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Published: 4 June 2021
Last updated: 7 February 2022

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1

service), SpringerLink (Online, ed. Transient Receptor Potential Channels. Dordrecht: Springer Science+Business Media B.V., 2011.

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2

Islam, Md Shahidul, ed. Transient Receptor Potential Channels. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0265-3.

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3

Flockerzi, Veit, and Bernd Nilius, eds. Transient Receptor Potential (TRP) Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-34891-7.

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4

Nilius, Bernd, and Veit Flockerzi, eds. Mammalian Transient Receptor Potential (TRP) Cation Channels. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-05161-1.

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5

Nilius, Bernd, and Veit Flockerzi, eds. Mammalian Transient Receptor Potential (TRP) Cation Channels. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54215-2.

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6

Wang, Yizheng, ed. Transient Receptor Potential Canonical Channels and Brain Diseases. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1088-4.

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7

Szallasi, Arpad. TRP channels in health and disease: Implications for diagnosis and therapy. Hauppauge, N.Y: Nova Science Publishers, 2010.

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8

Nilius, Bernd, and Veit Flockerzi. Transient Receptor Potential Channels. Springer, 2010.

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9

Islam, MD Shahidul. Transient Receptor Potential Channels. Springer, 2011.

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10

J, Abramowitz, Flockerzi Veit, and Nilius B, eds. Transient receptor potential (TRP) channels. Berlin: Springer, 2007.

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11

Nilius, Bernd, and Veit Flockerzi. Mammalian Transient Receptor Potential Cation Channels: Volume I. Springer, 2014.

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12

Wang, Yizheng. Transient Receptor Potential Canonical Channels and Brain Diseases. Springer, 2017.

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13

Nilius, Bernd, and Veit Flockerzi. Mammalian Transient Receptor Potential Cation Channels: Volume I. Springer, 2016.

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14

Wang, Yizheng. Transient Receptor Potential Canonical Channels and Brain Diseases. Springer, 2018.

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15

(Editor), Veit Flockerzi, and Bernd Nilius (Editor), eds. Transient Receptor Potential (TRP) Channels (Handbook of Experimental Pharmacology). Springer, 2007.

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16

Tsagareli, Merab G. Behavioral Study of Agonist-Evoked Activation of Transient Receptor Potential Channels. Nova Science Publishers, Incorporated, 2020.

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17

Tsagareli, Merab G. Behavioral Study of Agonist-Evoked Activation of Transient Receptor Potential Channels. Nova Science Publishers, Incorporated, 2020.

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18

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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19

Transient Receptor Potential (TRP) Channels in Drug Discovery: Old Concepts & New Thoughts. MDPI, 2018. http://dx.doi.org/10.3390/books978-3-03842-638-7.

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20

Trp Channels In Drug Discovery. Humana Press, 2012.

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21

Roedding, Angela S. Characterization of the transient receptor potential channels mediating lysophosphatidic acid-stimulated calcium mobilization in B lymphoblasts. 2006.

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22

Nagy, Istvan. VR1 in inflammatory thermal hyperalgesia. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0028.

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The landmark paper discussed in this chapter, published by Davis et al. in 2000, describes the role of the capsaicin receptor, which is called transient receptor potential cation channel subfamily vanilloid member 1 (TRPV1), in inflammatory thermal hyperalgesia. Capsaicin, the pungent agent found in hot peppers, has been linked to pain for centuries because it induces a burning pain sensation which, after prolonged application of the agent, turns into analgesia. Because of this, capsaicin has been used to relieve pain, most likely since prehistoric times. The elucidation of the role of TRPV1 in nociceptive processing was heralded as the starting point for the development of agents which would revolutionize pain management. Unfortunately, that promise is yet to be realized and apparently we need a more detailed understanding of the role of TRPV1 in physiological and pathological processes in order to fulfil the analgesic potential of drugs acting on this receptor.
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23

Mason, Peggy. Somatosensation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0017.

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Under normal circumstances, the somatosensory system contributes more to shaping movements than to perception. Yet damage to the somatosensory system can result in spontaneous pain and other abnormal somatic perceptions. An exploration of the mechanisms and pathways involved in touch perception is slanted toward understanding the contribution of the dorsal column–medial lemniscus pathway to the generation of paresthesia and dysesthesia. Peripheral somatosensory afferents that contribute to the perception of sharp or aching pain, temperature, and itch are described. The properties of transient receptor potential (TRP) channels on nociceptors and thermoreceptors are described. Physiological and pharmacological mechanisms that lead to neurogenic inflammation are considered. How peripheral and central changes triggered by acute injury or disease can lead to long-lasting changes that support chronic pain is described. Persistent pain that occurs independently of any stimulus is termed neuropathic. Mechanisms of referred pain from deep structures including viscera are introduced.
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24

Divya, Vohora, ed. The third histamine receptor: Selective ligands as potential therapeutic agents in CNS disorders. Boca Raton: CRC Press, 2009.

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25

The Third Histamine Receptor: Selective Ligands as Potential Therapeutic Agents in CNS Disorders. CRC, 2008.

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26

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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27

Patisaul, Heather B., and Scott M. Belcher. Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0005.

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In this chapter, the current understanding of the mechanisms of endocrine disruption on the brain and nervous system are presented. Because the overwhelming majority of mechanistic studies on EDCs have focused on the actions mediated by nuclear hormone receptors, this mechanisms is described in detail. The chapter also discusses the classic transcriptional mechanisms of steroid action and the impact of EDCs on rapid signaling (non-genomic) mechanisms. It presents an overview of the enzymes and pathways involved in the biosynthesis of steroid hormones, which are critical to proper functioning of the HPA and HPG axis, and the neuroactive steroids synthesized and active in the mammalian brain. The potential for EDCs to alter metabolic enzymes, with a focus on possible targets in the metabolic blood-brain barrier, is presented as a potential, though largely unexplored, mode of EDC action in the brain.
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28

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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29

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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30

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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31

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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32

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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33

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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34

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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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 intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), 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 lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. 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 prevented and modulated.
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35

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Abstract:
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 intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), 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 lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. 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 prevented and modulated.
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