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Books on the topic 'Targeted antagonist'

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Published: 1 February 2023

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1

A, Horton Michael, ed. Adhesion receptors as therapeutic targets. Boca Raton, Fla: CRC Press, 1996.

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2

Angerer, Erwin von. The estrogen receptor as a target for rational drug design. New York: Springer, 1995.

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3

Angerer, Erwin von. The estrogen receptor as a target for rational drug design. New York: Springer, 1995.

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4

K, Ghosh Arun. Aspartic acid proteases as therapeutic targets. Weinheim: Wiley-VCH, 2010.

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5

K, Ghosh Arun. Aspartic acid proteases as therapeutic targets. Weinheim: Wiley-VCH, 2010.

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6

1930-, Smith H. J., and Simons Claire, eds. Proteinase and peptidase inhibition: Recent potential targets for drug development. London: Taylor & Francis, 2002.

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7

1940-, Sanderson Colin J., ed. Interleukin-5: From molecule to drug target for asthma. New York: M. Dekker, 1999.

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8

Baldi, Elisabetta, and Corrado Bucherelli. Neuroscience. Florence: Firenze University Press, 2017. http://dx.doi.org/10.36253/978-88-6453-638-5.

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This bibliographic material is patrimony of our Laboratory of the Behavior Physiology. This research unit originated in 1972 by will of Aldo Giachetti (until 1990) and with the beginning of the activity of Corrado Bucherelli. In the early 1980s, with Carlo Ambrogi Lorenzini (until 2004), the cataloging became more capillary and systematic, to continue to this day. All the researchers who worked in our laboratory contributed to this collection (Giovanna Tassoni 1986-2000, Benedetto Sacchetti 1996-2002 and Elisabetta Baldi from 1991). The study of learning, memory and behavior requires to follow a broad spectrum of neuroscience topics, ranging from neuronal biochemistry to neuropsychology. The Authors’ idea of publishing this collection comes from believing that a such website, though not exhaustive, might be a useful and targeted tool for the selection of bibliographic material in the field of behavioral neuroscience. The bibliographic references present at the publication (29500), accompanied by a brief comment highlighting the contents, are organized in relation to the topics (represented by the 99 themes) constituting the publication itself. The intersection of several references will point out the topics that represent them simultaneously. Concerning neurotransmitters and neuromodulators, references to agonists, antagonists or molecules interfering with the activity of these synapses have been inserted in the pages of the implicated neurotransmitter (e.g. acetylcholine). The pages including topics that could have been dealt with separately (e.g. active and passive avoidance) are introduced by a short explanatory note. The comment of each publication highlights the animal species used. Each comment is intended to indicate the content rather than the experimental results of paper. This choice comes from wanting to provide the reader with a more objective and less speculative comment.
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9

Hendrickson, Rebecca C., and Murray A. Raskind. Pharmacological Treatment of Nightmares, Sleep Disturbance, and Daytime Hyperarousal in PTSD: The Role of Prazosin, Other Noradrenergic Modulators, and Sedative Hypnotics or Commonly Used Sedating Medications. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0035.

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Disruption of stress-response systems contributes to the pathophysiology of post-traumatic stress disorder (PTSD). Consistent with this, daytime hyperarousal and nighttime sleep disruption, including trauma-related nightmares, are core symptoms of the disorder, often requiring targeted pharmacologic treatment. Although a variety of medications that target sleep–wake and arousal mechanisms are commonly used for this purpose, there remains the best empirical support for prazosin, a brain-active antagonist of the α‎1 noradrenaline receptor, with emerging evidence for doxazosin, a longer-acting medication with the same mechanism of action. This chapter reviews the evidence for use of prazosin and doxazosin as well as for the sedative hypnotics (benzodiazepines, nonbenzodiazepine hypnotics, and related medications), antihistamines, and sedating antidepressants trazodone and nefazodone to address hyperarousal symptoms and trauma-associated nightmares in PTSD. Clinical recommendations for the use of prazosin in PTSD, as well as a discussion of emerging pharmacologic treatments, are also included.
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10

Budimirovic, Dejan B., and Megha Subramanian. Neurobiology of Autism and Intellectual Disability. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0052.

