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Books on the topic 'Receptor MET'

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Published: 4 June 2021
Last updated: 18 February 2022

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1

Somerset, David Alan. Hepatocyte growth factor (HGF) and its receptor c-met, in healthy and pathological human placentae. Birmingham: University of Birmingham, 2001.

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2

To, Christine Ting Ting. Overexpression of hepatocyte growth factor receptor/Met suppresses tumorigenecity of NCI-H1264 lung squamous carcimona cells. Ottawa: National Library of Canada, 1998.

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3

Spijker, Anke. Eten met plezier: Dieetinformatie en recepten voor nierpatiënten. 6th ed. Wormer: Inmerc, 2006.

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4

Rhoer, Sonja van de. Oranje Boven: Een culinaire geschiedenis met vorstelijke recepten. Houten: Van Dishoeck, 1997.

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5

Wouters, Valeer. Lekker West-Vlaanderen: Historische recepten met hedendaagse ingrediënten. Antwerpen: CODA, 1994.

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6

Bergman, Anneliese, Immy Timmerman, Miranda Castelein, and Annelène van Eijndhoven. Streep je slank..: Met 170 recepten & 70 tips & 40 oefeningen. 2nd ed. Hoofddorp: Sanoma, 2004.

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7

Koolsbergen, Titi. Vechten met gerechten tegen hoofdpijn en migraine: Voedingswijzer, recepten en adviezen. 's-Graveland: Fontaine Uitgevers, 2005.

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8

Hennie, Franssen-Seebregts, and efef com, eds. 500 chocoladegerechten: Heerlijke recepten voor groot en klein gebak met chocolade in de hoofdrol. Utrecht: Veltman Uitgevers, 2008.

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9

Boros, Peter. Hepatocyte growth factor: The basic principles. Austin: R.G. Landes, 1999.

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10

Gustave, Flaubert. Madame Bovary: Contexts, critical reception. Edited by Margaret Cohen. 2nd ed. New York, USA: W.W. Norton & Co., 2004.

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11

An encyclopedia of male homosexual poetry and its reception history. Edgecliff, N.S.W: Homo Poetry, 2002.

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12

1948-, Goldberg I. D., and Rosen E. M, eds. Hepatocyte growth factor-scatter factor (HGF-SF) and the C-met receptor. Basel: Birkhäuser, 1992.

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13

Benson, Roseann M., and James W. Janetka. Extracellular Targeting of Cell Signaling in Cancer: Strategies Directed at MET and RON Receptor Tyrosine Kinase Pathways. Wiley & Sons, Incorporated, John, 2018.

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14

Benson, Roseann M., and James W. Janetka. Extracellular Targeting of Cell Signaling in Cancer: Strategies Directed at MET and RON Receptor Tyrosine Kinase Pathways. Wiley & Sons, Incorporated, John, 2018.

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15

Long, Isolde Marie Seiden. Functional relationships between hepatocyte growth factor receptor (HGF)/Met signaling and Ki-ras oncogenic mutation in colon carcinoma cells. 2005.

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16

Kaar, Stephen J., Steven Potkin, and Oliver Howes. The neurobiology of antipsychotic treatment response and resistance. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0005.

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Dopamine D2/3 receptor occupancy by antipsychotic drugs is central to clinical response and many of their side effects. Yet the locus of dopaminergic alterations in the majority of patients with schizophrenia is not the D2/3 receptor but, instead, presynaptic, comprising elevated striatal dopamine synthesis and release capacity. However, whilst this explains why dopamine D2/3 receptor blockade is effective in many patients, a proportion of patients does not respond. In some this is because of inadequate antipsychotic blockade of dopamine receptors, but there are others who do not respond to antipsychotic treatment despite substantial dopamine D2/3 receptor blockade. The neurobiology of treatment resistance does not seem to involve the presynaptic dopamine dysfunction typically seen in patients, suggesting that it needs different treatments. Disruptions to the glutamatergic system, and to dopamine D1 and D2/3 receptors and serotonin 2A receptors have all been proposed as potential mechanisms underlying treatment resistance and as targets for novel treatments.
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17

Desroches, Julie. Peripheral analgesia involves cannabinoid receptors. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0034.

