10 results
One, two, three: portable sample size in agricultural research
- Hans-Peter Piepho, Doreen Gabriel, Jens Hartung, Andreas Büchse, Meike Grosse, Sabine Kurz, Friedrich Laidig, Volker Michel, Iain Proctor, Jan Erik Sedlmeier, Kathrin Toppel, Dörte Wittenburg
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- Journal:
- The Journal of Agricultural Science / Volume 160 / Issue 6 / December 2022
- Published online by Cambridge University Press:
- 25 August 2022, pp. 459-482
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Determination of sample size (the number of replications) is a key step in the design of an observational study or randomized experiment. Statistical procedures for this purpose are readily available. Their treatment in textbooks is often somewhat marginal, however, and frequently the focus is on just one particular method of inference (significance test, confidence interval). Here, we provide a unified review of approaches and explain their close interrelationships, emphasizing that all approaches rely on the standard error of the quantity of interest, most often a pairwise difference of two means. The focus is on methods that are easy to compute, even without a computer. Our main recommendation based on standard errors is summarized as what we call the 1-2-3 rule for a difference of two treatment means.
An Interesting Case of Nuchal Rigidity
- Christina Boettcher, Clemens Warnke, Stephan Macht, Hans-Peter Hartung, Bernd C. Kieseier
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- Canadian Journal of Neurological Sciences / Volume 38 / Issue 3 / May 2011
- Published online by Cambridge University Press:
- 02 December 2014, pp. 516-517
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A 34 year-old female without prior relevant medical history presented to our emergency room with a two-day history of neck pain, odynophagia and elevated body temperature up to 38.2° C. Her general practitioner had started the patient on antibiotic treatment with ciprofloxacin and referred her to our emergency department for further diagnostic workup and treatment of suspected meningitis. Initial neurological examination revealed neck rigidity and head pain without further focal neurological signs. Body temperature was 37.7 °C, blood analyses revealed a normal leukocyte count (8.900/μl) and normal C-reactive protein (<0.3mg/dl), blood cultures were sterile. Lumbar puncture was without pathological findings (<1 leukocytes/μl, normal levels for glucose, lactate and protein). Cervical magnetic resonance imaging could rule out osseous injury and cervical myelopathy, however a small prevertebral, retropharyngeal fluid collection was visible (Figure 1a-c). This prompted the diagnosis of acute retropharyngeal calcific tendinitis (RCT). This diagnosis was confirmed by conventional x-ray showing the presence of a characteristic amorphous calcification in the retropharyngeal space anterior to the C1-C2 segments (Figure 1d). Treatment with i.v. methylprednisolone (250mg) was started and pain was reduced shortly after the first infusion. The patient was discharged on tapered oral methylprednisolone and non-steroidal anti-inflammatory drug (NSAID) treatment. Symptoms resolved completely within a week.
Inflammatory Demyelinating Brain Lesions Heralding Primary CNS Lymphoma
- Leila Husseini, Andreas Saleh, Guido Reifenberger, Hans-Peter Hartung, Bernd C. Kieseier
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- Canadian Journal of Neurological Sciences / Volume 39 / Issue 1 / January 2012
- Published online by Cambridge University Press:
- 02 December 2014, pp. 6-10
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Brain biopsy plays a crucial role in the exploration of suspect white matter lesions in the differential diagnosis of primary central nervous system lymphoma (PCNSL) and inflammatory demyelination. We present the case of a previously healthy, immunocompetent woman, aged fifty-nine, who developed a histologically confirmed demyelinating white matter lesion months prior to the manifestation of a PCNSL. Similar cases of “sentinel lesions” preceding a PCNSL have been reported. In a literature review, we compared the diagnostic features that may be useful to differentiate a PCNSL from inflammatory demyelinating disease in older age. We conclude that the occurrence of large, contrast-enhancing cerebral lesions in older patients with a relapsing-remitting disease course and steroid-resistant vision disorders should lead to the consideration of a PCNSL.
