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Books on the topic 'Modulation of macrophage activation'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Kucey, Daryl Stanton. Modulation of macrophage procoagulant activity by platelet activating factor. National Library of Canada = Bibliothèque nationale du Canada, 1992.

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2

Russell, Stephen W., and Siamon Gordon, eds. Macrophage Biology and Activation. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77377-8.

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3

Therapeutic targets: Modulation, inhibition, and activation. John Wiley & Sons, 2012.

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4

1955-, Suttles Jill, ed. T-cell signaling of macrophage activation: Cell contact-dependent and cytokine signals. R.G. Landes, 1995.

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5

Adams, Dolph O. Macrophage Activation. Springer, 2013.

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6

Grom, Alexei A., and Athimalaipet V. Ramanan. Macrophage activation syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0168.

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Macrophage activation syndrome (MAS) is a life-threatening condition caused by excessive activation and proliferation of T lymphocytes and haemophagocytic macrophages. Although MAS has been reported in association with almost any rheumatic disease, it is by far most common in systemic juvenile idiopathic arthritis. Flares of the underlying disease or infection are most common triggers of MAS. The pathognomonic feature of MAS is typically found in bone marrow: numerous, well-differentiated macrophagic histiocytes phagocytosing normal haematopoietic elements. The expansion of these histiocytes l

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7

W, Russell Stephen, and Gordon Siamon, eds. Macrophage biology and activation. Springer-Verlag, 1992.

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8

Hussain Bhat, Khalid, ed. Macrophage Activation - Biology and Disease. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.79065.

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9

1943-, Zwilling Bruce S., and Eisenstein Toby K, eds. Macrophage-pathogen interactions. M. Dekker, 1994.

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10

Shukla, Supriya, Hridayesh Prakash, Jaya Talreja, and Manisha Yadav, eds. Modulation of Macrophage Signaling Pathways during Bacterial Infections. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-189-5.

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11

Botana, Luis M., and Mabel Loza. Therapeutic Targets: Modulation, Inhibition, and Activation. Wiley & Sons, Incorporated, John, 2012.

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12

Botana, Luis M., and Mabel Loza. Therapeutic Targets: Modulation, Inhibition, and Activation. Wiley & Sons, Incorporated, John, 2012.

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13

Botana, Luis M., and Mabel Loza. Therapeutic Targets: Modulation, Inhibition, and Activation. Wiley & Sons, Incorporated, John, 2012.

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14

Activation and Modulation of Mast Cells. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03936-564-7.

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15

Russell, Stephen W. Macrophage Biology and Activation (Current Topics in Microbiology and Immunology). Springer, 1992.

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16

Stout, Robert D. T-Cell Signaling of Macrophage Activation: Cell Contact-Dependent and Cytokine Signals (Archives of Toxicology). Springer, 1996.

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17

Russell, S., and S. Gordon. Current Topics in Microbiology and Immunology: Macrophage Biology and Activation (Current Topics in Microbiology and Immunology). Springer-Verlag Berlin and Heidelberg GmbH & Co. KG, 1992.

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18

Bucala, Richard. Mif Handbook. World Scientific Publishing Co Pte Ltd, 2012.

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19

J, Fritch Jennifer, Tash Joseph S, and United States. National Aeronautics and Space Administration., eds. A method for preparation, storage and activation of large populations of immotile sea urchin sperm. National Aeronautics and Space Administration, 1997.

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20

A method for preparation, storage and activation of large populations of immotile sea urchin sperm. National Aeronautics and Space Administration, 1997.

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21

Dackiw, Alan PB. Induction and modulation of monocyte/macrophage tissue factor/fibrin deposition and TNF secretion in the microenvironment of inflammation: The role of tyrosine phosphorylation. 1998.

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22

Murphy, Claire Louise, Yiannis Ioannou, and Nicola Ambrose. Juvenile systemic lupus erythematosus. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198739180.003.0008.

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Juvenile-onset systemic lupus erythematosus (JSLE) is similar to adult-onset SLE, but there are distinct differences in clinical features, serology, and management requirements. It is more aggressive than adult-onset SLE with frequent renal and haematological manifestations and higher mortality rates. The cause of JSLE is unknown but appears to be multifactorial with genetic, immunological, hormonal, and environmental influences. Macrophage activation syndrome is a potentially life-threatening complication, and may mimic the underlying disease or be confused with sepsis. Transferring care from

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23

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its a

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24

Sebastio, Gianfranco, Manuel Schiff, and Hélène Ogier de Baulny. Lysinuric Protein Intolerance and Hartnup Disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0025.

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Lysinuric protein intolerance (LPI) is an inherited aminoaciduria caused by defective cationic amino acid transport at the basolateral membrane of epithelial cells in intestine and kidney. LPI is caused by mutations in the SLC7A7 gene, which encodes the y+LAT-1 protein, the catalytic light chain subunit of a complex belonging to the heterodimeric amino acid transporter family. Symptoms usually begin after weaning with refusal of feeding, vomiting, and consequent failure to thrive. Hepatosplenomegaly, hematological anomalies, and neurological involvement including hyperammonemic coma will progr

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25

Baildam, Eileen. Juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0116.

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Juvenile idiopathic arthritis (JIA) is defined as arthritis lasting for 6 weeks or more presenting in childhood at any age up to 17 years. Arthritis is diagnosed clinically by the presence of joint pain, stiffness, and swelling with inflammation limiting the range of individual joint movement. There are subtypes that tend to follow distinct courses and with phenotypes that vary widely from a serious systemic inflammatory disorder of systemic JIA to single-joint monoarthritis. The differential diagnosis of JIA is wide and the best chance of long-term remission is where treatment is started as e

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26

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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27

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 p

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28

Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or

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