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This landmark paper by Agarwal and colleagues was published in 2007, when the exact contribution of the activation of the cannabinoid type 1 receptor (CB1) receptors expressed on the peripheral terminals of nociceptors in pain modulation was still uncertain. At that time, while it was clearly demonstrated that the central nervous system (CNS) was involved in the antinociceptive effects induced by the activation of the CB1 receptor, many strains of mice in which the gene encoding the CB1 receptor was deleted by conditional mutagenesis were used to study the specific role of these receptors in pain. Creating an ingenious model of genetically modified mice with a conditional deletion of the CB1 receptor gene exclusively in the peripheral nociceptors, Agarwal and colleagues were the first to unequivocally demonstrate the major role of this receptor in the control of pain at the peripheral level. In fact, these mutant mice lacking CB1 receptors only in sensory neurons (those expressing the sodium channel Nav1.8) have been designed to highlight that CB1 receptors on nociceptors, and not those within the CNS, constitute an important target for mediating local or systemic (but not intrathecal) cannabinoid analgesia. Overall, they have clarified the anatomical locus of cannabinoid-induced analgesia, highlighted the potential significance of peripheral CB1-mediated cannabinoid analgesia, and revealed important insights into how the peripheral endocannabinoid system works in controlling both inflammatory pain and neuropathic pain.
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18

Miller, Aaron E., and Teresa M. DeAngelis. NMDA Receptor Encephalitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199732920.003.0029.

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NMDA receptor encephalitis is a rare and underdiagnosed autoimmune mediated, often paraneoplastic, syndrome seen in young women with idiopathic neuropsychiatric illness. It is a potentially fatal illness and early identification and treatment can have critical prognostic implications. In this chapter, we review the typical clinical and laboratory features, which should raise suspicion for this condition, and therapeutic and supportive care recommendations.
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19

Nagy, Istvan. The capsaicin receptor. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0027.

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The landmark paper discussed in this chapter is ‘The capsaicin receptor: A heat activated ion channel in the pain pathway’, published by Caterina et al. in 1997. The identification of the molecular basis for the sensitivity of a major proportion of nociceptive primary sensory neurons for capsaicin, the pungent agent in chilli pepper, was undoubtedly one of the most significant pain-related discoveries in the twentieth century, for at least three reasons. First, the mechanism for capsaicin-induced responses could unequivocally be explained. Second, the discovery heralded the starting point for the development of a highly promising, mechanism-based means of analgesia. Third, the discovery also sparked studies which resulted in the discovery of the major cation channel family, the transient receptor potential (TRP) ion channel family, several members of which have also become putative targets for the development of analgesics.
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20

Hughes, Jim. Image receptors. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198813170.003.0003.

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The receptor head is the system that converts the X-ray beam into a visible image and allows it to be displayed. Modern systems accomplish this by using either an image intensifier (II) or a flat-panel detector (FPD). Both allow real-time fluoroscopy, as well as last-image hold, image storage and retrieval, and other features to assist in procedures or reduce radiation dose. This chapter covers the design and functions of image receptor heads used on C-arm systems that produce images from the incident X-ray beam. This includes the process of intensification and amplification of the image within an II system, as well as the function and the use of newer FPD systems.
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21

Lambert, David G. Mechanisms and determinants of anaesthetic drug action. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0013.

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This chapter is broken into two main sections: a general description of the principles of ligand receptor interaction and a discussion of the main groups of ‘targets’; and explanation of some common pharmacological interactions in anaesthesia, critical care, and pain management. Agonists bind to and activate receptors while antagonists bind to receptors and block the effects of agonists. Antagonists can be competitive (most common) or non-competitive/irreversible. The main classes of drug target are enzymes, carriers, ion channels, and receptors with examples of anaesthetic relevance interacting with all classes. There are many examples in anaesthesia where multiple interacting drugs are co-administered—polypharmacology. To give an example: neuromuscular blockade. Rocuronium is a non-depolarizing neuromuscular blocker acting as a competitive antagonist at the nicotinic acetylcholine receptor. Rocuronium competes with endogenous acetylcholine to shift the concentration–response curve for contraction to the right. The degree of contractility is less for a given concentration of acetylcholine (agonist) in the presence of rocuronium. Using the same principle, the rightward shift can be compensated by increasing the amount of acetylcholine (as long as the amount of rocuronium presented to the receptor as an antagonist remains unchanged, its action can be overcome by increased agonist). Acetylcholine at the effect site is increased by acetylcholinesterase inhibition with neostigmine. One of the side-effects of neostigmine is that it acts as an indirect parasympathomimetic. In the cardiovascular system this would lead to muscarinic receptor-mediated bradycardia; these effects are routinely reversed by the competitive muscarinic antagonist glycopyrrolate.
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22

Mason, Peggy. Receiving the Synaptic Message. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0013.