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Fragile X syndrome (FXS) is a neurodevelopmental disorder that manifests with a range of cognitive, behavioral, and social impairments. It is a monogenetic disease caused by silencing of the FMR1 gene, in contrast to autism spectrum disorder (ASD) that is a behaviorally-defined set of complex disorders. Because ASD is a major and growing public health concern, current research is focused on identifying common therapeutic targets among patients with different molecular etiologies. Due to the prevalence of ASD in FXS and its shared neurophysiology with ASD, FXS has been extensively studied as a model for ASD. Studies in the animal models have provided breakthrough insights into the pathophysiology of FXS that have led to novel therapeutic targets for its core deficits (e.g., mGluR theory of fragile X). Yet recent clinical trials of both GABA-B agonist and mGluR5 antagonist revealed a lack of specific and sensitive outcome measures capturing the full range of improvements of patients with FXS. Recent research shows promise for the mapping of the multitude of genetic variants in ASD onto shared pathways with FXS. Nonetheless, in light of the huge level of locus heterogeneity in ASD, further effort in finding convergence in specific molecular pathways and reliable biomarkers is required in order to perform targeted treatment trials with sufficient sample size. This chapter focuses on the neurobehavioral phenotype caused by a full-mutation of the FMR1 gene, namely FXS, and the neurobiology of this disorder of relevance to the targeted molecular treatments of its core symptoms.
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11

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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12

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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13

Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Targeted and biological therapies. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199689842.003.0009.

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Hormone therapy describes the role of hormones in the growth of a variety of cancers, and the therapeutic effects of manipulation of hormone levels in these diseases. Sex hormones stimulate the growth of breast and prostate cancers, many of which respond to surgical removal of the hormone-secreting gonad. Pharmacological measures to deliver hormone therapy in these diseases include luteinising hormone releasing hormone (LHRH) agonists and antagonists, inhibitors of sex hormone synthesis, and inhibitors of hormone-receptor binding. These treatments have established benefits in both in the control of advanced disease and the adjuvant therapy of early-stage disease. The pros and cons of combination hormone therapy are discussed. Resistance to hormone therapy may be primary or acquired, and the likely mechanisms are described.
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14

Karp, Daniel D., and Gerald S. Falchook. Handbook of Targeted Cancer Therapy. Lippincott Williams & Wilkins, 2014.

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15

Hoover, Robert N., Amanda Black, and Rebecca Troisi. Hormones and Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0022.

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Hormones are highly biologically active endogenous compounds that control the growth, development, physiology, and homeostasis of numerous organ systems. Because of this, they have long been thought likely to play key roles in both normal and abnormal (malignant) growth. They are also noteworthy for being produced away from the tissues that they control, and are thus secreted into circulating blood to reach their target organs. This combination of potent, targeted agents of growth and development that can be measured in available biologic fluids has made steroidal and peptide hormonesparticularly susceptible and relevant to epidemiologic investigation. In addition, medications containing hormones and hormone antagonists have come into widespread use, providing further opportunities for epidemiologic insights into hormonal carcinogenesis. The development of increasingly more accurate assays to measure sex hormones and their metabolites has resulted in major advances in understanding the hormonal etiology of breast and gynecologic malignancies.
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16

Preusser, Matthias, Gabriele Schackert, and Brigitta G. Baumert. Metastatic brain tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0019.

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Brain metastasis is a common clinical challenge in cancer patients, particularly those with lung cancer, breast cancer, and melanoma. The prognosis is poor, with median overall survival times measured in months for most patient populations. Established treatments include neurosurgical resection, radiotherapy (including stereotactic radiosurgery and stereotactic radiotherapy, whole-brain radiotherapy, and new radiation techniques), and supportive care measures. Recently, more and more targeted therapies such as EGFR inhibitors, HER2 antagonists, BRAF inhibitors, ALK inhibitors, and immune checkpoint inhibitors are demonstrating some efficacy in brain metastasis patients and should be considered in the clinical setting.
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17

(Editor), H. John Smith, and Claire Simons (Editor), eds. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. CRC, 2002.

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18

Simons, Claire, and H. John Smith. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. Taylor & Francis Group, 2002.

