David A. Eisner

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David Eisner
Eisner David A.jpg
David A. Eisner in 2016
Born
David Alfred Eisner

(1955-01-03) 3 January 1955 (age 69)
Manchester [1]
Awards Physiological Society Annual Review Prize Lecture (2017)
Scientific career
Institutions University College London, University of Liverpool, University of Manchester
Thesis The effects of sodium pump inhibition on the electrical and mechanical properties of mammalian cardiac muscle.  (1979)
Doctoral advisor Denis Noble

David Alfred Eisner, FRCP (Hon), FMedSci, [2] (born 3 January 1955) [1] [3] is British Heart Foundation Professor of Cardiac Physiology at the University of Manchester and editor-in-chief of The Journal of General Physiology (JGP). [4]

Contents

Education

Eisner was born in 1955 in Manchester, the son of the physicist and writer Herbert Eisner. [5] [3] [6] After attending Manchester Grammar School, he received his B.A. in natural sciences at King's College, Cambridge in 1976. In 1979 he obtained a D.Phil. in physiology at Oxford University in the laboratory of Denis Noble for work on the sodium pump in cardiac muscle.

Career

Following postdoctoral research at the University of Cambridge on the kinetics of the sodium pump [7] in the laboratory of Ian Glynn, he took up a lectureship in the Department of Physiology at University College London in 1980. In 1990 he moved to The University of Liverpool as professor of veterinary biology. In 1999 he took up a chair of cardiac physiology at the University of Manchester and, in 2000, was awarded the BHF Chair of Cardiac Physiology. [8]

Eisner was chair of the editorial board of The Journal of Physiology from 1997 to 2000 [9] and editor-in chief of the Journal of Molecular and Cellular Cardiology from 2007 to 2016. He was president of The Federation of European Physiological Societies (FEPS) from 2011-2015 [10] and The Physiological Society from 2016 to 2018.

Research

Eisner's early research focused on the regulation of intracellular sodium in cardiac muscle and the effects on contraction. [11] He then investigated the control of intracellular calcium concentration [12] and its role in the production of arrhythmias. [13] He has identified the factors that regulate the calcium content of the sarcoplasmic reticulum [14] [15] and how this is altered in disease. [16] His recent research has focused on the control of diastolic calcium [17] [18] and the effects of calcium buffering. [19] [20] He has also written [21] and spoken [22] about scientific reproducibility and fraud.

Personal life

Eisner is married to Susan Wray, professor of cellular and molecular physiology at the University of Liverpool, with whom he has three children. [6]

Honours and awards

Eisner was elected as a Fellow of The Academy of Medical Sciences in 1999 [23] and The International Society for Heart Research in 2001. [24] and as a Member of Academia Europaea in 2007. [25] He was elected to Honorary Fellowship of The Royal College of Physicians in 2010. In 2018 he received an honorary doctorate, Doctor Honoris Causa, from The University of Debrecen. [26] and, in 2021 from The University of Szeged. [27] Prizes awarded to him include: The GL Brown [28] [29] and Annual Review Lecture [30] of The Physiological Society; the Keith Reimer Lecture [31] [32] and the Peter Harris Distinguished Scientist Award of the International Society for Heart Research; the Carmeliet-Coraboeuf-Weidmann Lecture of the European Working Group on Cardiac Cellular Electrophysiology; [33] the Fabio Ruzzier Lecture of The Italian Physiological Society. [34] He has also delivered the Burdon-Sanderson Lecture (Oxford) in 2013. [35]

Related Research Articles

<span class="mw-page-title-main">Sodium–potassium pump</span> Enzyme found in the membrane of all animal cells

The sodium–potassium pump is an enzyme found in the membrane of all animal cells. It performs several functions in cell physiology.

