. 8 Program Overview. 9 Poster Titles. 20 Symposium Abstracts . 42 Slide Session Abstracts . 62 Poster Abstracts. .98 Index of Authors. 245 Participants . 247 Notes. 261 Maps. 267 SOCIETY FOR RESEARCH ON BIOLOGICAL RHYTHMS 1 President’s Welcome our standing committees on Animal Issues, chaired by Larry Morin; on ChronoHistory, chaired by Anna The Society for Research on Biological Rhythms Wirz-Justice; and on Communications, chaired by first convened in May 1986 at Wild Dunes, South Frank Scheer; as well as the Editorial Board of the Carolina. After 20 years, we continue to fulfill Journal of Biological Rhythms, chaired by Marty founding President Fred Turek's vision of a vibrant Zatz. Results of the election of the new SRBR board, society and a long series of successful meetings. Our coordinated by Rae Silver, chair of the Nominations goal remains to bring together researchers and their Committee, will be announced at the Business research on all aspects of biological rhythms. We Meeting on Wednesday. If you have ideas on ways encourage the exchange of information and ideas to enhance the activities of these arms of the society, during the scheduled scientific sessions, as well as the take the opportunity during the meeting to talk to enlightenment that comes from discussions exposed any member of these groups, which are listed in the to the sun, sand, and sea breeze. Program Book. Welcome to the 11th Biennial Meeting! We are Special thanks are due Michelle Chappell, Karen the beneficiaries of months of planning and work Nichols and Amy Hubbard at Conference & by many people. Program Chair Ravi Allada and Institutes of the University of Illinois, for their skill his committee have put together an outstanding set in organizing this event, coordinating with Sandestin of scientific sessions, diverse in form and content. and anticipating our needs, and ensuring that it all Facilities Chair Shelley Tischkau choreographed the holds together while it runs. We are deeply grateful complex shifts of space through time. Ken Wright, to our corporate and government sponsors for their Jr. and his committee have organized and established generous support. Their names are listed at the front the first full SRBR Trainee Professional Development of this book, and posted throughout Sandestin Day and overseen trainee awards for research Conference Center. Please take time to personally accomplishment. thank their representatives for their investment in the Various sub-groups will meet while we are here. We SRBR. have two satellite symposia, one honoring Aaron Last, but by no means least, I extend my thanks to Lerner’s discovery of melatonin, organized by Jo each of you, the speakers, presenters, and participants. Arendt and Al Lewy, and the other focused on Your passion, originality,
Recommended publications
  • Functions of the Mineralocorticoid Receptor in the Hippocampus By
    Functions of the Mineralocorticoid Receptor in the Hippocampus by Aaron M. Rozeboom A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Cellular and Molecular Biology) in The University of Michigan 2008 Doctoral Committee: Professor Audrey F. Seasholtz, Chair Professor Elizabeth A. Young Professor Ronald Jay Koenig Associate Professor Gary D. Hammer Assistant Professor Jorge A. Iniguez-Lluhi Acknowledgements There are more people than I can possibly name here that I need to thank who have helped me throughout the process of writing this thesis. The first and foremost person on this list is my mentor, Audrey Seasholtz. Between working in her laboratory as a research assistant and continuing my training as a graduate student, I spent 9 years in Audrey’s laboratory and it would be no exaggeration to say that almost everything I have learned regarding scientific research has come from her. Audrey’s boundless enthusiasm, great patience, and eager desire to teach students has made my time in her laboratory a richly rewarding experience. I cannot speak of Audrey’s laboratory without also including all the past and present members, many of whom were/are not just lab-mates but also good friends. I also need to thank all the members of my committee, an amazing group of people whose scientific prowess combined with their open-mindedness allowed me to explore a wide variety of interests while maintaining intense scientific rigor. Outside of Audrey’s laboratory, there have been many people in Ann Arbor without whom I would most assuredly have gone crazy.
    [Show full text]
  • Circadian Disruption: What Do We Actually Mean?
    HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Eur J Neurosci Manuscript Author . Author manuscript; Manuscript Author available in PMC 2020 May 07. Circadian disruption: What do we actually mean? Céline Vetter Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, USA Abstract The circadian system regulates physiology and behavior. Acute challenges to the system, such as those experienced when traveling across time zones, will eventually result in re-synchronization to the local environmental time cues, but this re-synchronization is oftentimes accompanied by adverse short-term consequences. When such challenges are experienced chronically, adaptation may not be achieved, as for example in the case of rotating night shift workers. The transient and chronic disturbance of the circadian system is most frequently referred to as “circadian disruption”, but many other terms have been proposed and used to refer to similar situations. It is now beyond doubt that the circadian system contributes to health and disease, emphasizing the need for clear terminology when describing challenges to the circadian system and their consequences. The goal of this review is to provide an overview of the terms used to describe disruption of the circadian system, discuss proposed quantifications of disruption in experimental and observational settings with a focus on human research, and highlight limitations and challenges of currently available tools. For circadian research to advance as a translational science, clear, operationalizable, and scalable quantifications of circadian disruption are key, as they will enable improved assessment and reproducibility of results, ideally ranging from mechanistic settings, including animal research, to large-scale randomized clinical trials.