Contributor affiliations
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- By Frank Andrasik, Melissa R. Andrews, Ana Inés Ansaldo, Evangelos G. Antzoulatos, Lianhua Bai, Ellen Barrett, Linamara Battistella, Nicolas Bayle, Michael S. Beattie, Peter J. Beek, Serafin Beer, Heinrich Binder, Claire Bindschaedler, Sarah Blanton, Tasia Bobish, Michael L. Boninger, Joseph F. Bonner, Chadwick B. Boulay, Vanessa S. Boyce, Anna-Katharine Brem, Jacqueline C. Bresnahan, Floor E. Buma, Mary Bartlett Bunge, John H. Byrne, Jeffrey R. Capadona, Stefano F. Cappa, Diana D. Cardenas, Leeanne M. Carey, S. Thomas Carmichael, Glauco A. P. Caurin, Pablo Celnik, Kimberly M. Christian, Stephanie Clarke, Leonardo G. Cohen, Adriana B. Conforto, Rory A. Cooper, Rosemarie Cooper, Steven C. Cramer, Armin Curt, Mark D’Esposito, Matthew B. Dalva, Gavriel David, Brandon Delia, Wenbin Deng, Volker Dietz, Bruce H. Dobkin, Marco Domeniconi, Edith Durand, Tracey Vause Earland, Georg Ebersbach, Jonathan J. Evans, James W. Fawcett, Uri Feintuch, Toby A. Ferguson, Marie T. Filbin, Diasinou Fioravante, Itzhak Fischer, Agnes Floel, Herta Flor, Karim Fouad, Richard S. J. Frackowiak, Peter H. Gorman, Thomas W. Gould, Jean-Michel Gracies, Amparo Gutierrez, Kurt Haas, C.D. Hall, Hans-Peter Hartung, Zhigang He, Jordan Hecker, Susan J. Herdman, Seth Herman, Leigh R. Hochberg, Ahmet Höke, Fay B. Horak, Jared C. Horvath, Richard L. Huganir, Friedhelm C. Hummel, Beata Jarosiewicz, Frances E. Jensen, Michael Jöbges, Larry M. Jordan, Jon H. Kaas, Andres M. Kanner, Noomi Katz, Matthew S. Kayser, Annmarie Kelleher, Gerd Kempermann, Timothy E. Kennedy, Jürg Kesselring, Fary Khan, Rachel Kizony, Jeffery D. Kocsis, Boudewijn J. Kollen, Hubertus Köller, John W. Krakauer, Hermano I. Krebs, Gert Kwakkel, Bradley Lang, Catherine E. Lang, Helmar C. Lehmann, Angelo C. Lepore, Glenn S. Le Prell, Mindy F. Levin, Joel M. Levine, David A. Low, Marilyn MacKay-Lyons, Jeffrey D. Macklis, Margaret Mak, Francine Malouin, William C. Mann, Paul D. Marasco, Christopher J. Mathias, Laura McClure, Jan Mehrholz, Lorne M. Mendell, Robert H. Miller, Carol Milligan, Beth Mineo, Simon W. Moore, Jennifer Morgan, Charbel E-H. Moussa, Martin Munz, Randolph J. Nudo, Joseph J. Pancrazio, Theresa Pape, Alvaro Pascual-Leone, Kristin M. Pearson-Fuhrhop, P. Hunter Peckham, Tamara L. Pelleshi, Catherine Verrier Piersol, Thomas Platz, Marcus Pohl, Dejan B. Popović, Andrew M. Poulos, Maulik Purohit, Hui-Xin Qi, Debbie Rand, Mahendra S. Rao, Josef P. Rauschecker, Aimee Reiss, Carol L. Richards, Keith M. Robinson, Melvyn Roerdink, John C. Rosenbek, Serge Rossignol, Edward S. Ruthazer, Arash Sahraie, Krishnankutty Sathian, Marc H. Schieber, Brian J. Schmidt, Michael E. Selzer, Mijail D. Serruya, Himanshu Sharma, Michael Shifman, Jerry Silver, Thomas Sinkjær, George M. Smith, Young-Jin Son, Tim Spencer, John D. Steeves, Oswald Steward, Sheela Stuart, Austin J. Sumner, Chin Lik Tan, Robert W. Teasell, Gareth Thomas, Aiko K. Thompson, Richard F. Thompson, Wesley J. Thompson, Erika Timar, Ceri T. Trevethan, Christopher Trimby, Gary R. Turner, Mark H. Tuszynski, Erna A. van Niekerk, Ricardo Viana, Difei Wang, Anthony B. Ward, Nick S. Ward, Stephen G. Waxman, Patrice L. Weiss, Jörg Wissel, Steven L. Wolf, Jonathan R. Wolpaw, Sharon Wood-Dauphinee, Ross D. Zafonte, Binhai Zheng, Richard D. Zorowitz
- Edited by Michael Selzer, Stephanie Clarke, Leonardo Cohen, Gert Kwakkel, Robert Miller, Case Western Reserve University, Ohio
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- Textbook of Neural Repair and Rehabilitation
- Published online:
- 05 May 2014
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- 24 April 2014, pp ix-xvi