<span class="mw-page-title-main">Cardiac muscle</span> Muscular tissue of heart in vertebrates

Cardiac muscle is one of three types of vertebrate muscle tissues, the others being skeletal muscle and smooth muscle. It is an involuntary, striated muscle that constitutes the main tissue of the wall of the heart. The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall and the inner layer, with blood supplied via the coronary circulation. It is composed of individual cardiac muscle cells joined by intercalated discs, and encased by collagen fibers and other substances that form the extracellular matrix.

<span class="mw-page-title-main">Frank–Starling law</span> Relationship between stroke volume and end diastolic volume

The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.

<span class="mw-page-title-main">Cardiac action potential</span> Biological process in the heart

Unlike the action potential in skeletal muscle cells, the cardiac action potential is not initiated by nervous activity. Instead, it arises from a group of specialized cells known as pacemaker cells, that have automatic action potential generation capability. In healthy hearts, these cells form the cardiac pacemaker and are found in the sinoatrial node in the right atrium. They produce roughly 60–100 action potentials every minute. The action potential passes along the cell membrane causing the cell to contract, therefore the activity of the sinoatrial node results in a resting heart rate of roughly 60–100 beats per minute. All cardiac muscle cells are electrically linked to one another, by intercalated discs which allow the action potential to pass from one cell to the next. This means that all atrial cells can contract together, and then all ventricular cells.

<span class="mw-page-title-main">Muscle contraction</span> Activation of tension-generating sites in muscle

Muscle contraction is the activation of tension-generating sites within muscle cells. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length, such as when holding something heavy in the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.

Ryanodine receptors form a class of intracellular calcium channels in various forms of excitable animal tissue like muscles and neurons. There are three major isoforms of the ryanodine receptor, which are found in different tissues and participate in different signaling pathways involving calcium release from intracellular organelles. The RYR2 ryanodine receptor isoform is the major cellular mediator of calcium-induced calcium release (CICR) in animal cells.

<span class="mw-page-title-main">T-tubule</span> Extensions in cell membrane of muscle fibres

T-tubules are extensions of the cell membrane that penetrate into the center of skeletal and cardiac muscle cells. With membranes that contain large concentrations of ion channels, transporters, and pumps, T-tubules permit rapid transmission of the action potential into the cell, and also play an important role in regulating cellular calcium concentration.

The sodium-calcium exchanger (often denoted Na+/Ca2+ exchanger, exchange protein, or NCX) is an antiporter membrane protein that removes calcium from cells. It uses the energy that is stored in the electrochemical gradient of sodium (Na+) by allowing Na+ to flow down its gradient across the plasma membrane in exchange for the countertransport of calcium ions (Ca2+). A single calcium ion is exported for the import of three sodium ions. The exchanger exists in many different cell types and animal species. The NCX is considered one of the most important cellular mechanisms for removing Ca2+.

<span class="mw-page-title-main">Calcium ATPase</span> Class of enzymes

Ca2+ ATPase is a form of P-ATPase that transfers calcium after a muscle has contracted. The two kinds of calcium ATPase are:

<span class="mw-page-title-main">Catecholaminergic polymorphic ventricular tachycardia</span> Medical condition

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited genetic disorder that predisposes those affected to potentially life-threatening abnormal heart rhythms or arrhythmias. The arrhythmias seen in CPVT typically occur during exercise or at times of emotional stress, and classically take the form of bidirectional ventricular tachycardia or ventricular fibrillation. Those affected may be asymptomatic, but they may also experience blackouts or even sudden cardiac death.

The Bowditch effect, also known as the Treppe phenomenon or Treppe effect or Staircase Phenomenon, is an autoregulation method by which myocardial tension increases with an increase in heart rate. It was first observed by Henry Pickering Bowditch in 1871.

<span class="mw-page-title-main">Ryanodine receptor 2</span> Transport protein and coding gene in humans

Ryanodine receptor 2 (RYR2) is one of a class of ryanodine receptors and a protein found primarily in cardiac muscle. In humans, it is encoded by the RYR2 gene. In the process of cardiac calcium-induced calcium release, RYR2 is the major mediator for sarcoplasmic release of stored calcium ions.

