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Books on the topic 'Airway inflammation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Rogers, Duncan F., and Louise E. Donnelly. Human Airway Inflammation. Humana Press, 2001. http://dx.doi.org/10.1385/1592591515.

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2

Tony, Eissa N., and Huston David P, eds. Therapeutic targets in airway inflammation. Marcel Dekker, 2003.

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3

1947-, Nijkamp Franciscus Petrus, ed. Mediators in airway hyperreactivity. Birkhäuser Verlag, 1990.

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4

1940-, Olivieri D., and Bianco S, eds. Airway obstruction and inflammation: Present status and perspectives. Karger, 1990.

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5

Just, Allan. Exposure to Phthalate Mixtures and Inner-City Pediatric Allergic Disease and Airway Inflammation. [publisher not identified], 2012.

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6

Rosa, Maria Jose. Ambient combustion by-product exposures and exhaled biomarkers of airway inflammation and oxidative stress. [publisher not identified], 2014.

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7

Underwood, Stephen L. Studies on the mechanisms of pulmonary inflammation and airway hyperreactivity in animal models of asthma. University of East London, 1997.

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8

Gosman, Margot Madeleine Elvira. From pathology to treatment in chronic obstructive pulmonary disease: Focus on inflammatory cells and airway hyperresponsiveness. [s.n.], 2006.

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9

Wong, Simon S. Role of neprilysin in airway inflammation induced by diesel exhaust emissions: With a critique by the HEI Health Review Committee. Health Effects Institute, 2011.

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10

Page, Clive P., Katharine H. Banner, and Domenico Spina, eds. Cellular Mechanisms in Airways Inflammation. Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1.

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11

M, Geddes Duncan, Kay A. B, and Friend J. A. R, eds. Inflammation: Its significance in airways disease. Medical Tribune Group, 1987.

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12

1953, Raeburn D., and Giembycz M. A. 1961-, eds. Airways smooth muscle: Neurotransmitters, amines, lipid mediators, and signal transduction. Birkhauser Verlag, 1995.

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13

Eissa, N. Tony, and David P. Huston, eds. Therapeutic Targets in Airway Inflammation. CRC Press, 2003. http://dx.doi.org/10.3109/9780203911471.

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14

Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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15

Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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16

Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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17

Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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18

Eissa, N. Tony, and David P. Huston. Therapeutic Targets in Airway Inflammation. Taylor & Francis Group, 2003.

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19

Obstructive Airway Diseases. Taylor & Francis Group, 2011.

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20

Rogers, Duncan F., and Louise E. Donnelly. Human Airway Inflammation: Sampling Techniques and Analytical Protocols. Humana Press, 2013.

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21

Human Airway Inflammation: Sampling Techniques and Analytical Protocols. Humana Press, 2004.

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22

Roldán, Nestor González, Otto Holst, Johannes Huebner, and Katarzyna Anna Duda, eds. Role of Lipids in the Dynamics of Allergic Airway Inflammation. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-315-6.

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23

(Editor), C. P. Page, Katharine H. Banner (Editor), and Domenico Spina (Editor), eds. Cellular Mechanisms in Airways Inflammation (Pir (Series).). Birkhauser, 2000.

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24

Ray, Abhijit. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2011.

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25

Ray, Abhijit, and Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2016.

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26

Ray, Abhijit, and Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2018.

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27

Ray, Abhijit, and Punit Kumar Srivastava. Obstructive Airway Diseases: Role of Lipid Mediators. Taylor & Francis Group, 2016.

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28

Olivieri, D. Airway Obstruction and Inflammation: Present Status and Perspectives (Progress in Respiratory Research). S. Karger AG (Switzerland), 1989.

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29

(Editor), Duncan F. Rogers, and Louise E. Donnelly (Editor), eds. Human Airway Inflammation: Sampling Techniques and Analytical Protocols (Methods in Molecular Medicine). Humana Press, 2001.

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30

Fahy, John Vincent. Cellular and biochemical analysis of induced sputum: A novel method for studying airway inflammation and mucus hypersecretion in asthmatic subjects. 2nd ed. 1995.

