Research Digest

Total Page:16

File Type:pdf, Size:1020Kb

Research Digest ERD Examine.com Research Digest Issue 7 ◆ May 2015 1 Table of Contents 05 Going nuts over infant peanut exposure Randomized trial of peanut consumption in infants at risk for peanut allergy 13 How the Food Industry Spins Science to Fit Its Agenda By Andy Bellatti, MS, RD 16 Non-celiac gluten sensitivity: much ado about something? Small Amounts of Gluten in Subjects with Suspected Nonceliac Gluten Sensitivity: a Randomized, Double-Blind, Placebo-Controlled, Cross-Over Trial 23 Baby probiotics for prevention of ADHD and Asperger’s A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood: a randomized trial 31 Putting the “D” in Death A reverse J-shaped association between serum 25- hydroxyvitamin D and cardio- vascular disease mortality – the CopD-study 40 Eggcellent Eggs: Is it safe for people with diabetes to eat a lot of eggs? The effect of a high-egg diet on cardiovascular risk factors in people with type 2 dia- betes: the Diabetes and Egg (DIABEGG) study—a 3-mo randomized controlled trial 46 Do BCAAs and arginine prevent central fatigue during exercise? Branched-chain amino acids and arginine improve performance in two consecutive days of simulated handball games in male and female athletes: a randomized trial 52 HMB-elly be gone β-Hydroxy-β-methylbutyrate (HMB) supplementation and resistance exercise sig- nificantly reduce abdominal adiposity in healthy elderly men 58 Spicing up your workout Curcumin supplementation likely attenuates delayed onset muscle soreness (DOMS) 65 INTERVIEW: Shawn Wells, MPH, RD 71 Ask the Researcher: James Heathers, Ph.D. 2 From the Editor Does “natural” matter in food and nutrition? inform what you eat. You MOST CERTAINLY don’t have to be anyone’s definition of “paleo”. Humans can eat a vari- I don’t think natural versus processed is just a fluff issue. ety of foods and thrive. Different people have astoundingly Many people use heuristics to guide how they eat, whether different reactions to food, due to their gut microbiomes, they know it or not. It’s hard for most people (Soylent aficio- disease states, and many other factors. nados excepted) to envision a mostly processed/powdered diet being healthier than a diet composed mostly of less Why does this matter for ERD and nutrition research in processed plants and animals. general? Well, it’s very easy to get caught up in research details and miss the big picture of health. Yes, heating toma- For ERD, we occasionally point out that certain nutrients toes increases lycopene absorption. Yes, piperine increases and supplements don’t need to come in pill form, and can absorption of curcumin. But so many people obsess over be ingested through food. But constantly telling people how details while missing the truly high impact habits, like cir- to eat sounds preachy from most anybody, and we are pretty cadian rhythm entrainment and stress reduction. Avoiding much evidence-conveyors rather than gurus. That doesn’t yo-yo dieting and enjoying wholesome meals is a good pre- mean we don’t have opinions on an individual level though. requisite to supplementation in general. And my personal opinion is that natural does probably matter. And while evidence is our bread and butter, know the lim- I don’t mean the literal definitions of natural and processed, itations of evidence. Just because research suggests that which gets into annoying semantics and downward spirals artificial sweeteners may be fairly safe, don’t take that as of argumentation. Yes, cutting a carrot is processing it. Yes, an excuse to drink two Diet Cokes every day for thirty applying heat can be considered processing. I’m not talking years. From reading ERD, you should be well aware that about gray areas though. This is about a smoothie versus a study findings don’t equal truth. Although evidence is Diet Coke. Pastured beef versus a zero carb protein bar with mixed, we’re just starting to find that artificial sweeteners thirty ingredients. may adversely impact the gut microbiome. While nutrition research is complex, nature is magnitudes of order more Don’t get me wrong: artificial foods can be magically deli- complex. It’s probably a good idea to consider both when cious. If you have enough self-control, Cheetos can be making decisions for your own health. worth every flourescent orange dusted finger that needs washing before using your laptop. A little bit, or even a moderate amount every once in a while, isn’t likely to be terrible for you. But that’s a guess. There will be no randomized trials on Cheetos (I think). What there is though, is history. Many thousands of years of humans eating food that can help Kamal Patel, Editor-in-Chief 3 Contributors Researchers Trevor Kashey Alex Leaf Courtney Silverthorn Zach Bohannan Anders