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Books on the topic 'Interleukin-6'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 July 2024

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1

Tamas, Bartfai, and Ottoson David 1918-, eds. Neuro-immunology of fever. Oxford [England]: Pergamon Press, 1992.

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2

Gregory, Bock, Marsh Joan, and Widdows Kate, eds. Polyfunctional cytokines: IL-6 and LIF. Chichester, Eng: Wiley, 1992.

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3

Young, Rosemary Irene. Cytokines and cancer: A focus on Interleukin-6. Manchester: University of Manchester, 1994.

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4

B, Sehgal Pravinkumar, Grieninger Gerd, Tosato Giovanna, New York Academy of Sciences., and National Foundation for Cancer Research., eds. Regulation of the acute phase and immune responses: Interleukin-6. New York, N.Y: New York Academy of Sciences, 1989.

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5

Michel, Revel, ed. IL-6: Physiopathology and clinical potentials. New York: Raven Press, 1992.

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6

Schwarze, Melinda Margarete K. Mechanisms of prevention of apoptosis in an interleukin-6-dependent myeloma cell line. Ottawa: National Library of Canada, 1995.

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7

Moldoveanu, Andrei Ion. Effects of prolonged endurance exercise on the gene expression and plasma levels of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. Ottawa: National Library of Canada, 1999.

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8

Cournoyer, Micheline. Circulating endotoxin, interleukin-6 and tumor necrosis factor alpha in a porcine model of intraabdominal sepsis. Ottawa: National Library of Canada, 1995.

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9

1946-, Kluger Matthew J., Oppenheim Joost J. 1934-, and Powanda M. C, eds. The Physiologic, metabolic, and immunologic actions of interleukin-1: Proceedings of a symposium held in Ann Arbor, Michigan, June 4-6, 1985. New York: Liss, 1985.

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10

Some aspects of induced protein synthesis in liver cells: Regulatory effects of interleukin-6, insulin, glicated proteins and polyglucans. Kraków: Wydawn. Uniwersytetu Jasgiellońskiego, 1997.

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11

Bernard, Klein. Cytokines in human multiple myeloma. Austin: R.G. Landes, 1994.

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12

Kishimoto, Tadamitsu. Interleukin-6. Springer, 2018.

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13

Interleukin-6. Nova Biomedical, 2013.

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14

Andrzej, Mackiewicz, Koj A, and Sehgal Pravinkumar B, eds. Interleukin-6-type cytokines. New York: New York Academy of Sciences, 1995.

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15

Schroeder, Joseph J. Roles of interleukin 6, zinc, and metallothionein in cytoprotection. 1990.

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16

Berrier, Allison Lyon. Mechanisms involved in regulating the expression and activity of the C/EBP protein nuclear factor-interleukin-6. 1998.

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17

Sehgal, Pravinkumar B., and Gerd Grieninger. Regulation of the Acute Phase and Immune Responses: Interleukin-6 (Annals of the New York Academy of Sciences, Vol. 557). New York Academy of Sciences, 1989.

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18

Hodgkiss, Andrew. Psychiatric consequences of particular cancers. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0004.

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Certain tumour types can cause psychopathology through direct biological mechanisms such as metastatic spread to the brain, release of onconeuronal antibodies, ectopic hormone secretion, or release of pro-inflammatory cytokines. Lung cancers, adenocarcinoma of the pancreas, brain tumours, and ovarian tumours are considered in detail. Confusional states due to brain metastases, syndrome of inappropriate ADH secretion, hypercalcaemia of malignancy, and anti-Hu encephalitis are found in lung cancers. Severe depression, due to interleukin-6 release and its actions on the HPA axis and tryptophan metabolism, is common in adenocarcinoma of the pancreas. Anti-NMDA-receptor limbic encephalitis, clinically indistinguishable from acute schizophrenia, can complicate teratomas. Gliomas, pituitary tumours, and thyroid, adrenal, and testicular tumours can also disrupt mental health through various biological mechanisms described here.

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19

Rock, Fernando Lloyd. High-level expression and structure-function analyses of recombinant human interleukin 6: structural roles of the Cysb4s5-Cysb5s1 and Cysb7s4-Cysb8s4 disulphide bonds. 1994.

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20

Klingenberg, Roland, and Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.

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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α‎ and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.

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21

Wang, Xu. Effect of controlled vitamin B-6 intake on in vitro lymphocyte proliferation and interleuken 2 production in young women. 1995.

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22

Richette, Pascal. Principles of gout management. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0044.