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31

(Editor), Johan Zaagsma, Herman Meurs (Editor), and Ad F. Roffel (Editor), eds. Muscarinic Receptors in Airways Diseases (Progress in Inflammation Research). Birkhauser, 2001.

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32

Jeffrey, Andrew, Abdul Nasimudeen, and Joshua Agbetile. Asthma. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0133.

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Asthma is a disorder of airway smooth muscle and airway inflammation, manifested by variable airflow limitation. This definition continues to be refined in light of developments in the understanding of asthma’s pathophysiology, immunology, and treatment.

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33

Williams, Erin S. Asthmatic for Adenotonsillectomy. Edited by Erin S. Williams, Olutoyin A. Olutoye, Catherine P. Seipel, and Titilopemi A. O. Aina. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190678333.003.0005.

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Asthma is a chronic reversible pulmonary condition. It is the most common respiratory disease as it affects 6 million to 9 million children in the United States. The patient with asthma can experience reversible bronchoconstriction, airway inflammation, airway hyperresponsivness, and increased mucus production. Inflammation is the fundamental abnormality. This dynamic process exists on a spectrum of mild, moderate, or severe. Patients may exhibit expiratory wheezing, obstruction to expiration, and/or inspiration, cough, and respiratory distress. Given the prevalence of asthma and its potential

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34

Redding, Amanda T., and Marc Hassid. Acute Severe Asthma and Bronchospasm. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0079.

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This chapter focuses on acute asthma and bronchospasm occurring in the perioperative period. Over 6% of the people in the United States have asthma, which is characterized by chronic inflammation, airway hyperresponsiveness, excessive mucus, and reversible airway obstruction. Due to generalized airway hyperreactivity, a history of asthma increases the risk of coughing, wheezing, bronchospasm, and oxygen desaturation. Although the incidence of bronchospasm associated with asthma is low, when it occurs it is often severe. A stepwise treatment algorithm is defined, which covers the use of first l

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35

Hebestreit, Helge, Susi Kriemler, and Thomas Radtke. Exercise, physical activity, and asthma. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0024.

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The incidence of asthma in children varies among countries and can be estimated to range between 5% and 20%. Exercise-induced asthma (EIA) is common in patients with asthma but can also occur in some children without asthma. Typical symptoms of EIA include cough, chest tightness, and shortness of breath shortly after exercise. The pathophysiology of EIA is not completely understood, but it has been shown that airway cooling and drying with increased ventilation during exercise and airway re-warming after exercise play a pivotal role. In addition, a lack of physical activity may also contribute

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36

Banner, Katharine H. Cellular Mechanisms in Airways Inflammation. Birkhauser Verlag, 2013.

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37

Page, C. P. Cellular Mechanisms in Airways Inflammation. Springer, 2012.

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38

(Editor), Clive P. Page, Katharine H. Banner (Editor), and Domenico Spina (Editor), eds. Cellular Mechanisms in Airways Inflammation (Progress in Inflammation Research). Birkhauser, 2000.

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39

Rello, Jordi, and Bárbara Borgatta. Pathophysiology of pneumonia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0115.

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Airway colonization, ventilator-associated tracheobronchitis (VAT), and hospital-acquired (HAP) and ventilator-associated pneumonia (VAP) are three manifestations having the presence of micro-organisms in airways in common. Newer definitions have to consider worsening of oxygenation, in addition to purulent respiratory secretions, chest-X rays opacities, and biomarkers of inflammation. Bacteria are the main causes of HAP/VAP. During hospitalization there’s a shift of airway’s colonizing flora from core organisms to enteric and non-fermentative ones. Macro- and micro-aspiration is the most impo

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40

Balhara, Kamna S., Basem F. Khishfe, and Jamil D. Bayram. Sepsis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0004.

