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Books on the topic 'Cholesterol and inflammatory molecules'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

Sharma, Ramesh Kumar, Maria Anna Coniglio, and Pasqualina Laganà. Natural Inflammatory Molecules in Fruits and Vegetables. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-88473-4.

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2

M, Harlan John, and Liu David Y. 1950-, eds. Adhesion: Its role in inflammatory disease. W.H. Freeman, 1992.

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3

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. Kluwer Academic Publishers, 1996.

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4

Keith, Lierre. The vegetarian myth: Food, justice and sustainability. Flashpoint Press, 2009.

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5

Sharma, Ramesh Kumar, Pasqualina Laganà, and Maria Anna Coniglio. Natural Inflammatory Molecules in Fruits and Vegetables. Springer International Publishing AG, 2022.

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6

(Editor), John M. Harlan, and David Y. Liu (Editor), eds. Adhesion: Its Role in Inflammatory Disease (Breakthroughs in Molecular Biology Series). Oxford University Press, USA, 1991.

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7

(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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8

Newcom, Gregory. Anti-Inflammatory Low Cholesterol Fast Track Cookbook - $10 Discount Now This Month Only! Blurb, 2023.

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9

Pezzi, Vincenzo, Rosa Sirianni, and Michihisa Umetani, eds. Cholesterol and Oxysterols as Signal Molecules in Human Pathophysiology and Cancer: Implications for New Therapeutic Strategies. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-278-7.

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10

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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11

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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12

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

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13

Fragoulis, George E., and Iain B. McInnes. Small molecules in the treatment of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0031.

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Psoriatic arthritis (PsA) is a chronic inflammatory arthritis, occurring in about one third of psoriasis patients, and exhibiting very varied clinical manifestations and comorbidities. Although the clinical outcome of the disease has been significantly improved recently, mainly due to utilization of novel agents targeting the IL-23/-17 axis, unmet needs still exist. Emerging insights into the disease’s pathogenesis led to development of new drugs acting against critical molecular targets and their efficacy in psoriasis and/or PsA has been tested in Phase III clinical trials. Some of these ther

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14

Bell, Robert M. Pathophysiology of coronary syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0145.

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The pathophysiology of acute coronary syndromes is characterized by an acute mismatch of blood supply to the myocardium to meet the prevailing metabolic need. By far the commonest aetiology of myocardial ischaemia is coronary artery disease . An inflammatory process that evolves over the period of many decades, coronary artery disease is characterized by the deposition of cholesterol and cholesterol laden macrophages within the intima of the vessel wall. This process can be accelerated by a number of cardiovascular risk factors (smoking, hypertension, hyperlipidaemia, hypercholesterolaemia, di

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15

Sokka, Tuulikki, Kari Puolakka, and Carl Turesson. Comorbidities of rheumatic disease. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0032.

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All other diseases that coexist with a disease of interest are called comorbidities. Comorbidities in inflammatory rheumatic diseases may be associated with persistent inflammatory activity or disease-related organ damage, or may be related to medications. Lifestyle choices such as smoking or physical inactivity contribute to comorbidity. Patients with rheumatic diseases meet health professionals regularly and are more often tested for osteoporosis or cholesterol levels than individuals without rheumatic disease, which may contribute to a higher prevalence of some comorbidities. Comorbidities

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16

Sokka, Tuulikki, Kari Puolakka, and Carl Turesson. Comorbidities of rheumatic disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0032_update_001.

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All other diseases that coexist with a disease of interest are called comorbidities. Comorbidities in inflammatory rheumatic diseases may be associated with persistent inflammatory activity or disease-related organ damage, or may be related to medications. Lifestyle choices such as smoking or physical inactivity contribute to comorbidity. Patients with rheumatic diseases meet health professionals regularly and are more often tested for osteoporosis or cholesterol levels than individuals without rheumatic disease, which may contribute to a higher prevalence of some comorbidities. Comorbidities

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17

Thomas, Ranjeny, and Andrew P. Cope. Pathogenesis of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0109.

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In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process

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18

Wainger, Brian J. Drug Discovery and Neuropathic Pain. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0117.

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Pain is one of the most common causes of physician visits and disability. Pain has been classified into specific subtypes. We refer to baseline or nociceptive pain as pain that results from an ongoing, high-threshold stimulus acting on an unenhanced somatosensory system. Inflammatory pain refers to pain in the setting of tissue damage and specifically the release of inflammatory molecules that activate and sensitize the nociceptive machinery. Hyperalgesia, or increased pain in response to a noxious stimulus, results from nociceptor sensitization whereas neuropathic pain results from a lesion o

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19

Levi, Marcel, and Tom van der Poll. Coagulation and the endothelium in acute injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0307.

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Vascular endothelial cells play a pivotal mediatory role in many responses to systemic inflammation, including the cross-talk between coagulation and inflammation in sepsis. Endothelial cells respond to the cytokines expressed and released by activated leukocytes, but can also release cytokines themselves. Furthermore, endothelial cells are able to express adhesion molecules and growth factors that may not only promote the inflammatory response further, but also affect a myriad of downstream responses. It has recently become clear that, in addition to these mostly indirect effects of the endot

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20

Teixeira, Antonio L., and Moises E. Bauer, eds. Immunopsychiatry. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190884468.001.0001.