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- By Frank Andrasik, Melissa R. Andrews, Ana Inés Ansaldo, Evangelos G. Antzoulatos, Lianhua Bai, Ellen Barrett, Linamara Battistella, Nicolas Bayle, Michael S. Beattie, Peter J. Beek, Serafin Beer, Heinrich Binder, Claire Bindschaedler, Sarah Blanton, Tasia Bobish, Michael L. Boninger, Joseph F. Bonner, Chadwick B. Boulay, Vanessa S. Boyce, Anna-Katharine Brem, Jacqueline C. Bresnahan, Floor E. Buma, Mary Bartlett Bunge, John H. Byrne, Jeffrey R. Capadona, Stefano F. Cappa, Diana D. Cardenas, Leeanne M. Carey, S. Thomas Carmichael, Glauco A. P. Caurin, Pablo Celnik, Kimberly M. Christian, Stephanie Clarke, Leonardo G. Cohen, Adriana B. Conforto, Rory A. Cooper, Rosemarie Cooper, Steven C. Cramer, Armin Curt, Mark D’Esposito, Matthew B. Dalva, Gavriel David, Brandon Delia, Wenbin Deng, Volker Dietz, Bruce H. Dobkin, Marco Domeniconi, Edith Durand, Tracey Vause Earland, Georg Ebersbach, Jonathan J. Evans, James W. Fawcett, Uri Feintuch, Toby A. Ferguson, Marie T. Filbin, Diasinou Fioravante, Itzhak Fischer, Agnes Floel, Herta Flor, Karim Fouad, Richard S. J. Frackowiak, Peter H. Gorman, Thomas W. Gould, Jean-Michel Gracies, Amparo Gutierrez, Kurt Haas, C.D. Hall, Hans-Peter Hartung, Zhigang He, Jordan Hecker, Susan J. Herdman, Seth Herman, Leigh R. Hochberg, Ahmet Höke, Fay B. Horak, Jared C. Horvath, Richard L. Huganir, Friedhelm C. Hummel, Beata Jarosiewicz, Frances E. Jensen, Michael Jöbges, Larry M. Jordan, Jon H. Kaas, Andres M. Kanner, Noomi Katz, Matthew S. Kayser, Annmarie Kelleher, Gerd Kempermann, Timothy E. Kennedy, Jürg Kesselring, Fary Khan, Rachel Kizony, Jeffery D. Kocsis, Boudewijn J. Kollen, Hubertus Köller, John W. Krakauer, Hermano I. Krebs, Gert Kwakkel, Bradley Lang, Catherine E. Lang, Helmar C. Lehmann, Angelo C. Lepore, Glenn S. Le Prell, Mindy F. Levin, Joel M. Levine, David A. Low, Marilyn MacKay-Lyons, Jeffrey D. Macklis, Margaret Mak, Francine Malouin, William C. Mann, Paul D. Marasco, Christopher J. Mathias, Laura McClure, Jan Mehrholz, Lorne M. Mendell, Robert H. Miller, Carol Milligan, Beth Mineo, Simon W. Moore, Jennifer Morgan, Charbel E-H. Moussa, Martin Munz, Randolph J. Nudo, Joseph J. Pancrazio, Theresa Pape, Alvaro Pascual-Leone, Kristin M. Pearson-Fuhrhop, P. Hunter Peckham, Tamara L. Pelleshi, Catherine Verrier Piersol, Thomas Platz, Marcus Pohl, Dejan B. Popović, Andrew M. Poulos, Maulik Purohit, Hui-Xin Qi, Debbie Rand, Mahendra S. Rao, Josef P. Rauschecker, Aimee Reiss, Carol L. Richards, Keith M. Robinson, Melvyn Roerdink, John C. Rosenbek, Serge Rossignol, Edward S. Ruthazer, Arash Sahraie, Krishnankutty Sathian, Marc H. Schieber, Brian J. Schmidt, Michael E. Selzer, Mijail D. Serruya, Himanshu Sharma, Michael Shifman, Jerry Silver, Thomas Sinkjær, George M. Smith, Young-Jin Son, Tim Spencer, John D. Steeves, Oswald Steward, Sheela Stuart, Austin J. Sumner, Chin Lik Tan, Robert W. Teasell, Gareth Thomas, Aiko K. Thompson, Richard F. Thompson, Wesley J. Thompson, Erika Timar, Ceri T. Trevethan, Christopher Trimby, Gary R. Turner, Mark H. Tuszynski, Erna A. van Niekerk, Ricardo Viana, Difei Wang, Anthony B. Ward, Nick S. Ward, Stephen G. Waxman, Patrice L. Weiss, Jörg Wissel, Steven L. Wolf, Jonathan R. Wolpaw, Sharon Wood-Dauphinee, Ross D. Zafonte, Binhai Zheng, Richard D. Zorowitz
- Edited by Michael E. Selzer, Stephanie Clarke, Leonardo G. Cohen, Gert Kwakkel, Robert H. Miller, Case Western Reserve University, Ohio
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- Textbook of Neural Repair and Rehabilitation
- Published online:
- 05 June 2014
- Print publication:
- 24 April 2014, pp ix-xvi
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Chapter 50 - Neuromuscular rehabilitation: diseases of the motor neuron, peripheral nerve, neuromuscular junction, and the muscle
- from Section 7 - Disease-specific neurorehabilitation systems
- Edited by Michael E. Selzer, Stephanie Clarke, Leonardo G. Cohen, Gert Kwakkel, Robert H. Miller, Case Western Reserve University, Ohio
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- Textbook of Neural Repair and Rehabilitation
- Published online:
- 05 June 2014
- Print publication:
- 24 April 2014, pp 655-673
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6 - Immunobiology of the oligodendrocyte
- Edited by Patricia Armati, University of Sydney, Emily Mathey, University of Sydney
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- The Biology of Oligodendrocytes
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- 05 August 2012
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- 21 October 2010, pp 115-136
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Summary
INTRODUCTION