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19

Simons, Claire, and H. John Smith. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. Taylor & Francis Group, 2002.

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20

Simons, Claire, and H. John Smith. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. Taylor & Francis Group, 2002.

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21

Simons, Claire, and H. John Smith. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. Taylor & Francis Group, 2002.

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22

Simons, Claire, and H. John Smith. Proteinase and Peptidase Inhibition: Recent Potential Targets for Drug Development. Taylor & Francis Group, 2002.

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23

Influenza Virus Sialidase A Drug Discovery Target. Birkhauser, 2010.

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24

Ferran, Christiane. Multiple Therapeutic Targets of A20. Springer London, Limited, 2014.

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25

Ferran, Christiane. The Multiple Therapeutic Targets of A20. Springer, 2016.

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26

Ferran, Christiane. The Multiple Therapeutic Targets of A20. Springer, 2014.

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27

Sullivan, Ryan J. BRAF Targets in Melanoma: Biological Mechanisms, Resistance, and Drug Discovery. Humana, 2014.

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28

Sullivan, Ryan J. BRAF Targets in Melanoma: Biological Mechanisms, Resistance, and Drug Discovery. Humana, 2016.

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29

Sullivan, Ryan J. BRAF Targets in Melanoma: Biological Mechanisms, Resistance, and Drug Discovery. Springer, 2014.

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30

Kevin M.K. Bottomley (Editor), David Bradshaw (Editor), and John S. Nixon (Editor), eds. Metalloproteinases as Targets for Anti-Inflammatory Drugs (Progress in Inflammation Research). Birkhäuser Basel, 1999.

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31

Miyamoto, Seiya, and Nobumi Miyake. Novel treatments and future directions. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198828761.003.0014.

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The advent of new-generation antipsychotic drugs has broadened the options for the pharmacological treatment of schizophrenia. However, there are still medical needs not met by current antipsychotic treatment, particularly for patients with negative symptoms and cognitive impairments, and for treatment-resistant schizophrenia. A growing body of research has identified new molecular mechanisms and novel pharmacological targets for treating schizophrenia beyond just dopamine D2 antagonism. This chapter provides a review of compounds in development and emerging non-pharmacological interventions for schizophrenia, and also considers approaches towards personalized and precision medicine for the disorder.
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32

Hoffmann, George. Background: Purging an Unreformed Past. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198808763.003.0002.

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Reformation satire grew out of the humanist reinvigoration of classical models but abandoned their convivial tone when reformers targeted Roman Eucharistic worship. Insofar as the Eucharist symbolized the social body, attacks against it could only be understood by readers as attacks against themselves. Iconoclasm drove reformers to this measure because the doctrine of “real presence” authorized reformers’ (disputed) charges of Roman idolatry. Efforts to mock the consequences of this doctrine pushed satires to vulgar and scatological extremes. The result proved an inimical posture which invalidated these works’ purported claims to persuade readers, making them instead serve as rites of passage by which reformers assumed an antagonistic role with respect to moderate French Gallicans.
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33

Numerof, R., Charles A. Dinarello, and Khusru Asadullah. Cytokines As Potential Therapeutic Targets for Inflammatory Skin Diseases. Springer Berlin / Heidelberg, 2014.

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34

Nutt, David J., and Liam J. Nestor. The opioid system and addiction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198797746.003.0010.

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The opioid system of the brain is the major target for opiate drugs such as morphine and heroin, and has been implicated in processes such as pain, stress and reward. Many of these effects take place at the mu opioid receptor (mOR), which is distributed throughout the brain. Significantly, genetic polymorphisms at the mOR may confer a greater dopamine response to the reinforcing effects of alcohol, and it has been suggested that addiction per se may be associated with alterations to the opioid system. There is evidence for the potential efficacy of mOR antagonists (e.g. naltrexone) in reducing drug and alcohol relapse, increasing treatment retention and attenuating the subjective effects of substances of abuse. Medications with partial agonist activity at the kappa opioid receptor (e.g. nalmefene) may also confer an additional clinical advantage by reducing binging following relapse.
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35

(Editor), R. Numerof, C. A. Dinarello (Editor), and K. Asadullah (Editor), eds. Cytokines as Potential Therapeutic Targets for Inflammatory Skin Diseases (Ernst Schering Research Foundation Workshop). Springer, 2005.