Nedergaard Jeff Rothschild Ph.D(c) M.S(c) Ph.D. M.S. Ph.D. M.Sc., RD Editors Gregory Lopez Pablo Sanchez Soria Kamal Patel Pharm.D. Ph.D. M.B.A., M.P.H., Ph.D(c) Reviewers Arya Sharma Natalie Muth Stephan Guyenet Sarah Ballantyne Katherine Rizzone Spencer Nadolsky Ph.D., M.D. M.D., M.P.H., RD Ph.D. Ph.D. M.D. D.O. Mark Kern Gillian Mandich Ph.D., RD Ph.D(c) 4 Going nuts over infant peanut exposure Randomized trial of peanut consumption in infants at risk for peanut allergy Introduction Peanut allergies are becoming more widespread across the globe. In the United States, up to 1.4% of the population, or as many as 4.4 million people have a peanut allergy. Peanut exposure is one of the leading causes of allergy-related deaths due to anaphylax- is, a set of symptoms that can include facial and oral swelling, difficulty breathing, a dangerous drop in blood pressure, and cardiac arrest. Other less severe symptoms include itchy skin and mouth, hives, and gastrointestinal distress. Unlike some other food allergies, like milk, soy, and egg, a pea- nut allergy rarely lessens with age. While there has been a lot research into possible therapies, there is currently no treatment other than complete avoidance, which requires hypervigilance in case of cross-contamination of other foods, leading to trace amounts of peanut in foods that would otherwise be assumed as safe. Many current research efforts focus instead on ways to prevent the development of severe allergies like this one. Researchers discovered that dietary antigens (foreign substanc- es that trigger the immune system to respond) for allergenic foods can pass through the placenta to the fetus, as well as pass through breast milk to an infant. Based on this finding, they hypothesized that preventing this early exposure would reduce the incidence of food allergies. 5 For most of the first decade of the 21st century, women Figure 1 - Peanuts: from snack darling were advised to avoid possible allergy triggers like peanuts, to object of constant vigilance dairy, and egg during their pregnancies, as well as to avoid feeding them to their infants. In spite of these efforts, epide- miological data show that the incidence of allergies actually increased. In fact, a meta-analysis of studies following chil- dren whose mothers had avoided dietary allergens found that those children developed allergies at approximately the same rate as children whose mothers did not adhere to the dietary recommendations. As a result, the recommendation to avoid dietary allergens during pregnancy was later aban- doned. Figure 1 notes some milestones from the past few decades with regards to peanut allergy. The increase in allergy rates in response to avoiding certain foods raises the question of whether deliberate exposure to potentially allergenic foods could reduce the incidence of allergies. This study was designed to investigate this ques- tion in the context of peanut allergies in infants. The number of people with a peanut allergy is increasing worldwide, which can result in a serious and sometimes life-threatening allergic reaction. Previous recommen- dations for mothers to avoid allergens during pregnancy and breastfeeding did not prevent the rise in allergies in children. The purpose of this study was to see if con- sumption of peanuts at an early age might help prevent development of peanut allergies in children. Who and what was studied? Infants from four to 11 months who had already been diag- nosed with severe eczema and/or egg allergy were included in this study. Because the study was on infants, and because of the possibility of serious allergic reactions, the trial was conducted as an ‘open-label’ study, rather than a blind or dou- ble-blind study. Both the researchers and the parents knew whether or not their child would receive the peanut snack. The infants were divided into two groups on the basis of a Source: Sicherer et al., J Allergy Clin Immunol. 2010 skin prick test (SPT) with peanut allergens. About 15% of 6 the infants in the study were assigned to one group after an Parents were provided with the peanut snacks to feed to initial positive SPT, defined as a skin wheal, or localized their child, with the option of substituting an equivalent region of redness and swelling, between one to four milli- amount of peanut butter instead. The researchers conducted meters. The 80% of the infants with a negative initial SPT in-person follow-up appointments at 12, 30, and 60 months were assigned to a second group. Infants with wheals larg- into the study. At each appointment, children were tested er than four millimeters were excluded from the study for for reactions to the peanut protein SPT. Researchers also safety reasons, as they would be expected to already have measured the levels of peanut-specific antibodies.