Oligodendrocytes, as the myelin-producing cells of the central nervous system (CNS), are exactly what their Greek-derived name “oligodendroglia” suggests: they, alongside astrocytes, the non-neural microglia and ependymal cells, have been characterized as the “glue” that holds together the intricate apparatus of our brain. The fact that oligodendrocyte and astrocyte cells outnumber neurons by ten to one illustrates their importance, which is particularly highlighted by the oligodendrocyte's role in accelerating transmission of axonal action potentials. On the other hand, oligodendrocytes are involved in a number of serious diseases of viral, metabolic and immunological origin. This chapter tries to shed light on the immunobiological properties of oligodendroglial cells in the healthy and diseased CNS. We will begin with an overview of diseases featuring oligodendrocyte/immune system interactions and will then, in the second part, focus on the molecular repertoire that allows these cells to interact directly or indirectly with immune cells. Subsequently, we will discuss oligodendrocytes as antigen-presenting cells and finally we will present data on direct oligodendroglial/immune cell interactions.
IMMUNE-MEDIATED DISEASES AFFECTING OLIGODENDROCYTES
Multiple sclerosis
Multiple sclerosis (MS), which was first described by the French neurologist Jean-Martin Charcot in 1868 (Charcot, 1868), is a chronic inflammatory disease of the CNS of unknown etiology (Hemmer et al., 2006). Although an ideal system for the classification of different MS stages does not yet exist (Van der Valk and De Groot, 2000) there is broad consensus that loss of myelin due to oligodendrocyte damage or death together with axonal degeneration leading to reactive glial scar formation are the key hallmarks of this disease (Trapp and Nave, 2008).
7 - Schwann cells as immunomodulatory cells
- Edited by Patricia Armati, University of Sydney
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- The Biology of Schwann Cells
- Published online:
- 13 August 2009
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- 15 February 2007, pp 118-125
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Summary
INTRODUCTION
The nervous system has long been considered an immunologically privileged site. This concept was based on the premises that: (1) there is a more or less strict anatomic separation between the systemic immune compartment (blood) and the neural tissue; (2) molecules required for antigen presentation are absent under normal circumstances; (3) there is no lymphatic drainage; and (4) immune surveillance by T cells is lacking. It is now obvious that most of these assumptions are not tenable. The blood–nerve barrier (BNB) does restrict access of immune cells and soluble mediators to a certain degree; however, this restriction is not complete, either anatomically (e.g. the BNB is absent or relatively deficient at the roots, in the ganglia and the motor terminals) or functionally. Activated T lymphocytes can penetrate intact barriers irrespective of their antigen specificity, and, under certain circumstances, release cytokines that upregulate the expression of major histocompatibility complex (MHC) class II molecules, key molecules required for antigen presentation. In the central nervous system (CNS) tissue-resident neuroglial cells are present that actively participate in the regulation of immune responses within the tissue. In recent years, several lines of evidence have pointed to Schwann cells as immunocompetent cells within the peripheral nervous system (PNS), which, in addition to their physiological roles, exhibit a broad spectrum of immune-related functions and might be involved in the local immune response in the PNS. In this chapter we will elaborate on the expanding recognition of Schwann cells as immunocompetent cells that form part of the local immune circuitry within the PNS. Interestingly, present data suggest that the entire spectrum of an immune response can be displayed by Schwann cells; recognition of antigens, presentation of antigens, mounting an immune response, and, finally, terminating an immune response within the inflamed peripheral nerve.