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Ionotropic and metabotropic receptors differ in their speed of action, the variety of effects produced after ligand-binding, and in the number of types present in the nervous system. The participation of two ionotropic glutamate receptors in synaptic plasticity is thought to be the cellular basis of learning. The actions of acetylcholine on nicotinic acetylcholine receptors present at the neuromuscular junction are described. The pharmacological profile of the GABAA receptor, central to most neural functions, is introduced. The properties of metabotropic receptors that are coupled to G proteins, termed G protein-coupled receptors (GPCRs), are detailed. Three canonical second-messenger systems through which GPCRs act are briefly described. An introduction to clinical pharmacology focused on how drugs acting on muscarinic and adrenergic receptors produce peripheral and central psychotropic effects is provided. Finally, the role of connexins and gap junctions in myelination and hearing is introduced.
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23

Knaggs, Roger D. The molecular structure of the μ‎-opioid receptor. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0038.

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The landmark paper discussed in this chapter describes the crystal structure of the μ‎-opioid receptor (also known as MOP-1). Opioids are some of the oldest known drugs and have been used for over 4,000 years; however, in addition to having beneficial analgesic effects, they are associated with a myriad of side effects that can minimize their use. Although the gene sequences of the opioid receptors were determined in the 1990s it has taken much longer to translate this into visualizing their three-dimensional structure. The μ‎-opioid receptor consists of seven transmembrane α‎-helices that are connected by three extracellular loops and three intracellular loops, with a wide open binding pocket which offers many potential ligand interaction sites, and evidence of dimerization. Understanding the crystal structure of the μ‎-opioid receptor in much more detail aids explanation of the molecular determinants of ligand recognition and selectivity and will be of use in designing novel opioids with improved efficacy and fewer side effects.
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24

Maljaars, C. Mediterrane keuken recepten en tips, koken met diabetes. Bohn Stafleu van Loghum, 2009.

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25

Doedens, Gina. Hollandse Keuken Recepten en Tips: Koken Met Diabetes. Bohn Stafleu en van Loghum, 2008.

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26

NA. Hollandse keuken recepten en tips, koken met diabetes. Bohn Stafleu van Loghum, 2007.

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27

Wells, Elizabeth M. Anti-N-Methyl-D-Aspartate Receptor Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0091.

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Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe but treatable recently identified form of immune-mediated encephalitis associated with antibodies in serum and cerebrospinal fluid (CSF) against the GluN1 subunit of the NMDAR. Research has rapidly expanded the understanding of disease mechanisms and how the condition manifests in different populations (e.g., pediatrics vs. adult, cancer vs. noncancer, male vs. female). Immunocytochemical, physiological, and molecular studies of the effects of human CSF on the rodent and murine brain in vitro and in vivo indicate a noncytotoxic antibody-mediated mechanism of disease pathogenesis. Finding positive antibodies prompts a search for occult neoplasm, most likely ovarian teratoma in young women; other age groups and male patients are less likely to have tumor but need to be screened. Fifty percent of patients respond to first line steroids, IVIG, plasma exchange or a combination, and many others improve with addition of rituximab or cyclophosphamide. Cured patients may have cognitive or motor sequelae, and refractory disease and death may occur despite treatment. Knowledge about etiology and biomarkers of refractory disease are lacking. Additional work is needed to further elucidate the origin of the immune-mediated response, to determine optimal clinical management and develop effective therapies for refractory patients.
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28

Hohmann, Andrea G. Control of pain initiation by endogenous cannabinoids. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0033.