Recommended publications
  • American Heart Association Preview 2017.Pdf
    NovemberNovember 11-15 11-15 Anaheim,Anaheim, California California PREVIEWTHE IN CLASS CARDIOVASCULAR CONFERENCE EDUCATIONAL SESSIONS FOR ALL CAREER STAGES WITH GLOBAL THOUGHT LEADERS innovative FACULTY PROVIDING INTERACTIVE, network PERSONALIZED EDUCATION world- renowned PAID ADVERTISEMENT PICK UP A FREE COPY AT: AHA HeartQuarters, booth #355 Wolters Kluwer, booth #439 Wiley, booth #545 FIND THE ENTIRE AHA /ASA JOURNALS’ TREND WATCH COLLECTION ONLINE DOWNLOAD ALL 3 ISSUES TODAY! Freely 450+ Available Articles INTERACTIVE MAGAZINE DOWNLOAD THE BLIPPAR APP App required for free, full-text Download the latest issue and view access to Trend Watch. a video demonstration at AVAILABLE ON www.ahajournals.org/site/trendwatch American Heart Association American Heart Association National Center 7272 Greenville Ave. Dallas, TX 75231 214-373-6300 800-242-2453 professional.heart.org Registration INSIDE Convention Data Services 107 Waterhouse Road THE PREVIEW Bourne, MA 02532 800-748-3583 (inside U.S.) 508-743-8517 (outside U.S.) Join the [email protected] AHA Scientific Sessions 2017 conversation Housing 2 Welcome from the program chair onPeak 4 What’s hot at AHA Scientific Sessions 2017 381 Park Ave. S., Third Floor 6 Expect the best in 2017 New York, NY 10 Week at a glance facebook.com/ 800-221-3531 (inside U.S.) ahameetings 312-527-7300 (outside U.S.) [email protected] Advance programming and faculty Facility Anaheim Convention Center 14 Programming information and schedule @AHAmeetings 800 W. Katella Ave. #AHA17 Anaheim, CA 92802 14 CE/CME
    [Show full text]
  • Omega-3 Fatty Acids and Their Role in Cardiac Arrhythmogenesis Workshop Research Challenges and Opportunities
    National Heart, Lung, and Blood Institute and the Office of Dietary Supplements National Institutes of Health Omega-3 Fatty Acids and their Role in Cardiac Arrhythmogenesis Workshop Research Challenges and Opportunities August 29-30, 2005 Embassy Suites Hotel at the Chevy Chase Pavilion 4300 Military Road, NW Washington, District of Columbia 20015 AGENDA Omega-3 Fatty Acids and their Role in Cardiac Arrhythmogenesis Workshop: Research Challenges and Opportunities Day 1: Monday, August 29, 2005 9:00 a.m. Call to Order 9:30 a.m. Welcome and Opening Remarks Dr. David Lathrop Dr. Rebecca Costello 9:35 a.m. Workingshop Goals and Objectives Dr. Barry London (Chair) Session I - Background: Evidence for Antiarrhythmic Effects of Omega-3 (n-3) Fatty Acids 9:50 a.m. Evidence for Antiarrhythmic Effects from Epidemiologic Dr. Christine Albert Studies 10:20 a.m. Agency for Healthcare Research and Quality Dr. Ethan Balk (AHRQ): Evidence Reports on the Cardiovascular Ms. Mei Chung Effects of n-3 Fatty Acids 10:50 a.m. Discussion All Participants 11:05 a.m. Break . Session II –NHLBI-supported Trials to Determine the Antiarrhythmic Effects of n-3 Fatty Acids 11:15 a.m. The Fatty Acid Antiarrhythmia Trial (FATT) (R01 Dr. Alexander Leaf HL062154) 11:55 a.m. The Antiarrhythmic Effects of n-3 Fatty Acids Study (R01 Dr. John McAnulty HL061682) 12:35 p.m. Discussion All Participants 12:50 p.m. Lunch Session III – Possible Basic Mechanisms of Action 1:50 p.m. Dietary Source of n-3 Fatty Acids: Metabolic Pathways Dr. Bill Lands and Sites of Interaction 2:20 p.m.