    [Show full text]
  • Familial Neurohypophyseal Diabetes Insipidus in 13 Kindreds and 2
    3 181 G Patti, S Scianguetta and Familial centralQ1 diabetes 181:3 233–244 Clinical Study others insipidus Familial neurohypophyseal diabetes insipidus in 13 kindreds and 2 novel mutations in the vasopressin gene Giuseppa Patti1,*, Saverio Scianguetta2,*, Domenico Roberti2, Alberto Di Mascio3, Antonio Balsamo4, Milena Brugnara5, Marco Cappa6, Maddalena Casale2, Paolo Cavarzere5, Sarah Cipriani7, Sabrina Corbetta8, Rossella Gaudino5, Lorenzo Iughetti9, Lucia Martini5, Flavia Napoli1, Alessandro Peri7, Maria Carolina Salerno10, Roberto Salerno11, Elena Passeri8, Mohamad Maghnie1, Silverio Perrotta2 and Natascia Di Iorgi1 1Department of Pediatrics, IRCCS Istituto Giannina Gaslini Institute, University of Genova, Genova, Italy, 2Department of Women, Child and General and Specialized Surgery, University of Campania ‘Luigi Vanvitelli’, Naples, Italy, 3University of Trieste, Trieste, Italy, 4Pediatrics Unit, Policlinico S. Orsola-Malpighi, Bologna, Italy, 5Department of Surgical Sciences, Dentistry, Gynecology and Pediatrics, University of Verona, Verona, Italy, 6Unit of Endocrinology, Bambino Gesù Children’s Hospital, IRCCS, Roma, Italy, 7Endocrine Unit, Department of Experimental and Clinical Biomedical Sciences ‘Mario Serio’, University of Firenze, Correspondence Ospedale Careggi Firenze, Firenze, Italy, 8Endocrinology and Diabetology Service, IRCCS Istituto Ortopedico Galeazzi, should be addressed University of Milan, Milan, Italy, 9Policlinico Universitario Modena, Modena, Italy, 10Department of Translational to M Maghnie or S Perrotta Medical Sciences-Pediatric Section, University of Naples Federico II, Naples, Italy, and 11SOD Endocrinologia, DAI Email Medico-Geriatrico, AOU Careggi Florence, Florence, Italy mohamadmaghnie@gaslini. *(G Patti and S Scianguetta contributed equally to this work) org or silverio.perrotta@ unicampania.it Abstract Background: Autosomal dominant neurohypophyseal diabetes insipidus (adNDI) is caused by arginine vasopressin (AVP) deficiency resulting from mutations in the AVP-NPII gene encoding the AVP preprohormone.
    [Show full text]
  • A Murine Model of Autosomal Dominant Neurohypophyseal Diabetes Insipidus Reveals Progressive Loss of Vasopressin- Producing Neurons
    A murine model of autosomal dominant neurohypophyseal diabetes insipidus reveals progressive loss of vasopressin- producing neurons Theron A. Russell, … , Jeffrey Weiss, J. Larry Jameson J Clin Invest. 2003;112(11):1697-1706. https://doi.org/10.1172/JCI18616. Article Endocrinology Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disorder caused by mutations in the arginine vasopressin (AVP) precursor. The pathogenesis of FNDI is proposed to involve mutant protein–induced loss of AVP-producing neurons. We established murine knock-in models of two different naturally occurring human mutations that cause FNDI. A mutation in the AVP signal sequence [A(–1)T] is associated with a relatively mild phenotype or delayed presentation in humans. This mutation caused no apparent phenotype in mice. In contrast, heterozygous mice expressing a mutation that truncates the AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these features of DI progressively worsened with age. Studies of the paraventricular and supraoptic nuclei revealed induction of the chaperone protein BiP and progressive loss of AVP-producing neurons relative to oxytocin-producing neurons. In addition, Avp gene products were not detected in the neuronal projections, suggesting retention of WT and mutant AVP precursors within the cell bodies. In summary, this murine model of FNDI recapitulates many features of the human disorder and demonstrates that expression of the mutant AVP precursor leads to progressive neuronal cell loss. Find the latest version: https://jci.me/18616/pdf A murine model of autosomal See the related Commentary beginning on page 1641. dominant neurohypophyseal diabetes insipidus reveals progressive loss of vasopressin-producing neurons Theron A.