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The landmark paper discussed in this chapter, published by Calignano et al. in 1998, focuses on the control of pain initiation by endogenous cannabinoids. In the paper, analgesic lipid mediators are shown to be present in peripheral paw tissue where they control the ability of pain signals to ascend to the central nervous system (CNS). Anandamide acts through a peripheral mechanism to suppress inflammatory pain via cannabinoid type 1 receptors. Palmitoylethanolamine, subsequently identified as an endogenous ligand for peroxisome proliferator-activated receptor-α‎, produces peripheral antinociceptive effects via a mechanism similar to that for the cannabinoid type 2 receptor. These lipids do not serve redundant functions and, in combination, produce synergistic antinociceptive effects. These observations suggested that drug-development efforts targeting peripheral control of pain may elucidate improved pharmacotherapies that lack the unwanted CNS side effects of current treatments.
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29

Mogil, Jeffrey S. Genetic differences in opiate receptors. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0010.

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The 1975 manuscript ‘Opioid receptors in mice: Genetic differences’ by Baran and colleagues was the first published paper to forward a hypothesis as to what might underlie mouse strain differences in opioid analgesic response. A strain was identified, CXBK, that exhibited both deficient morphine analgesia and low μ‎-opioid receptor density. Further study of this strain over the next two decades proved very useful, and the phenotype of CXBK mice has now been explained at the molecular level. The Baran et al. paper presaged the modern genetic studies of the μ‎-opioid gene, OPRM1, and was an important early example of the very active modern field of pain genetics.
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30

Vincent, Angela. Neuroimmunology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0015.

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This chapter relates to antibody-mediated disorders throughout the nervous system. Early papers recall how use of bungarotoxin, passive transfer experiments in mice, and clinical response to plasma exchange confirmed the role of acetylcholine receptor antibodies in myasthenia gravis. Cutting edge techniques subsequently discovered other key neuromuscular junctional proteins, including muscle-specific kinase an additional target for antibodies. Later papers report the link between brain inflammation and severe amnesia, paraneoplastic and non-paraneoplastic, and the identification of the first pathogenic antibodies to a central nervous system (CNS) receptor in Rasmussen’s syndrome. The first report of “Morvan’s syndrome” is followed by a single patient with antibodies immunoprecipitating potassium channels who improved remarkably with plasma exchange. Lastly, the patients in the 1920’s encephalitis lethargica epidemic described in detail by von Economo, exhibited many of the features now recognised as caused by antibodies to various CNS receptors and associated membrane proteins.
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31

Trepiccione, Francesco, and Giovambattista Capasso. Calcium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0026.

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Ca2+ homeostasis is achieved through a fine balance among three main organs: the intestine, the kidney, and bone. Blood levels of Ca2+ are accurately tuned through the Ca2+ sensing receptors and regulated by several hormones, including parathyroid hormone (PTH), active vitamin D, and calcitonin. The most recent findings in Ca2+ handling are described. The role of the Ca2+ sensing receptor, as well as Klotho, a new player participating in Ca2+ homeostasis, are described. Finally, the effects of diuretics, calcineurin inhibitors, and the link between hypertension and Ca2+ metabolism are reviewed.
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32

Henter, Ioline D., and Rodrigo Machado-Vieira. Novel therapeutic targets for bipolar disorder. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198748625.003.0030.

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The long-term course of bipolar disorder (BD) comprises recurrent depressive episodes and persistent residual symptoms for which standard therapeutic options are scarce and often ineffective. Glutamate is the major excitatory neurotransmitter in the central nervous system, and glutamate and its cognate receptors have consistently been implicated in the pathophysiology of mood disorders and in the development of novel therapeutics for these disorders. Since the rapid and robust antidepressant effects of the N-methyl-D-aspartate (NMDA) antagonist ketamine were first observed in 2000, other NMDA receptor antagonists have been studied in major depressive disorder (MDD) and BD. This chapter reviews the clinical evidence supporting the use of novel glutamate receptor modulators for treating BD—particularly bipolar depression. We also discuss other promising, non-glutamatergic targets for potential rapid antidepressant effects in mood disorders, including the cholinergic system, the melatonergic system, the glucocorticoid system, the arachidonic acid (AA) cascade, and oxidative stress and bioenergetics.
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33

Feng, Alexander J., George C. Chang Chien, and Alan D. Kaye. NMDA Receptor Antagonists, Gabapentinoids, Alpha-2 Agonists, and Dexamethasone. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0002.