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In recent years, great attention has been devoted to the understanding of the immune dysfunction that is associated with major psychiatric disorders. In the context of the reconceptualization of the immune system as a homeostatic system, immune cells, molecules and mechanisms are highly promising as new diagnostic and therapeutic targets to reduce the burden of mental/psychiatric disorders. In this regard, immune cells, molecules and mechanisms are highly promising. The literature on immunology of psychiatric disorders is still disperse, and only very few attempts have been done so far to cons

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21

Sedel, Frédéric. Niemann-Pick Disease Type C. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0053.

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Niemann-Pick disease type C (NPC) is a fatal neurovisceral lipid storage disease of autosomal inheritance resulting from mutations in either the NPC1 (95% of families) or NPC2 gene. The encoded proteins appear to be involved in lysosomal/late endosomal transport of cholesterol, glycolipids, and other molecules, but their exact function is still unknown. The clinical spectrum of the disease ranges from a neonatal rapidly fatal disorder to an adult-onset chronic neurodegenerative disease characterized prominently by psychiatric disorders, cerebellar ataxia, cognitive decline, and vertical supran

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22

Landmesser, Ulf, and Wolfgang Koenig. From risk factors to plaque development and plaque destabilization. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0003.

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This chapter begins with a discussion of recent vascular research that has unveiled the complex interaction between exposure to risk factors and pathological changes at the vessel wall. Risk factors such as smoking or hyperlipidaemia first cause a pre-morbid phenotype with reversible dysfunction of flow-mediated vasodilation, known as endothelial dysfunction (ED). If exposure to risk factor(s) does not cease, ED develops into the first morphological vascular changes that finally lead to atherosclerosis. Cholesterol crystals have been shown to lead to pro-inflammatory activation of macrophages.

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23

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of

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24

Ho, Vanessa P., and Philip S. Barie. Acute acalculous cholecystitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0188.

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Acute acalculous cholecystitis (AAC) may occur in surgical or injured, critically-ill, and systemically-ill patients, with diabetes mellitus, malignant disease, abdominal vasculitis, congestive heart failure, cholesterol embolization, shock, and cardiac arrest. Children may also be affected, especially following a viral illness. The pathogenesis of AAC is complex and multifactorial. Ischaemia/reperfusion injury and the associated pro-inflammatory response and oxidative tissue stress, appear to be the central mechanisms, but bile stasis, opioid therapy, positive-pressure ventilation, and parent

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25

Yu, Shirley P., and David J. Hunter. Prospects for disease modification. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0035.

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The tremendous individual and societal burden underpin a strong rationale for the development of disease-modifying agents for osteoarthritis. Current approaches to managing the disease remain largely palliative and focused on alleviating symptoms, specifically pain and functional limitation. The chapter considers the multitude of tissues that potentially can be targeted in this heterogeneous disease of osteoarthritis and the agents that can modify these tissues. It first focuses on molecules targeting inflammatory pathways and then breaks that down by particular tissue targeted: specifically a

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26

Jay, Taylor R., Shane M. Bemiller, Lee E. Neilson, Paul J. Cheng-Hathaway, and Bruce T. Lamb. Neuroinflammation and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0004.

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Neuroinflammation has long been associated with many neurodegenerative diseases (NDDs). Immune-related genetic and environmental risk factors have recently been identified for NDDs, suggesting that neuroinflammation can play an active role in modifying NDD pathologies. Immune cells that underlie this neuroinflammatory response can have both beneficial and detrimental roles in NDDs. These cells can engage in clearance of debris and provide important survival factors to neighboring neurons. However, these cells can also release inflammatory molecules that promote oxidative stress and excitotoxic

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27

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

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28

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of

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29

Voll, Reinhard E., and Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.

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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms

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30

Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s

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31

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

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32

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

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33

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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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

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34

Gonder, Ulrike, ed. Ethisch Essen mit Fleisch: Eine Streitschrift über nachhaltige und ethische Ernährung mit Fleisch und die Missverständnisse und Risiken einer streng vegetarischen und veganen Lebensweise. Riva, 2021.

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35

El mito vegetariano: Comida, Justicia, Sostenibilidad. Capitán Swing Libros, 2018.

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36

Le Mythe végétarien: Nourriture, justice et pérennité. Les Editions Pilule Rouge, 2013.

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37

Keith, Lierre. Vegetarian Myth: Food, Justice, and Sustainability. PM Press, 2010.

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38

El Mito Vegetariano: Alimento, justicia y sustentabilidad. FisicalBook, 2012.

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39

Keith, Lierre. Vegetarian Myth: Food, Justice, and Sustainability. PM Press, 2009.

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40

Keith, Lierre. The Vegetarian Myth: Food, Justice, and Sustainability. ReadHowYouWant, 2013.

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