    [Show full text]
  • And Low-Dose Melatonin Therapies
    diseases Review Divergent Importance of Chronobiological Considerations in High- and Low-dose Melatonin Therapies Rüdiger Hardeland Johann Friedrich Blumenbach Institute of Zoology and Anthropology, University of Göttingen, 37073 Göttingen, Germany; [email protected] Abstract: Melatonin has been used preclinically and clinically for different purposes. Some applica- tions are related to readjustment of circadian oscillators, others use doses that exceed the saturation of melatonin receptors MT1 and MT2 and are unsuitable for chronobiological purposes. Conditions are outlined for appropriately applying melatonin as a chronobiotic or for protective actions at elevated levels. Circadian readjustments require doses in the lower mg range, according to receptor affinities. However, this needs consideration of the phase response curve, which contains a silent zone, a delay part, a transition point and an advance part. Notably, the dim light melatonin onset (DLMO) is found in the silent zone. In this specific phase, melatonin can induce sleep onset, but does not shift the circadian master clock. Although sleep onset is also under circadian control, sleep and circadian susceptibility are dissociated at this point. Other limits of soporific effects concern dose, duration of action and poor individual responses. The use of high melatonin doses, up to several hundred mg, for purposes of antioxidative and anti-inflammatory protection, especially in sepsis and viral diseases, have to be seen in the context of melatonin’s tissue levels, its formation in mitochondria, and detoxification of free radicals. Citation: Hardeland, R. Divergent Keywords: circadian; entrainment; inflammation; melatonin; mitochondria; receptor saturation Importance of Chronobiological Considerations in High- and Low-dose Melatonin Therapies. Diseases 2021, 9, 18.
    [Show full text]
  • MELATONIN and HUMAN RHYTHMS INTRODUCTION It Has
    Chronobiology International, 23(1&2): 21–37, (2006) Copyright # 2006 Taylor & Francis Group, LLC ISSN 0742-0528 print/1525-6073 online DOI: 10.1080/07420520500464361 MELATONIN AND HUMAN RHYTHMS Josephine Arendt Centre for Chronobiology, School of Biomedical and Molecular Sciences, University of Surrey, Guildford, England Melatonin signals time of day and time of year in mammals by virtue of its pattern of secretion, which defines ‘biological night.’ It is supremely important for research on the physiology and pathology of the human biological clock. Light suppresses melatonin secretion at night using pathways involved in circadian photoreception. The melatonin rhythm (as evidenced by its profile in plasma, saliva, or its major metabolite, 6-sulphatoxymelatonin [aMT6s] in urine) is the best peripheral index of the timing of the human circadian pacemaker. Light suppression and phase-shifting of the melatonin 24 h profile enables the characterization of human circadian photore- ception, and circulating concentrations of the hormone are used to investigate the general properties of the human circadian system in health and disease. Suppression of melatonin by light at night has been invoked as a possible influence on major disease risk as there is increasing evidence for its oncostatic effects. Exogenous melatonin acts as a ‘chronobiotic.’ Acutely, it increases sleep propensity during ‘biological day.’ These properties have led to successful treatments for serveal circadian rhythm disorders. Endogenous melatonin acts to reinforce the functioning of the human circadian system, probably in many ways. The future holds much promise for melatonin as a research tool and as a therapy for various conditions. Keywords Melatonin, Light, Circadian and Circaanual Rhythms, Chronobiotic, Sleep, Sleep Disorders, Photoperiodism INTRODUCTION It has been nearly 50 yrs since Aaron Lerner identified melatonin and, after self-administration, reported that it made him feel sleepy (Lerner et al., 1958).