<span class="mw-page-title-main">HRC (gene)</span> Protein-coding gene in the species Homo sapiens

Sarcoplasmic reticulum histidine-rich calcium-binding protein is a protein that in humans is encoded by the HRC gene.

CXL 1020 is an experimental drug that is being investigated as a treatment for acute decompensated heart failure. CXL 1020 functions as a nitroxyl donor; nitroxyl is the reduced, protonated version of nitric oxide. Nitroxyl is capable of enhancing left ventricular contractility without increasing heart rate by modifying normal Ca2+ cycling through the sarcoplasmic reticulum as well as increasing the sensitivity of cardiac myofilaments to Ca2+.

<span class="mw-page-title-main">Istaroxime</span> Chemical compound

Istaroxime is an investigational drug under development for treatment of acute decompensated heart failure

Calcium buffering describes the processes which help stabilise the concentration of free calcium ions within cells, in a similar manner to how pH buffers maintain a stable concentration of hydrogen ions. The majority of calcium ions within the cell are bound to intracellular proteins, leaving a minority freely dissociated. When calcium is added to or removed from the cytoplasm by transport across the cell membrane or sarcoplasmic reticulum, calcium buffers minimise the effect on changes in cytoplasmic free calcium concentration by binding calcium to or releasing calcium from intracellular proteins. As a result, 99% of the calcium added to the cytosol of a cardiomyocyte during each cardiac cycle becomes bound to calcium buffers, creating a relatively small change in free calcium.

Cardiac excitation-contraction coupling (CardiacEC coupling) describes the series of events, from the production of an electrical impulse (action potential) to the contraction of muscles in the heart. This process is of vital importance as it allows for the heart to beat in a controlled manner, without the need for conscious input. EC coupling results in the sequential contraction of the heart muscles that allows blood to be pumped, first to the lungs (pulmonary circulation) and then around the rest of the body (systemic circulation) at a rate between 60 and 100 beats every minute, when the body is at rest. This rate can be altered, however, by nerves that work to either increase heart rate (sympathetic nerves) or decrease it (parasympathetic nerves), as the body's oxygen demands change. Ultimately, muscle contraction revolves around a charged atom (ion), calcium (Ca2+), which is responsible for converting the electrical energy of the action potential into mechanical energy (contraction) of the muscle. This is achieved in a region of the muscle cell, called the transverse tubule during a process known as calcium induced calcium release.

<span class="mw-page-title-main">David Paterson (physiologist)</span> New Zealand-born British physiologist and academic

David James Paterson MAE Hon FRSNZ is a New Zealand-born British physiologist and academic. He is a Fellow of Merton College, Oxford at the University of Oxford. He is also the Head of the Department of Physiology, Anatomy and Genetics at Oxford, and immediate Past President of The Physiological Society of the United Kingdom and Republic of Ireland. Paterson is best known for his work in cardiac neurobiology, linking the nervous system to heart rhythm, which was featured in the 2012 BBC Four documentary Heart v Mind: What Makes Us Human?, and associated interviews on RNZ National Science programme Heart v Mind. In 2018 he co-authored with Neil Herring the text book Levick's Introduction to Cardiovascular Physiology, 6th edition.

Dario DiFrancesco is a Professor Emeritus (Physiology) at the University of Milano. In 1979, he and collaborators discovered the so-called "funny" current in cardiac pacemaker cells, a new mechanism involved in the generation of cardiac spontaneous activity and autonomic regulation of heart rate. That initiated a new field of research in the heart and brain, where hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels, the molecular components of "funny" channels cloned in the late 90's, are today known to play fundamental roles in health and disease. Clinically relevant exploitation of the properties of "funny" channels has developed a channel blocker with specific heart rate-slowing action, ivabradine, marketed for the therapy of coronary artery disease, heart failure and the symptomatic treatment of chronic stable angina.