    [Show full text]
  • Remodeling of Myocardial Passive Electrical Properties: Insights Into the Mechanisms of Malignant Arrhythmias and Sudden Cardiac Death
    Remodeling of Myocardial Passive Electrical Properties: Insights into the Mechanisms of Malignant Arrhythmias and Sudden Cardiac Death. DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Carlos Luis del Rio, M.S. Graduate Program in Electrical and Computer Science The Ohio State University 2015 Dissertation Committee: Professor Bradley D. Clymer, Ph.D., Advisor Professor George E. Billman, Ph.D., Co-Advisor Professor Furrukh S. Khan, Ph.D. Copyright by Carlos Luis del Rio 2015 Abstract Despite extensive research, sudden cardiac death (SCD) resulting from ischemia-induced malignant arrhythmias, such as ventricular fibrillation (VF), remains a leading cause of death, particularly following myocardial infarction (MI). Furthermore, SCD is generally the first and most common manifestation of the disease, as current risk-stratifying tools are inaccurate and insufficient. Acute/chronic changes in the passive electrical properties governing electrotonic coupling in the myocardium have been proposed as a potential mechanism mediating both the onset and maintenance of arrhythmias, as the loss of homogenizing electrotonic coupling can exacerbate intrinsic pro-arrhythmic electrical heterogeneities within the ventricle, especially during repolarization. However, no study to date has assessed the ability of indices reflective of electrotonic changes to stratify intrinsic arrhythmic susceptibility in vivo. Leveraging a well-established in vivo post-MI canine model of SCD and lethal arrhythmias, this research work investigates the pro-arrhythmic role of changes in the passive electrical properties of the myocardium, as measured by its complex electrical impedance spectrum (MEI). The studies were performed under the general hypothesis that the loss of electrotonic coupling accompanies and facilitates the development of malignant arrhythmias in the setting of ischemia and post-MI ventricular/autonomic remodeling.
    [Show full text]
  • Relengthening RT50, Fig 3C-G)
    Neuronal Nitric Oxide Synthase Signaling Contributes to the Beneficial Cardiac Effects of Exercise DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Steve R. Roof Biomedical Sciences Graduate Program The Ohio State University 2012 Dissertation Committee: Dr. Mark T. Ziolo, PhD Advisor Dr. George E. Billman, PhD Dr. Sandor Gyorke, PhD Dr. Brandon Biesidecki, PhD ABSTRACT Exercise is beneficial to one’s health, reduces the risk of cardiomyopathies, and is utilized as a therapeutic intervention after disease [2-7]. This is due, in part, due to the beneficial chronic adaptations that enhance contraction and accelerate relaxation [8]. These intrinsic exercise-induced adaptations are observed at the level of the cardiomyocyte [9]. That is, ventricular myocytes from exercised (Ex) mice exhibit increased Ca2+ cycling and contraction-relaxation rates [6, 9-12]. Additionally, cardiac growth (physiological hypertrophy) and an increase in aerobic fitness (VO2max) are hallmark cardiac adaptations due to exercise training. The molecular mechanisms that explain how the heart adapts are not fully understood and studies examining signaling pathways are limited. A signaling molecule with a potential role in cardiac adaptations to exercise is nitric oxide (NO). Nitric Oxide (NO) has been shown to be a key regulator of myocyte contractile function. NO, produced via the neuronal nitric oxide synthase (nNOS or NOS1), enhances basal contraction by increasing Ca2+ cycling through the sarcoplasmic reticulum (SR) [13-15]. Data suggest that NOS1 signaling increases Ca2+ uptake by targeting the SR Ca2+ ATPase (SERCA2a)/phospholamban (PLB) complex. NOS1 signaling also targets the SR Ca2+ release channel (ryanodine receptor - RYR2) to increase its open time probability [16].
