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Books on the topic 'Anti-inflammatory molecules'

Author: Grafiati
Published: 9 March 2023

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1

G, Bazán Nicolás, Botting Jack H, and Vane John R, eds. New targets in inflammation: Inhibitors of COX-2 or adhesion molecules : proceedings of a conference held on April 15-16, 1996, in New Orleans, USA, supported by an educational grant from Boehringer Ingelheim. Dordrecht: Kluwer Academic Publishers, 1996.

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2

W, Pruzanski, and Vadas P. 1953-, eds. Novel molecular approaches to anti-inflammatory therapy. Basel: Birkhäuser Verlag, 1995.

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3

Pruzanski, Waldemar, and Peter Vadas, eds. Novel Molecular Approaches to Anti-Inflammatory Therapy. Basel: Birkhäuser Basel, 1995. http://dx.doi.org/10.1007/978-3-0348-7276-8.

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4

N, Cohn Jay, and Abrams William B, eds. Cardiovascular drugs. Mount Kisco, N.Y: Futura Pub. Co., 1985.

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5

W, Houde Raymond, Ley Timothy J, and Hollister Leo E. 1920-, eds. Analgesics and NSAID. Mount Kisco, N.Y: Futura Pub. Co., 1985.

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6

(Editor), N. Bazan, Jack H. Botting (Editor), and Sir John R. Vane (Editor), eds. New Targets in Inflammation: Inhibitors of COX-2 or Adhesion Molecules. Springer, 1996.

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7

Bazan, N., Jack H. Botting, and Sir John R. Vane. New Targets in Inflammation: Inhibitors of COX-2 or Adhesion Molecules Proceedings of a Conference Held on April 15-16, 1996, in New Orleans, USA, Supported by an Educational Grant from Boehringer Ingelheim. Springer London, Limited, 2012.

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8

Bazan, N., Jack H. Botting, and Sir John R. Vane. New Targets in Inflammation: Inhibitors of COX-2 or Adhesion Molecules Proceedings of a Conference Held on April 15-16, 1996, in New Orleans, USA, Supported by an Educational Grant from Boehringer Ingelheim. Springer, 2012.

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9

Parlato, Marianna, and Jean-Marc Cavaillon. Innate immunity and the inflammatory cascade. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0299.

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Inflammation results from a complex interaction between a large number of mediators able to induce each other and to favour the generation of other inflammatory molecules (e.g. free radicals, lipid mediators, and proteases). The perpetuation of inflammation by these cascades of mediators is favoured by their ability to induce coagulation, leukocyte recruitment, and cell and tissue alteration (apoptosis, necrosis, and barrier disruption). Other cascades of mediators occur to generate anti-inflammatory mediators favouring the healing process. A neuroendocrine loop and neuromediators from central and peripheral nervous system are also involved in the process, allowing a return to homeostasis.
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10

Vadas, Peter, and Waldemar Pruzanski. Novel Molecular Approaches to Anti-Inflammatory Therapy. Springer Basel AG, 2013.

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11

(Editor), Paul G. Winyard, and Derek A. Willoughby (Editor), eds. Inflammation Protocols (Methods in Molecular Biology). Humana Press, 2003.

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12

Baier, Gottfried, Burkhart Schraven, Ulrich Zügel, and Arne Bonin. Sparking Signals: Kinases as Molecular Signaltransducers and Pharmacological Drug Targets in Inflammation. Springer, 2010.

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13

Baier, Gottfried, Burkhart Schraven, Ulrich Zügel, and Arne Bonin. Sparking Signals: Kinases As Molecular Signaltransducers and Pharmacological Drug Targets in Inflammation. Springer London, Limited, 2008.

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14

Brune, Kay, Stefan Laufer, and Steffen Gay. Inflammation and Rheumatic Diseases: The Molecular Basis of Novel Therapies. Thieme Medical Publishers, 2003.

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15

Inflammation and rheumatic diseases: The molecular basis of novel therapies. Stuttgart: Thieme, 2003.

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16

Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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17

McMahon, Francis Gilbert. Principles and Techniques of Human Research and Therapeutics: Selected Topics : Immunology and Monoclonal Antibodies (Principles and Techniques of Human Research and Therapeutics). Blackwell/Futura, 1985.

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18

Sjøgren, Per, Frank Elsner, and Stein Kaasa. Non-opioid analgesics. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0096.