    [Show full text]
  • Tumour-Specific Arginine Vasopressin Promoter Activation in Small-Cell
    British Journal of Cancer (1999) 80(12), 1935–1944 © 1999 Cancer Research Campaign Article no. bjoc.1999.0623 Tumour-specific arginine vasopressin promoter activation in small-cell lung cancer JM Coulson, J Stanley and PJ Woll CRC Department of Clinical Oncology, University of Nottingham, City Hospital, Hucknall Rd, Nottingham NG5 1PB, UK Summary Small-cell lung cancer (SCLC) can produce numerous mitogenic neuropeptides, which are not found in normal respiratory epithelium. Arginine vasopressin is detected in up to two-thirds of SCLC tumours whereas normal physiological expression is essentially restricted to the hypothalamus. This presents the opportunity to identify elements of the gene promoter which could be exploited for SCLC- specific targeting. A series of human vasopressin 5′ promoter fragments (1048 bp, 468 bp and 199 bp) were isolated and cloned upstream of a reporter gene. These were transfected into a panel of ten cell lines, including SCLC with high or low endogenous vasopressin transcription, non-SCLC and bronchial epithelium. All these fragments directed reporter gene expression in the five SCLC cell lines, but had negligible activity in the control lines. The level of reporter gene expression reflected the level of endogenous vasopressin production, with up to 4.9-fold (s.d. 0.34) higher activity than an SV40 promoter. The elements required for this strong, restricted, SCLC-specific promoter activity are contained within the 199-bp fragment. Further analysis of this region indicated involvement of E-box transcription factor binding sites, although tumour-specificity was retained by a 65-bp minimal promoter fragment. These data show that a short region of the vasopressin promoter will drive strong expression in SCLC in vitro and raise the possibility of targeting gene therapy to these tumours.
    [Show full text]
  • Familial Neurohypophyseal Diabetes Insipidus—An Update Jane H
    Familial Neurohypophyseal Diabetes Insipidus—An Update Jane H. Christensen* and Søren Rittig† Although molecular research has contributed significantly to our knowledge of familial neurohypophyseal diabetes insipidus (FNDI) for more than a decade, the genetic back- ground and the pathogenesis still is not understood fully. Here we provide a review of the genetic basis of FNDI, present recent progress in the understanding of the molecular mechanisms underlying its development, and survey diagnostic and treatment aspects. FNDI is, in 87 of 89 kindreds known, caused by mutations in the arginine vasopressin (AVP) gene, the pattern of which seems to be largely revealed as only few novel mutations have been identified in recent years. The mutation pattern, together with evidence from clinical, cellular, and animal studies, points toward a pathogenic cascade of events, initiated by protein misfolding, involving intracellular protein accumulation, and ending with degener- ation of the AVP producing magnocellular neurons. Molecular research has also provided an important tool in the occasionally difficult differential diagnosis of DI and the opportunity to perform presymptomatic diagnosis. Although FNDI is treated readily with exogenous administration of deamino-D-arginine vasopressin (dDAVP), other treatment options such as gene therapy and enhancement of the endoplasmic reticulum protein quality control could become future treatment modalities. Semin Nephrol 26:209-223 © 2006 Elsevier Inc. All rights reserved. KEYWORDS neurohypophyseal diabetes
    [Show full text]
  • Dark-Phase Light Contamination Disrupts Circadian Rhythms in Plasma Measures of Endocrine Physiology and Metabolism in Rats
    Comparative Medicine Vol 60, No 5 Copyright 2010 October 2010 by the American Association for Laboratory Animal Science Pages 348–356 Dark-Phase Light Contamination Disrupts Circadian Rhythms in Plasma Measures of Endocrine Physiology and Metabolism in Rats Robert T Dauchy,1,* Erin M Dauchy,1 Robert P Tirrell,2 Cody R Hill,1 Leslie K Davidson,2 Michael W Greene,2 Paul C Tirrell,2 Jinghai Wu,2 Leonard A Sauer,2 and David E Blask1 Dark-phase light contamination can significantly disrupt chronobiologic rhythms, thereby potentially altering the endocrine physiology and metabolism of experimental animals and influencing the outcome of scientific investigations. We sought to de- termine whether exposure to low-level light contamination during the dark phase influenced the normally entrained circadian rhythms of various substances in plasma. Male Sprague–Dawley rats (n = 6 per group) were housed in photobiologic light-exposure chambers configured to create 1) a 12:12-h light:dark cycle without dark-phase light contamination (control condition; 123 µW/cm2, lights on at 0600), 2) experimental exposure to a low level of light during the 12-h dark phase (with 0.02 , 0.05, 0.06, or 0.08 µW/cm2 light at night), or 3) constant bright light (123 µW/cm2). Dietary and water intakes were recorded daily. After 2 wk, rats underwent 6 low-volume blood draws at 4-h intervals (beginning at 0400) during both the light and dark phases. Circadian rhythms in dietary and water intake and levels of plasma total fatty acids and lipid fractions remained entrained during exposure to either control conditions or low-intensity light during the dark phase.