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Surgical pain is a major obstacle in the recovery of patients. Effective pain management is of upmost importance to optimize a patient’s recovery, decrease medical complications, and increase patient satisfaction. Traditional pain management with opioids and nonsteroidal anti-inflammatory drugs have significant side effect profiles leading to medical complications or insufficient pain management from reluctance of use. Adjuvant analgesic can provide improved pain management with significantly less side effect profile. In addition, the clinician can, with synergistic effects of adjuvant medications, lower the total dosages used, thus lessening the likelihood of the side effects that occur when medications are used alone at a higher dosage. This chapter presents several adjuvant analgesics—NMDA receptor antagonists, gabapentinoids, alpha-2 agonists, and dexamethasone—and evidence for their use. Ultimately, through the use of traditional pain management options along with adjuvant analgesics, the effectiveness of acute pain management can be increased while adverse outcomes are reduced and functional recovery and quality of life improved.
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34

Livingston, Schuyler, Benjamin Young, Martin Markowitz, Poonam Mathur, and Bruce L. Gilliam. HIV Virology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0017.

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HIV is a member of the lentivirus subfamily of retroviruses. Two distinct groups of viruses are pathogenic in humans: HIV-1 and HIV-2. Both are transmitted sexually and known to cause immunodeficiency disease. HIV enters the cell through use of the CD4 receptor and chemokine co-receptors, primarily CCR5 and CXCR4. The viral genome is transcribed from RNA to DNA by reverse transcriptase and integrated into the host genome by integrase. The HIV genome encodes 15 proteins, comprising three categories: structural, regulatory, and accessory. After budding from the host cell, the virus matures into its infectious form through cleavage of viral precursor proteins by protease.
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35

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, Gareth Morris-Stiff, and Amen Sibtain. Colorectal cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0015_update_001.

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Breast cancer reviews the epidemiology and aetiology of this malignancy, with particular attention to the genetics underlying familial breast cancer, its pathology along with its receptors, oestrogen receptor (ER), the growth factor receptor HER2, and epidermal growth factor receptor (EGFR), and the bearing these have on treatment and prognosis. The benefits of breast cancer screening in the population and families at higher risk are discussed. Presenting symptoms and signs are followed by investigation including examination, bilateral mammography, and core biopsy of suspicious lesions. Management of non-invasive in situ disease is considered. Invasive breast cancer is staged according to TNM guidelines. Early breast cancer is defined, managed frequently by breast conserving surgery and sentinel node biopsy from the axilla. A positive sentinel node biopsy requires clearance of the axilla. Larger lesions may require mastectomy. Breast radiotherapy is indicated after breast conserving surgery. Following surgery, the risk of systemic micrometastatic disease is estimated from the primary size, lymph node spread, and tumour grade. Adjuvant chemotherapy improves treatment outcome in all but very good prognosis premenopausal breast cancer, and intermediate or poor prognosis postmenopausal breast cancer. This is combined with trastuzumab in HER2 positive disease. Adjuvant endocrine therapy is recommended for all ER positive breast cancer, tamoxifen in premenopausal, aromatase inhibitors in postmenopausal women. Neoadjuvant chemotherapy may be used in large operable breast cancers to facilitate breast conserving surgery. Locally advanced breast cancer is defined, its high risk of metastatic disease requiring full staging before treatment. Systemic therapy is often best first treatment, according to receptor profile. Metastatic breast cancer although incurable can be controlled for years using endocrine therapy, chemotherapy, trastuzumab, palliative radiotherapy, and bisphosphonates as appropriate. Male breast cancer is uncommon, but management similar.
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36

Abood, Mary E., and Thomas Gamage. The cloning and characterization of the cannabinoid type 1 receptor. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0025.

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The cloning and characterization of the first cannabinoid receptor (now known as the cannabinoid type 1 (CB1) receptor) by Matsuda et al. in the landmark paper discussed in this chapter was a seminal discovery in 1990. While the analgesic properties of marijuana had been known for thousands of years, the mechanisms through which marijuana produces analgesia were not understood. The identification and functional characterization of the CB1 receptor led to the discovery of an endogenous cannabinoid system (the endocannabinoid system), which has now been shown to be important not only for acute and chronic pain states, but also for a whole host of physiological and pathophysiological disorders.
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37

Bradbury, Elizabeth J., and Nicholas D. James. Mapping of neurotrophin receptors on adult sensory neurons. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0022.