<span class="mw-page-title-main">Peter Kohl (scientist)</span>

Peter Kohl FAHA FHRS FTPS FIUPS is a scientist specializing in integrative cardiac research. He studies heterocellular electrophysiological interactions in cardiac tissue, myocardial structure-function relationships using 'wet' and 'dry' lab models, and mechano-electrical autoregulation of the heart.

References

  1. 1 2 "CURRICULUM VITAE – David Alfred Eisner" (PDF). ae-info.org. Academia Europaea. November 2009. Retrieved 30 April 2017.
  2. ↑ "Professor of Cardiac Physiology: Prof David Eisner M.A. D.Phil, FRCP (Hon), FMedSci". University of Manchester. Retrieved 30 April 2017.
  3. 1 2 ‘EISNER, Prof. David Alfred’, Who's Who 2017, A & C Black, an imprint of Bloomsbury Publishing plc, 2017; online edn, Oxford University Press, 2016; online edn, Nov 2016
  4. ↑ "Editors and Staff". rupress.org. Retrieved 2 January 2020.
  5. ↑ "Herbert Eisner". The Daily Telegraph. 28 July 2011. ISSN   0307-1235 . Retrieved 17 November 2018.
  6. 1 2 "European Perspectives". Circulation. 122 (3). 20 July 2010. doi: 10.1161/cir.0b013e3181e8eb7f . ISSN   0009-7322.
  7. ↑ Eisner DA, Richards DE (1981). "The interaction of potassium ions and ATP on the sodium pump of resealed red cell ghosts". The Journal of Physiology. 319: 403–18. doi:10.1113/jphysiol.1981.sp013917. PMC   1243847 . PMID   7320919.
  8. ↑ "BHF Professor David Eisner – heart attack and arrhythmias". British Heart Foundation. Retrieved 30 April 2017.
  9. ↑ "Past Officers of the Physiological Society (1876–2001)" (PDF). physoc.org. Retrieved 30 April 2017.
  10. ↑ "Past Officers of FEPS". www.feps.org. Retrieved 10 November 2022.
  11. ↑ Eisner DA, Lederer WJ, Vaughan-Jones RD (August 1981). "The dependence of sodium pumping and tension on intracellular sodium activity in voltage-clamped sheep Purkinje fibres". The Journal of Physiology. 317: 163–87. doi:10.1113/jphysiol.1981.sp013819. PMC   1246783 . PMID   7310731.
  12. ↑ Allen DG, Eisner DA, Orchard CH (May 1984). "Factors influencing free intracellular calcium concentration in quiescent ferret ventricular muscle". The Journal of Physiology. 350: 615–30. doi:10.1113/jphysiol.1984.sp015221. PMC   1199289 . PMID   6747860.
  13. ↑ Orchard CH, Eisner DA, Allen DG (1983). "Oscillations of intracellular Ca2+ in mammalian cardiac muscle". Nature. 304 (5928): 735–8. Bibcode:1983Natur.304..735O. doi:10.1038/304735a0. PMID   6888540. S2CID   4306804.
  14. ↑ Eisner DA, Trafford AW, Díaz ME, Overend CL, O'Neill SC (June 1998). "The control of Ca release from the cardiac sarcoplasmic reticulum: regulation versus autoregulation". Cardiovascular Research. 38 (3): 589–604. doi: 10.1016/s0008-6363(98)00062-5 . PMID   9747428.
  15. ↑ Trafford AW, Díaz ME, Eisner DA (February 2001). "Coordinated control of cell Ca(2+) loading and triggered release from the sarcoplasmic reticulum underlies the rapid inotropic response to increased L-type Ca(2+) current". Circulation Research. 88 (2): 195–201. doi: 10.1161/01.res.88.2.195 . PMID   11157672.
  16. ↑ Kashimura T, Briston SJ, Trafford AW, Napolitano C, Priori SG, Eisner DA, Venetucci LA (December 2010). "In the RyR2(R4496C) mouse model of CPVT, β-adrenergic stimulation induces Ca waves by increasing SR Ca content and not by decreasing the threshold for Ca waves". Circulation Research. 107 (12): 1483–9. doi: 10.1161/CIRCRESAHA.110.227744 . PMID   20966392.