    [Show full text]
  • Role of Melatonin in the Regulation of Human Circadian Rhythms and Sleep
    Journal of Neuroendocrinology, 2003, Vol. 15, 432–437 Role of Melatonin in the Regulation of Human Circadian Rhythms and Sleep C. Cajochen, K. Kra¨ uchi and A. Wirz-Justice Center for Chronobiology, Psychiatric University Clinic, Basel, Switzerland. Key words: chronobiotic, soporific, EEG power density, thermoregulation, sleepiness. Abstract The circadian rhythm of pineal melatonin is the best marker of internal time under low ambient light levels. The endogenous melatonin rhythm exhibits a close association with the endogenous circadian component of the sleep propensity rhythm. This has led to the idea that melatonin is an internal sleep ‘facilitator’ in humans, and therefore useful in the treatment of insomnia and the readjustment of circadian rhythms. There is evidence that administration of melatonin is able: (i) to induce sleep when the homeostatic drive to sleep is insufficient; (ii) to inhibit the drive for wakefulness emanating from the circadian pacemaker; and (iii) induce phase shifts in the circadian clock such that the circadian phase of increased sleep propensity occurs at a new, desired time. Therefore, exogenous melatonin can act as soporific agent, a chronohypnotic, and/or a chronobiotic. We describe the role of melatonin in the regulation of sleep, and the use of exogenous melatonin to treat sleep or circadian rhythm disorders. entrained (6, 7) and in sighted subjects with non 24-sleep–wake Endogenous melatonin and the circadian sleep–wake cycle syndrome (8, 9). Even more impressive are the results cycle and thermoregulation obtained from studies using the forced desynchrony protocol to Under entrained conditions, the phase relationship between the separate out circadian- and wake-dependent components of beha- endogenous circadian rhythm of melatonin and the sleep–wake viour.
    [Show full text]
  • Central Diabetes Insipidus (CDI) 15035X Mutations
    Central Diabetes Insipidus (CDI) 15035X Mutations Clinical Use Clinical Background • Differentiate inherited CDI from CDI is an acquired or autosomal acquired CDI dominant inherited disorder character- • Screen for CDI carrier status in at- ized by polyuria, polydipsia, a low risk individuals urinary specific gravity, and high risk of severe dehydration. Arginine Reference Range vasopressin (AVP), also known as Negative (no mutations detected) antidiuretic hormone (ADH), is absent. CDI stems from the degenera- Interpretive Information tion or destruction of cells in the posterior pituitary, the site of AVP Mutation present production. Thus, it is also referred to • Central diabetes insipidus (affected as pituitary, neurohypophyseal, or or carrier) neurogenic diabetes insipidus. The disorder typically presents in infancy or early childhood, although late-onset cases have been reported. Although rare, inherited CDI can be caused by mutations in the AVP gene on chromosome 20. Prepro-AVP, the initial protein product of the AVP gene, undergoes several post-transla- tional steps to yield AVP, neurophysin, and glycoprotein. When mutations in the AVP gene are present, cytotoxic products that lead to destruction of the secretory neurons are generated. Since more than 30 relevant mutations have been identified, gene sequencing is the method of choice for diagnosis of the inherited form. After identifica- tion of a mutation in an affected indi- vidual, genetic testing can be used to evaluate other family members. Method • Polymerase chain reaction (PCR) and DNA sequencing • Analytical specificity: mutations in 3 exons of the AVP gene Specimen Requirements 5 mL room temperature whole blood 3 mL minimum Collect blood in a lavender-top (EDTA) or yellow-top (ACD solution B) tube.
    [Show full text]
  • Photoperiodic Responses on Expression of Clock Genes, Synaptic Plasticity Markers, and Protein Translation Initiators the Impact of Blue-Enriched Light
    Photoperiodic Responses on Expression of Clock Genes, Synaptic Plasticity Markers, and Protein Translation Initiators The Impact Of Blue-Enriched Light Master report Jorrit Waslander, s2401878 Behavioral Cognitive Neuroscience research master, N-track University of Groningen, the Netherlands Internship at: Bergen Stress and Sleep Group, University of Bergen, Norway Date: 13-7-2018 Internal supervisor, University of Groningen: P. (Peter) Meerlo External supervisor, University of Bergen: J. (Janne) Grønli Daily supervisor, University of Bergen: A. (Andrea) R. Marti Photoperiodic Responses in the PFC Table of Contents Summary ................................................................................................................................................. 3 Introduction ............................................................................................................................................. 5 Research Objective .............................................................................................................................. 8 Hypotheses .......................................................................................................................................... 8 Methods ................................................................................................................................................ 10 Experimental procedure .................................................................................................................... 10 Ethics ............................................................................................................................................
    [Show full text]