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Gotowe bibliografie tematyczne / Humoral immunity / Książki

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Książki na temat „Humoral immunity”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 29 stycznia 2023

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Sprawdź 22 najlepszych książek naukowych na temat „Humoral immunity”.

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1

1928-, Gupta A. P., red. Hemocytic and humoral immunity in arthropods. New York: Wiley, 1986.

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2

Giuseppe, Remuzzi, red. Humoral immunity in kidney transplantation: What clinicians need to know. Basel: Karger, 2009.

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Karcher, D. Humoral Immunity in Neurological Diseases. Springer, 2014.

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4

Karcher, D. Humoral Immunity in Neurological Diseases. Springer, 2012.

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Karcher, D. Humoral Immunity in Neurological Diseases. Springer London, Limited, 2013.

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6

Remuzzi, G., S. Chiaramonte, N. Perico i C. Ronco, red. Humoral Immunity in Kidney Transplantation. S. Karger AG, 2008. http://dx.doi.org/10.1159/isbn.978-3-8055-8959-8.

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7

M, Snapper Clifford, red. Cytokine regulation of humoral immunity: Basic and clinical aspects. Chichester: J. Wiley, 1996.

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8

Snapper, Clifford M. Cytokine Regulation of Humoral Immunity: Basic and Clinical Aspects. Wiley & Sons, Incorporated, John, 2008.

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9

Cytokine Regulation of Humoral Immunity: Basic and Clinical Aspects. Wiley, 1996.

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10

Valanne, Susanna, Dan Hultmark i Laura Vesala, red. Recent Advances in Drosophila Cellular and Humoral Innate Immunity. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-191-6.

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11

E, Sim, red. Humoral factors. Oxford: IRL Press at Oxford University Press, 1993.

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12

Whitney, Allene M. Effects of fluoride on humoral immunity in Eisenia foetida (Annelida). 1998.

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13

Roxburgh, Campbell S. D., i Donald C. McMillan. Cancer, immunity, and inflammation. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199656103.003.0012_update_001.

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The chapter focuses on the role of immunity and inflammation in established cancer. From the evidence reviewed it is clear that immune and inflammatory responses, innate, humoral and adaptive, local and systemic, are intimately linked to the tumour and themselves and impact on cancer survival. It is also possible to identify key mediators that may be targeted in the cancer patient. However, further work is required to elucidate the mechanisms by which these immune and inflammatory responses are activated, maintained, and interact. Therapeutic intervention using non-selective anti-inflammatory agents is widely advocated and likely to become part of routine clinical practice in the near future. Selective therapeutic intervention directed at the immune and inflammatory responses in cancer is in its infancy. Therefore, it would appear that, at least in non-hereditary disease, immune and inflammatory responses are of key, if not of prime, importance in tumour progression and dissemination.

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14

A, Sacher Ronald, i American Association of Blood Banks., red. Cellular and humoral immunotherapy and apheresis. Arlington, Va: American Association of Blood Banks, 1991.

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15

M. Poorghasemi, A. Seidavi, A.A.A. Qotbi, J.R. Chambers, V. Laudadio i V. Tufarelli. Effect of dietary fat source on humoral immunity response of broiler chickens. Verlag Eugen Ulmer, 2015. http://dx.doi.org/10.1399/eps.2015.92.

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16

1938-, Goidl Edmond A., red. Aging and the immune response: Cellular and humoral aspects. New York: Dekker, 1987.

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17

M. Vilić, Jadranka Pejaković Hlede, Jelena Dotur, S. Pašić, Ivona Žura Žaja, Marija Majer i Ž. Gottstein. Acute whole-body low dose gamma irradiation does not affect humoral immunity in chicken. Verlag Eugen Ulmer, 2016. http://dx.doi.org/10.1399/eps.2016.120.

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18

Shaw, Robert Patrick. Assessing the role of humoral immunity in the resistance to infection with mouse hepatitis virus type 3. 1986.

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19

Raghavan, Sri. Infection in the Cancer Patient. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0054.

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Cancer patients have increased susceptibility to a variety of both common and atypical infections due to the steady increase in outpatient chemotherapy regimens, these patients are presenting more often to the emergency department when acutely ill. Already immunocompromised, patients’ chemotherapy regimens lead to neutropenia, deficits in cellular and humoral immunity, and disruption of mucosal barriers that predisposing them to severe disease presentations with high morbidity and mortality rates. There are different subsets of oncologic patients predisposed to specific infections. One of the most common presentations of oncologic chemotherapy patients is neutropenic fever caused by bacterial infection; neutropenic patients are also highly susceptible to fungal infections. Patients with hematologic malignancies, particularly those undergoing chemotherapy or bone marrow transplant, can present with inflammation of the cecum with high risk for bacterial translocation and possible perforation. Patients who have indwelling catheters or mediports are at risk for catheter-associated bloodstream infections.

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20

Vaheri, Antti, James N. Mills, Christina F. Spiropoulou i Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.

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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.

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21

Izzedine, Hassan, i Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Redaktor Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.

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22

Ammen, Sharon. Causes and Compromise. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252040658.003.0007.

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This chapter looks at the variety of causes Irwin was involved in, from animal rights to suffragism to pacifism. The chapter reviews the anti-trust movement led by Theodore Roosevelt and blossoming during Woodrow Wilson’s push for progressivism. Irwin’s immunity to anti-immigrant sentiment because of her Scottish roots is discussed. Her reason for opposition to the new Actors Equity Association is covered. As the calls for suffragism grow, Irwin lends her voice to the cause, as do other actress suffragists, including Mary Shaw and Lillian Russell. She urges Woodrow Wilson to appoint her as “Secretary of Laughter.” Through it all, she stresses the strong connection between women and humor and her belief that women have a greater sense of humor than men do.

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