    [Show full text]
  • Regulation of Cardiac Voltage Gated Potassium Currents in Health and Disease
    REGULATION OF CARDIAC VOLTAGE GATED POTASSIUM CURRENTS IN HEALTH AND DISEASE DISSERTATION Presented in Partial Fulfillment of the Requirements for The Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Arun Sridhar, M.S. ****** The Ohio State University 2007 Dissertation Committee: Dr. Cynthia A. Carnes, Pharm.D, PhD Approved By: Dr. Robert L. Hamlin, DVM, PhD ______________________ Dr. Sandor Gyorke, PhD Advisor Dr. Mark T. Ziolo, PhD Graduate Program in Biophysics ABSTRACT Cardiovascular disease (CVD) is a major cause of mortality and morbidity worldwide. CVD accounts for more deaths than all forms of cancer in the United States. Hypertension, Heart Failure and Atrial Fibrillation are the most common diagnosis, hospitalization cause and the sustained cardiac arrhythmia respectively in the US. Sudden cardiac death is the one of the most common causes of cardiovascular mortality after myocardial infarction, and a common cause of death in heart failure patients. This has been attributed to the development of ventricular tachyarrhythmias. In addition, most forms of acquired CVD have been shown to produce electrophysiological changes due to very close interactions between structure, signaling pathways and ion channels. Due to the increased public heath burden caused by CVD, a high impetus has been placed on identifying novel therapeutic targets via translational research. Identification of novel therapeutic targets to treat heart failure and sudden death is underway and is still in a very nascent stage. In addition, ion channel blockers, more specifically “atrial-specific” ion channel blockers have proposed to be a major therapeutic target to treat atrial fibrillation without the risk of ventricular pro- arrhythmia.
    [Show full text]
  • The Benefits of Marine Omega-3S for Preventing Arrhythmias
    Open access Editorial Open Heart: first published as 10.1136/openhrt-2018-000904 on 4 February 2020. Downloaded from The benefits of marine omega- 3s for preventing arrhythmias James J DiNicolantonio, James OKeefe To cite: DiNicolantonio JJ, MARINE OMEGA-3S FOR THE PREVENTION OF polyunsaturated fatty acids (PUFAs) can also OKeefe J. The benefits of marine ARRHYTHMIAS be liberated from lipoproteins via lipoprotein omega- 3s for preventing and hepatic lipase and picked up by albumin arrhythmias. Open Heart Omega- 3s have been theorised to increase 2020;7:e000904. doi:10.1136/ membrane fluidity by reducing compression via fatty acid- binding sites. The omega- 3s are openhrt-2018-000904 of the acyl chains of membrane phospholipid then carried by albumin to the heart, brain fatty acids, which can lead to a reduction in and other tissues for entrance into membrane 4 Received 17 July 2018 the ‘spring- like’ tension on membrane ion phospholipids and stored as triglycerides. Revised 29 September 2018 channels. This spring-like tension can reduce However, it is the liberated ‘free- fatty acid’ Accepted 12 October 2018 the ability of ions to freely move in and out form of omega-3s that are thought to produce of the ion channel and hence reduce its the antiarrhythmic properties. This free conductance. This is known as the ‘Andersen form of omega-3 can be mobilised from the membrane spring- like tension hypothesis’ plasma phospholipid during states of stress and is just one way marine omega- 3s may (severe exertion, sympathetic discharge) via prevent arrhythmias.1 This theory states that phospholipases.5 6 If consumed on a regular the phospholipid cell membrane curves near basis, omega- 3s will be adequately stored the ion protein channel in order for the in the heart waiting to be released in order hydrophobic domains of the cell membrane to protect against fatal arrhythmias.
    [Show full text]
  • Effect of Omega-3 Fatty Acids on Ventricular Action Potentials in a Canine Model of Sudden Cardiac Death
    Effect of omega-3 fatty acids on ventricular action potentials in a canine model of sudden cardiac death THESIS Presented in Partial Fulfillment of the Requirements for the Degree Master of Science in the Graduate School of The Ohio State University By Sarmistha Mazumder Graduate Program in Pharmacy The Ohio State University 2010 Master's Examination Committee: Cynthia Carnes, PharmD, PhD, Advisor Terry S. Elton, PhD George E. Billman, PhD Copyright by Sarmistha Mazumder 2010 Abstract Background : Sudden cardiac death (SCD) is the most common cause of death in the United States and in most developed countries, accounting for ~ 50% of total mortality. The most common underlying cause of SCD is “ventricular fibrillation” (VF). Several clinical trials have reported conflicting results on the benefits of omega-3 fatty acids for the prevention of lethal ventricular arrhythmias following infarction. The explanation for these inconsistent results remains to be determined. Methods : Dogs with healed left ventricular anterior wall myocardial infarctions (MI, 3-4 weeks post- MI, n = 76) were subjected to an exercise and ischemia test to stratify animals by arrhythmia risk as VF susceptible, VF + (n = 46) and VF resistant, VF - (n = 30). The animals were then assigned to omega-3 fatty acid ethyl esters (1-4 grams/day, n = 45) or corn-oil treatment (placebo, n = 31) for 3 months. Following treatment, arrhythmia inducibility was re-evaluated with the exercise and ischemia test. The left ventricular myocytes were isolated one week following the exercise plus ischemia test. Five age matched dogs served as controls (non-infarcted). Action potentials were recorded by perforated whole cell patch clamp studies (T= 36 ± 0.5ºC) to measure the resting membrane potentials (RMP) and the action potential duration at 90% repolarization (APD 90 ).