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36

Downes, Alexander B. Catastrophic Success. Cornell University Press, 2021. http://dx.doi.org/10.7591/cornell/9781501761140.001.0001.

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This book compiles all instances of regime change around the world over the past two centuries. In doing so, the book shows that regime change increases the likelihood of civil war and violent leader removal in target states and fails to reduce the probability of conflict between intervening states and their targets. As the book demonstrates, when a state confronts an obstinate or dangerous adversary, the lure of toppling its government and establishing a friendly administration is strong. The historical record, however, shows that foreign-imposed regime change is, in the long term, not consistently successful. The strategic impulse to forcibly oust antagonistic or non-compliant regimes overlooks two key facts. First, the act of overthrowing a foreign government sometimes causes its military to disintegrate, sending thousands of armed men into the countryside where they often wage an insurgency against the intervener. Second, externally imposed leaders face a domestic audience in addition to an external one, and the two typically want different things. These divergent preferences place imposed leaders in a quandary: taking actions that please one invariably alienates the other. Regime change thus drives a wedge between external patrons and their domestic protégés or between protégés and their people. The book provides sober counsel for leaders and diplomats. Regime change, the book urges, should be reserved for exceptional cases. Interveners must recognize that, absent a rare set of promising preconditions, regime change often instigates a new period of uncertainty and conflict that impedes their interests from being realized.
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37

T, Baird David, Schütz G. 1940-, and Krattenmacher R. 1957-, eds. Organ-selective actions of steroid hormones. Berlin: Springer-Verlag, 1995.

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38

Baird, David T. Organ Selective Actions of Steroid (Universitext). Springer, 1995.

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39

Sanderson, Colin. Interleukin-5: From Molecule to Drug Target for Asthma (Lung Biology in Health and Disease , Vol 125). Informa Healthcare, 1999.

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40

Ferro, Charles J., and Khai Ping Ng. Recommendations for management of high renal risk chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0099.

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Poorer renal function is associated with increasing morbidity and mortality. In the wider population this is mainly as a consequence of cardiovascular disease. Renal patients are more likely to progress to end-stage renal disease, but also have high cardiovascular risk. Aiming to reduce both progression of renal impairment and cardiovascular disease are not contradictory. Focusing on the management of high-risk patients with proteinuria and reduced glomerular filtration rates, it is recommended that blood pressure should be kept below 140/90, or 130/80 if proteinuria is > 1 g/24 h (protein:creatinine ratio (PCR) >100 mg/mmol or 0.9 g/g). These targets may be modified according to age and other factors. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor antagonists should form part of the therapy for patients with proteinuria > 0.5 g/24 h (PCR > 50 mg/mmol or 0.45 g/g). Use of ACEIs or angiotensin receptor blockers in patients with lower levels of proteinuria may be indicated in some patient groups even in the absence of hypertension, notably in diabetic nephropathy. Evidence that other agents that reduce proteinuria bring additional benefits is weak at present. The best studies of ‘dual-blockade’ with various combinations of ACEIs, ARBs, and renin inhibitors have shown additional hazard with little evidence of additional benefit. Hyperlipidaemia—regardless of lipid levels, statin therapy is indicated in secondary cardiovascular prevention, and in primary prevention where cardiovascular risk is high, noting that current risk estimation tools do not adequately account for the increased risk of patients with CKD. There is not substantial evidence that lipid lowering therapy impacts on average rates of loss of GFR in progressive CKD. Non-drug lifestyle interventions to reduce cardiovascular risk, including stopping smoking, are important for all. Acidosis—in more advanced CKD it is justified to treat acidosis with oral sodium bicarbonate. Diet—sodium restriction to < 100 mmol/day (6 g/day) and avoidance of excessive dietary protein are justified in early to moderate CKD. Recommendations to limit levels of protein to 0.8 g/kg body weight are suggested by some, but additional protective effects of this are likely to be slight in patients who are otherwise well managed. Low-protein diets may carry some risk. Lower-protein diets may however be used to prevent symptoms in advanced CKD not treated by dialysis.
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