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Non-opioid analgesics encompass the non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol (acetaminophen). The NSAIDs include acetylsalicylic acid (ASA, aspirin), dipyrone (metamizole), and numerous other drugs in diverse classes. The NSAIDs have potent anti-inflammatory, analgesic and antipyretic activity, and are among the most widely used drugs worldwide. In palliative medicine, they represent the first step of the World Health Organization’s analgesic ladder used for mild pain and they are an important supplement to opioids and adjuvant drugs at higher steps of the ladder. The disadvantages of non-opioid analgesics include a ceiling effect for pain relief and the risk of side effects. NSAIDs are also associated with an increased risk of adverse gastrointestinal, renal, and cardiovascular effects and hepatotoxicity can result from overdosing with paracetamol. This chapter describes the clinical pharmacology of NSAIDs, their classification, molecular mechanisms of action and adverse effects, as well as some recent developments aimed at designing effective anti-inflammatory agents with improved safety and tolerability profiles.
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19

Ribeiro, Carla Maria Pedrosa, Noel Gerard McElvaney, and Giulio Cabrini, eds. Novel Anti-inflammatory Approaches for Cystic Fibrosis Lung Disease: Identification of Molecular Targets and Design of Innovative Therapies. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88971-941-9.

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20

Bagchi, Debasis, Siba P. Raychaudhuri, and Sashwati Roy. Chronic Inflammation: Molecular Pathophysiology, Nutritional and Therapeutic Interventions. Taylor & Francis Group, 2016.

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21

Bagchi, Debasis, Siba P. Raychaudhuri, and Sashwati Roy. Chronic Inflammation: Molecular Pathophysiology, Nutritional and Therapeutic Interventions. Taylor & Francis Group, 2012.

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22

Bagchi, Debasis, Siba P. Raychaudhuri, and Sashwati Roy. Chronic Inflammation: Molecular Pathophysiology, Nutritional and Therapeutic Interventions. Taylor & Francis Group, 2012.

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23

McMahon, Francis Gilbert. Principles and Techniques of Human Research and Therapeutics: Selected Topics : Analgesics and Nsaid (Principles and Techniques of Human Research and Therapeutics). Blackwell/Futura, 1985.

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24

McMahon, Francis Gilbert. Principles and Techniques of Human Research and Therapeutics: Selected Topics : Cardiovascular Drugs/Antiarrhythmics. Blackwell/Futura, 1985.

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25

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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26

Farquhar-Smith, Paul. The key role of nerve growth factor in inflammatory pain processing. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0021.

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This paper was one of several that cemented the key role of nerve growth factor (NGF) in sensory neurons in inflammatory pain processing. It used a novel way of biologically ‘removing’ NGF using a sequestration molecule that could then investigate the effect of the absence of NGF in pain paradigms. These data contributed to the robust evidence base indicating the importance of NGF and, although there had been issues in developing usable anti-NGF moieties in human pain conditions, this study could be considered part of the journey that has led to the introduction of antagonists to NGF actions for the treatment of pain in bone.
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27

Zhang, Xuehong, Eunyoung Cho, and Hans-Olov Adami. Kidney Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676827.003.0023.

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The etiology of kidney cancer remains largely unknown. Cigarette smoking, obesity, and hypertension are well-established risk factors for kidney cancer. Although the current evidence is relatively mixed, other emerging risk factors include use of nonsteroidal anti-inflammatory drugs (NSAIDs), occupational exposure to trichloroethylene, and high parity in women. In contrast, physical activity and alcohol consumption have been consistently inversely associated with risk of kidney cancer. There is no convincing evidence of a causal link with any other specific food items or nutrients. Most kidney cancers are sporadic, and current studies of common genetic variants report mixed results, but genetic variations may also contribute to the etiology of kidney cancer. Further research is warranted to identify new environmental causes, to better understand the genetic and molecular processes, and to account for different molecular subtypes with specific genetic or tumor characteristics.
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28

Thursfield, Rebecca, Chris Orchard, Rosanna Featherstone, and Jane C. Davies. Future treatments. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0013.

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There are only a relatively limited armoury of drugs, the majority of which are aimed at downstream symptoms of cystic fibrosis. Therapies targeting the basic defect in CF as well as continued availability of more conventional drugs are required. Progress in gene therapy has been limited by the significant barriers to gene transfer of the CF lung, but the UK is hosting a large repeated dose trial of nebulized non-viral gene therapy designed around clinically meaningful outcomes. The UK CF Gene Therapy Consortium is also seeking to develop a promising modified lentiviral approach, although this is some years off. Perhaps the exciting development of recent decades has come from small molecule CFTR modulators, driven by an understanding of basic pathophysiological mechanisms. Ivacaftor is the first drug to be licensed, having proved itself highly clinically efficacious in patients with the class-3 gating mutation G551D. The trial pipeline seeks to expand indications for this and to explore the potential of Phe508del correctors. Finally, a number of anti-inflammatory and anti-infective strategies are being pursued. The emerging global problem of antibiotic resistance is leading to exciting alternatives such as biofilm disruption and bacteriophage to be explored.
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