    [Show full text]
  • Letter to President Obama Vivisection Marlene Phelan March 17, 2011
    letter to president obama vivisection marlene phelan March 17, 2011 1 March 17th, 2011 The White House 1600 Pennsylvania Ave. NW Washington, D.C. 20500 Dear Mr. President; I would like to speak out for 115 million individuals a year whose voices will never be heard. I would like to speak of their outrageous, heartbreaking suffering. “Sanitized Sadism” is what it has been called by one human. This legalized torture is hidden in buildings without windows. It takes place in basements, cellars, and underground rooms. George Bernard Shaw once said, “There are hundreds of paths to scientific knowledge. The cruel ones can teach us only what we ought not to know.” This sanitized sadism costs the United States taxpayers over 18 billion dollars annually. This tragic waste of life is represented here in print, photos and DVD’s of numerous undercover investigations of laboratories in the United States. These animals are voiceless victims of a devious atrocity that is called vivisection. Vivisection is a method of “science”, which was labeled by Dr. Frederic Mayo, founder of the Mayo clinic, as “Evil.” “My own conviction is that the study of human physiology by way of experiments on animals is the most grotesque and fantastic 2 error ever committed in the whole range of human intellectual ability.” (Dr. G.F. Walker in “Medical World” Dec. 8, 1933). The victims of these scientific atrocities have faces. I would like to introduce you to one rare survivor known formerly only as “CH 411”. (“CH 411”,Tom, 1965-2009) 3 “CH 411” was the way he was referred to by laboratory workers that kept him in a cage for 30 years.
    [Show full text]
  • Future Physiologists Early Career Special Issue Experimental Models in Physiology 27 - 29 June 2018 | University of Exeter, UK
    PN Issue 109 / Winter 2017 Physiology News Future physiologists Early career special issue Experimental models in physiology 27 - 29 June 2018 | University of Exeter, UK The Mighty Mouse and the might of other models Why is the mouse not so mighty? Complementary models Pathophysiological models: Cells to complex systems Insights from animal models of human disease Towards human models Future directions: Opportunities and challenges www.physoc.org/models Physiology News Scientific Editor Roger Thomas We welcome feedback on our membership magazine, or letters and suggestions for (University of Cambridge) articles for publication, including book reviews, from our Members. Managing Editor Please email Julia Turan at [email protected] Julia Turan Editorial Board Physiology News is one of the benefits of membership, along with reduced registration rates Karen Doyle for our high-profile events, free online access to our leading journals,The Journal of Physiology, (NUI Galway) Experimental Physiology and Physiological Reports, and travel grants to attend scientific Rachel McCormick meetings. Membership offers you access to the largest network of physiologists in Europe. (University of Liverpool) Keith Siew Join now to support your career in physiology: (University of Cambridge) Visit www.physoc.org/membership or call 0207 269 5721 Austin Elliott (University of Manchester) Mark Dallas (University of Reading) Membership Fees for 2017 FEES Fiona Hatch Fellow £120 (Cello Health Communications iScience, Member £90 Medical writer) [email protected] Retired Member – Affiliate £40 www.physoc.org Associate £30 Undergraduate – @ThePhySoc /physoc Opinions expressed in articles and letters submitted by, or commissioned from, Members, Affiliates or outside bodies are not necessarily those of The Physiological Society.