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The paper discussed in this chapter describes the first mapping of neurotrophin receptors in adult sensory neurons. Neurotrophins and their receptors were a particularly hot topic at the time, but the primary focus of interest had been in their role in development. In this paper, McMahon and colleagues characterized both mRNA and protein expression of the recently discovered trk receptors on defined populations of adult sensory neurons, correlating trk expression with other primary afferent projection neuron properties such as cell size and neuronal function. Furthermore, by showing clear correlations between the expression of different trk receptors and the physical and functional properties of defined primary afferent projections, the authors provided key evidence suggesting that nerve growth factor and neurotrophin-3 acted on functionally distinct populations of adult sensory neurons. This paper provided the basis for subsequent research on neurotrophin signalling and function in both the healthy and the diseased nervous system.
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38

Kettenmann, Helmut, and Robert Zorec. Release of Gliotransmitters and Transmitter Receptors in Astrocytes. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0017.

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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...
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39

Boddeke, Erik W. G. M., Bart J. L. Eggen, and Knut P. H. Biber. Cytokine, Chemokine, and Growth Factor Receptors and Signaling. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0022.

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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...
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40

Gulini, U., U. Gulini, W. Quaglia, G. Marucci, and M. Gianella. Receptor Chemistry Towards the Third Millennium. Elsevier Science Publishing Company, 2000.

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41

Montgomery, Erwin B. Principles of Electrophysiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0003.

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In many ways, post-operative DBS programming is “prescribing electricity” in much the same sense as “prescribing medications.” The principles of pharmacokinetics and pharmacodynamics that guide the rational use of medications find parallels in DBS. Many drugs have their effect by binding to ligand-gated channels, particularly channels that control the flow of electrical charges, in the form of ions across the cell membrane of the neuron in the soma. The binding of drugs to receptors can open the receptor to approximate the normal opening by endogenous neurotransmitters, or to block the channel from opening when endogenous neurotransmitters are released. In the case of DBS, the electrical charges manipulated in the nervous system similarly affect neuronal membrane channels; however, these initially and primarily are voltage gated ionic conductance channels, which are described in detail in this chapter.
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42

Ren, Ke, and Ronald Dubner. The first crystal structure of an ionotropic glutamate receptor ligand-binding core. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0032.

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The known functional ionotropic glutamate receptors (iGluRs) are composed of three major subtypes: AMPA, NMDA, and kainate. In 1998, in the landmark paper discussed in this chapter, Armstrong et al. provided the first crystal structure of an iGluR-subunit ligand-binding core, the S1S2 region of the rat GluA2 ‘flop’ isoform. They solved its structure with X-ray crystallography from selenomethonine crystals. They also identified residues involved in kainate binding, analysed allosteric sites that regulate affinity and specificity of the agonist, and mapped potential subunit–subunit interaction sites. They also proposed that binding of different agonists may result in variable degrees of domain closure. This work has profound impact on the field and it has been importantly cited. Subsequently, numerous high-resolution crystal structures of ligand-binding domains of iGluRs in complex with ligands, both agonists and antagonists, have been solved.
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43

Alharbi, Yousef, Manish S. Patankar, and Rebecca J. Whelan. Antibody-Based Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0006.

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With their role in connecting disease-associated antigens to the cellular immune response, antibodies hold considerable promise as therapeutic agents. This chapter discusses three classes of therapeutic antibodies that have been developed for use in ovarian cancer therapy. The first includes antibodies selected against tumor-associated antigens such as MUC16/CA125, mesothelin, epithelial cell adhesion molecule, and folate receptor α‎. Antibodies in the second class target proteins such as CTLA-4 and PD1 that act as immune response checkpoint receptors. The third class of antibodies target secreted factors that promote tumor growth: targets in this class include vascular endothelial growth factor, cytokines, and chemokines. The development of each of these is described. The chapter also discusses the complications presented by soluble antigens, which serve to limit the applicability of antigens (such as MUC16/CA125) that are both cell-surface associated and circulating and the prospects for the combination of antibody-based immunotherapy and chemotherapy.
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Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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Reddy, Ugan, and Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.