40 - Neuromuscular rehabilitation: diseases of the motor neuron, peripheral nerve and neuromuscular junction
- from Section C - Disease-specific neurorehabilitation systems
- Edited by Michael Selzer, University of Pennsylvania, Stephanie Clarke, Université de Lausanne, Switzerland, Leonardo Cohen, National Institute of Mental Health, Bethesda, Maryland, Pamela Duncan, University of Florida, Fred Gage, Salk Institute for Biological Studies, San Diego
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- Textbook of Neural Repair and Rehabilitation
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- 04 August 2010
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- 16 February 2006, pp 657-676
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Summary
This chapter describes the current knowledge on the pathogenesis, the clinical symptoms, and deficits and current therapy concepts during the acute disease state and for rehabilitation including long-term impairment of activities of daily living. It focuses on rehabilitation of patients with diseases of the motor neuron like amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA) and polio. Rehabilitation in polio and post-polio patients is aimed at improving muscle strength, lowering muscle and joint pain, increasing physical independence and quality of life not only of the patient but also of the caregiver. The chapter also explains the rehabilitation of patients with diseases of the peripheral nervous system, especially acute and chronic inflammatory polyneuropathies Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP) and other neuropathies. Finally, it also discusses diseases of the neuromuscular junction (myasthenia gravis and Lambert-Eaton myasthenic syndrome (LEMS)).
92 - Immune mechanisms in neurological disease
- from PART XII - AUTOIMMUNE DISORDERS
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- By Hans-Peter Hartung, Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany, Klaus V. Toyka, Department of Neurology, Julius-Maximilians-University, Würzburg, Germany, Bernd C. Kieseier, Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany
- Edited by Arthur K. Asbury, University of Pennsylvania School of Medicine, Guy M. McKhann, The Johns Hopkins University School of Medicine, W. Ian McDonald, University College London, Peter J. Goadsby, University College London, Justin C. McArthur, The Johns Hopkins University School of Medicine
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- Diseases of the Nervous System
- Published online:
- 05 August 2016
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- 11 November 2002, pp 1501-1526
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Summary
The following chapter reviews principles of immunology to provide an understanding of how components of the nervous system are recognized by the immune system, how an autoimmune response is mounted, how immune cells and mediators enter the nervous tissue, and how tolerance against neural antigens is induced, maintained, and broken. Most of the general principles have been discovered since the 1980s but only with the new technology of targeted deletions and mutations (permanent and conditional knockout, knockin) can these principles be systematically explored at the molecular level. A brief discussion of multiple sclerosis, the Guillain–Barré syndrome, and myasthenia gravis will follow, while clinical aspects and disease-specific pathomechanisms of immune-mediated neurological disorders are presented in greater detail in individual chapters. Therapeutic consequences based on immunological principles are discussed in Chapter 93.
Categories of the immune response
The immune system is a multifaceted system of cells and molecules with specialized tasks in defending the organism from external agents, infectious or toxic. Moreover, the immune system plays a pivotal role in maintaining antigenic homeostasis in the body. Two types of responses to invading organisms can take place: an acute response launched within hours, and a delayed response occurring within days. The immediately responding system is termed innate immune system, and it evolves stereotypically and at the same magnitude regardless how often the infectious agent is encountered. In contrast, a more delayed response is delivered by the adaptive or acquired immune system and provides a more specific immunologic reaction which improves in efficiency on repeated exposure to a given infective agent, capitalizing on the formation of immunological memory. The immune system has traditionally been divided into innate and adaptive systems, each containing different cellular and molecular components. The main distinction between these two systems lies in the mechanisms and receptors used for immune recognition. These two systems are not separated, but are functionally connected allowing for intensive interactions (Carroll & Prodeus, 1998; Ochsenbein & Zinkernagel, 2000).
The innate immune system
During evolution, the innate immune system appeared before the adaptive immune system, and some form of innate immunity probably exists in all multicellular organisms. Characteristically, innate immune responses consist of all the immune defence mechanisms that do not require immunologic memory. Genetically, the molecular mediators and their receptors are highly conserved between species as far apart as Caenorhabditis elegans, Drosophila, and mammals.