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Sepsis is a clinical syndrome characterized by systemic inflammation in the presence of infection. The source of infection may be occult. One must be aware of the epidemiology, presenting features and complications, diagnostic considerations and tests, and the organisms involved. Bacteria (gram positive and negative) are most commonly associated with sepsis, although fungi, viruses, and parasites can cause sepsis. Infections in the lungs, urinary tract, abdomen, skin, brain, and other areas can cause bacteremia and lead to sepsis. Treatment includes airway, breathing, and circulation (ABCs) ma

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41

Inflammatory disorders of the airways. Saunders, 1988.

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42

Wecksell, Matthew, and Kenneth Fomberstein. Traumatic Brain Injury and C-Spine Management. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0020.

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Traumatic brain injury encompasses two different types of pathology: that caused at the time of the initial physical insult, called primary injury, and then further, secondary injury caused by either host cellular responses such as oxidative injury and inflammation or by physiological insults such as ischemia, hypoxia, hypo- or hypercapnia, intracranial hypertension, and hypo- or hyperglycemia. While primary injury falls to the realm of public health (e.g., encouraging helmet use for sports, discouraging impaired driving, etc.), many secondary injuries are avoidable with proper medical managem

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43

Kriemler, Susi, Thomas Radtke, and Helge Hebestreit. Exercise, physical activity, and cystic fibrosis. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0027.

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Cystic fibrosis (CF) is a genetic disease resulting in an impaired mucociliary clearance, chronic bacterial airway infection, and inflammation. The progressive destruction of the lungs is the main cause of morbidity and premature death. Diverse other organ systems such as heart, muscles, bones, gastro-intestinal tract, and sweat glands are often also affected and interfere with exercise capacity. Hence, exercise capacity is reduced as the disease progresses mainly due to reduced functioning of the muscles, heart, and/or lungs. Although there is still growing evidence of positive effects of exe

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44

Loukides, Stelois. Non-Invasive Assessment of Airways Inflammation in Asthma and COPD. Green Stem Press, 2011.

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45

Frew, Anthony. Air pollution. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0341.

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Any public debate about air pollution starts with the premise that air pollution cannot be good for you, so we should have less of it. However, it is much more difficult to determine how much is dangerous, and even more difficult to decide how much we are willing to pay for improvements in measured air pollution. Recent UK estimates suggest that fine particulate pollution causes about 6500 deaths per year, although it is not clear how many years of life are lost as a result. Some deaths may just be brought forward by a few days or weeks, while others may be truly premature. Globally, household

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46

Gilchrist, Francis J., and Alex Horsley. Management of respiratory exacerbations. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0005.

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Cystic fibrosis lung disease is characterized by chronic infection, inflammation and a progressive loss of lung function. Patients are also affected by recurrent episodes of increased respiratory symptoms, called exacerbations which have a detrimental effect on quality of life, the rate of lung function decline, and mortality. Early diagnosis and treatment is vital. Diagnosis relies on a combination of symptoms, examination findings, the results of laboratory tests, and lung function. Antibiotics are the mainstay of treatment but airway clearance, nutrition, and glucose homeostasis must also b

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47

Raeburn, D. Ed. Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators & Signal Transduction (Exs). Birkhauser, 1996.

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48

Davey, Patrick, Sherif Gonem, and David Sprigings. Interstitial lung disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0139.

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The interstitial lung diseases, also known as the diffuse or diffuse parenchymal lung diseases, are a broad group of pulmonary disorders which mainly affect the lung parenchyma as opposed to the airways. By convention, infectious and malignant conditions are excluded from this definition. Thus, the interstitial lung diseases comprise a group of conditions characterized by variable degrees of inflammation and fibrosis, centred on the lung interstitium and alveolar airspaces.

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49

Airways Smooth Muscle: Neurotransmitters, Amines, Lipid Mediators and Signal Transduction (Respiratory Pharmacology and Pharmacotherapy). Birkhauser Boston, 1995.

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50

Inflammation,its significance in airways disease: Proceedings of a series of symposia held in Edinburgh, London and Chester in October and November, 1986. Education in Practice, 1987.

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