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Books on the topic 'Mucosal surfaces'

To see the other types of publications on this topic, follow the link: Mucosal surfaces.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Nataro, James P., Paul S. Cohen, Harry L. T. Mobley, and Jeffrey N. Weiser, eds. Colonization of Mucosal Surfaces. Washington, DC, USA: ASM Press, 2005. http://dx.doi.org/10.1128/9781555817619.

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2

Kraehenbuhl, Jean-Pierre, and Marian R. Neutra, eds. Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59951-4.

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3

Warren, Strober, ed. Mucosal immunity and infections at mucosal surfaces. New York: Oxford University Press, 1988.

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4

Colonization Of Mucosal Surfaces. ASM Press, 2005.

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5

Leceta, Javier, Rosa Del Campo, Stefan Jordan, and Christoph Siegfried Niki Klose, eds. Immunoregulation at Mucosal Surfaces. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-014-9.

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6

Nataro, James P., Paul S. Cohen, Harry L. T. Mobley, and Jeffrey N. Weiser. Colonization of Mucosal Surfaces. Wiley & Sons, Limited, John, 2014.

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7

Defense of mucosal surfaces: Pathogenesis, immunity and vaccines. Berlin: Springer, 1999.

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8

-P, Kraehenbuhl J., and Neutra M. R, eds. Defense of mucosal surfaces: Pathogenesis, immunity and vaccines. Berlin: Springer, 1999.

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9

Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Springer, 2011.

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10

Kraehenbuhl, Jean-Pierre, and Marian R. Neutra. Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Springer London, Limited, 2012.

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11

Kraehenbuhl, Jean-Pierre, and Marian R. Neutra. Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines. Springer London, Limited, 2011.

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12

(Editor), J. P. Kraehenbuhl, and M. R. Neutra (Editor), eds. Defense of Mucosal Surfaces: Pathogenesis, Immunity and Vaccines (Current Topics in Microbiology and Immunology). Springer-Verlag Telos, 1999.

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13

Khan, Nadeem, Ramkumar Mathur, and Murugaiyan Gopal, eds. Cross-Talk Between Inflammation and Barrier Framework at Mucosal Surfaces in the Lung: Implications for Infections and Pathology. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-175-6.

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14

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Incorporated, John, 2012.

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15

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Incorporated, John, 2011.

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16

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Incorporated, John, 2012.

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17

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Incorporated, John, 2011.

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18

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Incorporated, John, 2011.

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19

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Incorporated, John, 2011.

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20

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences. Wiley & Sons, Limited, John, 2011.

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21

Williams, Andrew E. Immunology: Mucosal and Body Surface Defences with Exploring Immunology Set. Wiley & Sons, Incorporated, John, 2012.

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22

Nadel, Simon, and Johnny Canlas. Epidemiology, diagnosis, and assessment of meningitis and encephalitis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0240.

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Despite advances in antimicrobial therapy, central nervous system infections have a high morbidity and mortality. Most pathogens reach the brain by haematogenous spread following invasion through the mucosal surface of the nasopharynx. The cerebrospinal fluid inflammatory response is responsible for most of the deleterious effects of the infection. Understanding this response has allowed a more rational approach to therapy. Patients may present with non-specific features, especially neonates, infants, post-neurosurgical patients, and the elderly. This chapter will review the epidemiology, pathophysiology, clinical presentation, and diagnosis of acute bacterial meningitis and encephalitis.

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23

Beebe-Dimmer, Jennifer L., Fawn D. Vigneau, and David Schottenfeld. Small Intestine Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0035.

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The small intestine extends 6–7 meters from the gastric pylorus to its insertion into the large intestine. Its mucosal surface contains 90% of the absorptive surface area of the digestive tract. Remarkably, in 2015, only about 3% of digestive system cancers and less than 1% of digestive cancer deaths in the United States were observed in the small intestine. In contrast, approximately 50% of cancers in the digestive tract were diagnosed in the large intestine, which measures just 1.5 meters in length. Cancers of the small intestine are among the most heterogeneous of gastrointestinal neoplasms, encompassing pathologic subtypes of neuroendocrine carcinoid, adenocarcinoma, lymphoma, and gastrointestinal stromal tumors. Adenocarcinoma accounted for ~25% to–35% of cancers in the small intestine, in contrast to over 90% of cancers in the large intestine. Genetic syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC), predispose to adenocarcinoma in the small intestine.

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24

Coppola, Silvia, and Franco Valenza. Inhalation injury in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0107.

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Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.

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