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The general goals of gout therapy are to manage acute flares and to prevent recurrences and prevent or reverse the complications of urate deposition by lowering urate levels. The choice of drug should be made on the basis of the patient’s co-morbidities, other medications, and side effect profile. Treatment of flares can be achieved with non-steroidal anti-inflammatory drugs, colchicine, or corticosteroids (systemic or intra-articular). Interleukin-1 blockers could become an alternative in patients contraindicated for traditional anti-inflammatory agents. Lowering of urate levels below monosodium urate (MSU) saturation point with both a non-pharmacological and pharmacological approach allows to dissolve MSU crystals and to cure gout. Serum urate (SUA) levels should be maintained below 6 mg/dL (360 μ‎mol/L) or below 5 mg/dL (300 μ‎mol/L) in patients with severe gout to facilitate faster dissolution of crystals. Urate-lowering therapy (ULT) should be initiated close to the first diagnosis of gout. Allopurinol and febuxostat are the most widely used xanthine oxidase inhibitors to lower SUA levels. If the SUA target cannot be reached by these agents, uricosurics are indicated, either alone or in combination with a xanthine oxidase inhibitor. In patients with severe tophaceous gout in whom the SUA target cannot be reached with any other available drug, pegloticase is indicated. Since ULT initiation may trigger acute attacks of gout, prophylaxis with an anti-inflammatory agent is recommended, mostly with low-dose colchicine. Of note, patient education, appropriate lifestyle advice, and treatment of comorbidities are also important parts of the management of patients with gout.

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23

Gray, Andrew C. Orthopaedic approach to the multiply injured patient. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012003.

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♦ Major trauma results in a systemic stress response proportional to both the degree of initial injury (1st hit) and the subsequent surgical treatment (2nd hit).♦ The key physiological processes of hypoxia, hypovolaemia, metabolic acidosis, fat embolism, coagulation and inflammation operate in synergy during the days after injury/surgery and their effective management determines prognosis.♦ The optimal timing and method of long bone fracture fixation after major trauma remains controversial. Two divergent views exist between definitive early intramedullary fixation and initial external fixation with delayed conversion to an intramedullary nail once the patient’s condition has been better stabilised.♦ There is agreement that the initial skeletal stabilisation should not be delayed and that the degree of initial injury has a more direct correlation with outcome and the development of subsequent systemic complications rather than the method of long bone fracture stabilisation.♦ Trauma patients can be screened to identify those more ‘at risk’ of developing systemic complications such as respiratory insufficiency. Specific risk factors include: A high injury severity score; the presence of a femoral fracture; the combination of blunt abdominal or thoracic injury combined with an extremity fracture; physiological compromise on admission and uncorrected metabolic acidosis prior to surgery.♦ The serum concentration of pro-inflammatory cytokine interleukin (IL) 6 may offer an accurate method of quantifying the degree of initial injury and the response to surgery.♦ The effective management of the polytraumatised patient involves a team approach and effective communication with allied specialties and theatre staff. A proper hierarchy of the injuries sustained can then be compiled and an effective surgical strategy made.

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24

M, Glauert Audrey, Strangeways Research Laboratory (Cambridge, England), and International Symposium on "The Control of Tissue Damage" (1987 : Babraham, England), eds. The Control of tissue damage: Strangeways Research Laboratory 75th anniversary symposium, 6-8 April 1987. Amsterdam: Elsevier, 1988.

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25

Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.

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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ‎ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.

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26

Bending, David, Kiran Nistala, and Lucy R. Wedderburn. Pathogenesis of juvenile idiopathic arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0060.

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Although the term juvenile idiopathic arthritis (JIA) encompasses a heterogeneous group of diseases, they all share a common pathological hallmark: inflammation of the synovium. Highly activated T cells, monocytes, and neutrophils are attracted to the joint and secrete mediators that not only perpetuate inflammation but also may attenuate immune regulation. In the oligoarticular and polyarticular forms of JIA, which are thought to be autoimmune conditions, dysregulated adaptive immunity is a likely factor in disease pathogenesis; the nature of the interactions between T effector (Teff) cells and T regulatory cells (Treg) is probably a key factor in controlling disease progression. Factors that affect the frequency and function of Tregs and/or the sensitivity of Teffs to mechanisms of immune suppression will therefore impact on the disease course. In the systemic form of JIA, however, dysregulation of innate immune pathways appears more central to disease pathogenesis resulting in augmented levels of interleukins IL-1β‎, IL-6, and IL-18. In the end, a final, common pathological pathway in JIA is the activation of monocytes and neutrophils, which are the principal mediators of joint inflammation and damage. This is supported by the fact that the therapies that have targeted innate cytokine pathways have shown greater success in the treatment of JIA.

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