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Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR resulting in a decreased receptor density resulting in a reduced postsynaptic end-plate potential following motor nerve stimulation and leading to muscle weakness. Although all voluntary muscles can be affected, ocular, bulbar, respiratory, and proximal limb weakness predominates. In the majority of seronegative patients, an antibody directed towards a NMJ protein called muscle specific tyrosine kinase (MUSK) is found. Anti-MUSK MG is characterized by severe bulbar and respiratory muscle weakness. Diagnosis of MG requires a high degree of clinical suspicion coupled with pharmacological and electrophysiological testing, and detection of the various causative antibodies. Treatment of MG involves enhancing neuromuscular transmission with long-acting anticholinesterase agents and immunosuppression. Acute exacerbations are treated with either plasma exchange or intravenous immunoglobulin. Myasthenic crisis is associated with severe muscle weakness that necessitates tracheal intubation and mechanical ventilation. LEMS is an autoimmune disease in which IgG antibodies are directed towards the pre-synaptic voltage-gated calcium channels at the NMJ. It is often associated with malignant disease (usually small cell carcinoma of the lung). Autonomic dysfunction is prominent and patients show abnormal responses to neuromuscular blocking drugs.
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De Backer, Daniel, and Patrick Biston. Vasopressors in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0034.

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Vasopressors are used in various shock states to correct hypotension, aiming at restoring or improving organ and tissue perfusion. Vasopressor therapy may be associated with excessive vasoconstriction, but also metabolic and other side-effects. Hence, the ideal target for arterial pressure remains undetermined. Adrenergic agents remain the most commonly used vasopressor agents. Adrenergic agents increase arterial pressure through stimulation of alpha-adrenergic receptors. The effects of the different adrenergic agents differ mostly due to variable associated beta-adrenergic effects. Epinephrine and norepinephrine are strong and equipotent vasopressor agents. Their impact on outcome is as yet unanswered, but there is no sign that epinephrine might be associated with better outcomes. Accordingly, norepinephrine is the adrenergic agent of choice, especially in patients with cardiogenic shock. Vasopressin is a non-adrenergic vasopressor acting via V1 receptor stimulation, with weak vasopressor effects in normal conditions, but markedly increased vascular tone in shock states, especially in septic shock. Splanchnic vasoconstriction may occur. Arginine vasopressin at low doses appears to be a promising alternative to adrenergic agents, but its exact place is not yet well defined.
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Wiersinga, W. Joost, and Tom van der Poll. The host response to infection in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0303.

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Infection continues to be a leading cause of intensive care unit death. The host response to infection can be seen as a pattern recognition receptor (PRR)-mediated dysregulation of the immune system following pathogen invasion in which a careful balance between inflammatory and anti-inflammatory responses is vital. A measured and rapid response to microbial invasion is essential to health. The same immunological and coagulation systems that protect against localized infection can act to our disadvantage when these systems are activated systemically during generalized microbial infection. Toll-like receptors (TLR), the inflammasomes and other PRRs initiate the host response after recognition of pathogen-associated-molecular-patterns (PAMPs) or endogenous danger-associated-molecular-patterns (DAMPs). The systemic host response to infection will result in activation of coagulation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Further dissection of the role of host–pathogen interactions, the cytokine response, the coagulation cascade and their multidirectional interactions in sepsis should lead towards the development of new therapeutic approaches in the critically ill who are faced with infection.
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Ramrakha, Punit, and Jonathan Hill, eds. Drugs for the heart. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199643219.003.0002.

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Antiplatelet agents 82Antiplatelet agents: aspirin 84Antiplatelet agents: thienopyridines 88Antiplatelet agents: clopidogrel 90Antiplatelet agents: prasugrel 94Intravenous antiplatelet agents 96Angiotensin-converting enzyme inhibitors 98Angiotensin receptor blockers (ARBs, also referred to as angiotensin II receptor antagonists, AIIRAs) 102Aldosterone antagonists 106Beta-adrenoceptor blockers (...
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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Tran, Anh Q. When the Cross Met the Lotus. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190677602.003.0002.

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Chapter 1 considers the Catholic presence in Tonkin and its interaction with Vietnamese religions. It begins by describing the sociopolitical situation of Tonkin as a land of two kings. The chapter then narrates the development of Vietnamese Christianity from its beginning in the Jesuit, Augustinian, and Dominican missions to the eighteenth century. The chapter charts the varied reception of Christianity by the ruling class of Tonkin, and Christianity’s relationship with Confucianism. It ends with a narrative of the protracted Chinese Rites Controversy, describing the attempts to reconcile Catholic dogma with Vietnamese cultural and religious practices, especially regarding those pertaining to filial piety, and a description of the Controversy’s long-lasting effects in Vietnam.
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