  17. ↑ Eisner, David A.; Caldwell, Jessica L.; Trafford, Andrew W.; Hutchings, David C. (31 January 2020). "The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications". Circulation Research. 126 (3): 395–412. doi: 10.1161/CIRCRESAHA.119.315891 . ISSN   0009-7330. PMC   7004450 . PMID   31999537.
  18. ↑ Sankaranarayanan R, Kistamás K, Greensmith DJ, Venetucci LA, Eisner DA (August 2017). "i regulates diastolic levels in rat ventricular myocytes". The Journal of Physiology. 595 (16): 5545–5555. doi:10.1113/JP274366. PMC   5556151 . PMID   28617952.
  19. ↑ Smith GL, Eisner DA (May 2019). "Calcium Buffering in the Heart in Health and Disease". Circulation. 139 (20): 2358–2371. doi:10.1161/CIRCULATIONAHA.118.039329. PMC   6520234 . PMID   31082292.
  20. ↑ Eisner, David; Neher, Erwin; Taschenberger, Holger; Smith, Godfrey (16 June 2023). "Physiology of intracellular calcium buffering". Physiological Reviews. 103 (4): 2767–2845. doi: 10.1152/physrev.00042.2022 . ISSN   1522-1210. PMID   37326298.
  21. ↑ Eisner, D. A. (January 2018). "Reproducibility of science: Fraud, impact factors and carelessness". Journal of Molecular and Cellular Cardiology. 114: 364–368. doi:10.1016/j.yjmcc.2017.10.009. ISSN   1095-8584. PMC   6565841 . PMID   29079076.
  22. ↑ "Does the 'system' reward fraud?". Youtube. 17 April 2020. Archived from the original on 25 June 2021.
  23. ↑ "Professor David Eisner | The Academy of Medical Sciences". Acmedsci.ac.uk. Retrieved 30 April 2017.
  24. ↑ "Fellows of the ISHR". International Society for Heart Research. Retrieved 30 April 2017.
  25. ↑ "Academy of Europe: Eisner David". Ae-info.org. Retrieved 30 April 2017.
  26. ↑ születnek, www.WebDeb.hu – ahol a weblapok. "University of Debrecen -". edu.unideb.hu. Retrieved 15 June 2018.
  27. ↑ "Szeged University, University Day 2021". 13 November 2021. Archived from the original on 16 November 2021.
  28. ↑ "GL Brown Prize Lecture | Physiological Society". Physoc.org. 29 May 2011. Retrieved 30 April 2017.
  29. ↑ "Calcium in the heart: from physiology to disease – David Eisner (GL Brown Lecture 2014)". 16 May 2014. Retrieved 30 April 2017– via YouTube.
  30. ↑ Eisner DA (January 2018). "Ups and downs of calcium in the heart". The Journal of Physiology. 596 (1): 19–30. doi:10.1113/JP275130. PMC   5746526 . PMID   29071725.
  31. ↑ "ISHR Hall of Fame". International Society for Heart Research. Retrieved 30 April 2017.
  32. ↑ Eisner DA, Kashimura T, O'Neill SC, Venetucci LA, Trafford AW (April 2009). "What role does modulation of the ryanodine receptor play in cardiac inotropy and arrhythmogenesis?". Journal of Molecular and Cellular Cardiology. 46 (4): 474–81. doi:10.1016/j.yjmcc.2008.12.005. PMID   19150449.
  33. ↑ escardio (25 October 2013). "The Carmeliet-Coraboeuf-Weidmann Lecture – David Eisner".{{cite journal}}: Cite journal requires |journal= (help)
  34. ↑ "Lectures". FEPS SIF 2019. Retrieved 25 June 2019.
  35. ↑ "Sir John Burdon-Sanderson Prize Lecture Series – Physiology, Anatomy and Genetics". University of Oxford. Archived from the original on 18 February 2020. Retrieved 26 February 2020.
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