    [Show full text]
  • DAVID C. RANDALL DATE of BIRTH April 23, L945 DEGREES HELD BA
    DAVID C. RANDALL DATE OF BIRTH April 23, l945 DEGREES HELD B.A. (scl) physics, chemistry Taylor University, l967 Ph.D. physiology University of Washington, l972 POSITIONS HELD 2007 - present Donald T. Frazier Professor, Department of Physiology and Biophysics, College of Medicine, University of Kentucky 1985 - present Professor, Department of Physiology and Biophysics, College of Medicine, University of Kentucky 1978 - 1985 Associate Professor, Department of Physiology and Biophysics, College of Medicine, University of Kentucky 1981 - 1984 Director of Graduate Studies, Department of Physiology and Biophysics, University of Kentucky 1981 Visiting Associate Professor, Department of Neurobiology and Behavior, State University of New York at Stony Brook 1979 - 2014 Part-time Instructor, Asbury University, Wilmore, KY 1975 - 1978 Assistant Professor, Department of Physiology & Biophysics, College of Medicine, University of Kentucky 1972 - 1975 Assistant Professor, Division of Behavioral Biology, Department of Psychiatry and Behavioral Sciences, The Johns Hopkins University School of Medicine JOINT APPOINTMENTS 1987 - Present Professor, Graduate Center for Biomedical Engineering, University of Kentucky (Executive Committee, 1990 - 1992) 2004 - Present Associate Faculty, University of Kentucky Spinal Cord and Brain Injury Research Center MEMBERSHIP ON PUBLIC ADVISORY GROUPS American Heart Association, Kentucky Affiliate Research Peer Review Committee (1980 - 1990; chair, 1985 – 1987) Resource Allocation Committee, (member, 1986 - 1992; chair,
    [Show full text]
  • Physiologynews
    PHYSIOLOGYNEWS winter 2006 | number 65 Meetings Bristol Brazil Heidelberg International Workshop, Kiev Also featuring A century of research in sugar transport A summer in the life of a retiring physiologist Did evolution go the wrong path for the human lung? Acute pain Legs pay out for cost of breathing! Long and tortuous goodbye to Stud Muffin No 1 A publication of The Physiological Society IMAGES OF BRAZIL JOINT INTERNATIONAL MEETING WITH THE BRAZILIAN PHYSIOLOGICAL SOCIETY Ribeirão Preto, Brazil 27-30 August 2006 For more images of Brazil, including flora and fauna, see the inside back cover (photos by Prem Kumar) PHYSIOLOGYNEWS Editorial 3 Meetings Bristol Focused Meeting Johannes Reul, Astrid Linthorst, 4 The Society’s dog. ‘Rudolf Magnus gave Stafford Lightman me to Charles Sherrington, who gave me Heidelberg Focused Meeting Joseph Bruton 5 to Henry Dale, who gave me to The Images of Brazil inside front and back covers Physiological Society in October 1942’ Living history The surface energy of water from 1908 Wilfred Widdas 7 A summer in the life of ... Published quarterly by The Physiological Society An (endless?) summer in the life of a retiring physiologist 11 Contributions and Queries David Miller Executive Editor Features Linda Rimmer The Physiological Society Publications Office What structures bear the tension and store energy in lengthening 13 P O Box 502 muscle? Gavin Pinniger, K W Ranatunga, Gerald Offer Cambridge CB1 0AL Acidification protects skeletal muscle volume during anaerobic 15 UK exercise Juliet Usher-Smith,
    [Show full text]
  • Proquest Dissertations
    INFORMATION TO USERS This manuscript has been reproduced from the microfilm master. UMI films the text directly from the original or copy submitted. Thus, some thesis and dissertation copies are in typewriter face, while others may t>e from any type of computer printer. The quality of this reproduction is dependent upon tfie quality of the copy submitted. Broken or indistmct print, colored or poor quality illustrations and photographs, print bleedthrough, substandard margins, and improper alignment can adversely affect reproduction. In the unlikely event tfiat the author did not send UMI a complete manuscript and there are missing pages, these will t>e noted. Also, if unauthorized copyright material had te be removed, a note will indicate the deletion. Oversize materials (e.g., maps, drawings, charts) are reproduced by sectioning the original, t>eginning at the upper left-hand comer and continuing from left to right in equal sections with small overlaps. Photographs included in the original manuscript have been reproduced xerographically in this copy. Higher quality 6” x 9” black and white photographic prints are available for any photographs or illustrations appearing in this copy for an additional charge. Contact UMI directly to order. Bell & Howell Information and Learning 300 North Zeeb Road, Ann Arbor, Ml 48106-1346 USA UIVLI800-521-0600 ENHANCED IN VIVO AND IN VITRO RESPONSE TO BETA-2 ADRENERGIC RECEPTOR STIMULATION IN ANIMALS SUSCEPTIBLE TO VENTRICULAR FIBRILLATION DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Melanie Taghon Houle, M.S.
    [Show full text]