Bibliografías temáticas / Lungs Inflammation / Libros

Libros sobre el tema "Lungs Inflammation"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 27 de enero de 2023

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1

Symposium, on Airway Obstruction and Inflammation (1988 Florence Italy). Airway obstruction and inflammation: Present status and perspectives. Basel: Karger, 1990.

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2

Criner, Gerard J., William D. Cornwell y Thomas J. Rogers. Smoking and lung inflammation: Basic, pre-clinical, and clinical research advances. New York: Springer, 2013.

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3

L, Kradin Richard y Robinson Bruce W. S, eds. Immunopathology of lung disease. Boston: Butterworth-Heinemann, 1996.

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4

Bertolini, Renzo. Animal and vegetable dusts as a cause of deep lung inflammation. Hamilton: CCOHS, 1988.

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5

Michel, Chignard y Conference on Cytokines and Adhesion Molecules in Lung Inflammation (1995 : Paris, France), eds. Cytokines and adhesion molecules in lung inflammation. New York: New York Academy of Sciences, 1996.

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6

F, Donner C., ed. COPD is/is not a systemic disease? Hauppauge, NY: Nova Science, 2009.

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7

1952-, Strieter Robert M., Kunkel S. L y Standiford Theodore J, eds. Chemokines in the lung. New York: Marcel Dekker, Inc., 2003.

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8

Rogers, Thomas J., Gerard J. Criner y William D. Cornwell, eds. Smoking and Lung Inflammation. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7351-0.

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9

Dubinett, Steven M., ed. Inflammation and Lung Cancer. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2724-1.

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10

Alper, Scott y William J. Janssen, eds. Lung Innate Immunity and Inflammation. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8570-8.

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11

Wang, Yong-Xiao, ed. Lung Inflammation in Health and Disease, Volume I. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63046-1.

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12

Wang, Yong-Xiao, ed. Lung Inflammation in Health and Disease, Volume II. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68748-9.

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13

Pokorski, Mieczyslaw. Pulmonary Infection and Inflammation. Springer London, Limited, 2016.

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14

Pokorski, Mieczyslaw. Pulmonary Infection and Inflammation. Springer, 2018.

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15

Pokorski, Mieczyslaw. Pulmonary Infection and Inflammation. Springer, 2016.

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16

Dubinett, Steven M. Inflammation and Lung Cancer. Springer, 2015.

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17

Dubinett, Steven M. Inflammation and Lung Cancer. Springer, 2016.

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18

Dubinett, Steven M. Inflammation and Lung Cancer. Springer, 2015.

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19

Rogers, Thomas J., Gerard J. Criner y William D. Cornwell. Smoking and Lung Inflammation: Basic, Pre-Clinical and Clinical Research Advances. Springer, 2016.

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20

Martin, Thomas. Cytokines in Pulmonary Disease: Infection and Inflammation (Lung Biology in Health & Disease). Informa Healthcare, 2000.

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21

Strieter, Robert M., Steven L. Kunkel y Theodore J. Standiford. Chemokines in the Lung. Taylor & Francis Group, 2003.

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22

Michel, Chignard, ed. Cells and cytokines in lung inflammation. New York, NY: New York Academy of Sciences, 1994.

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23

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

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24

(Editor), Trevor T. Hansel y Peter J. Barnes (Editor), eds. Recent Advances in the Pathophysiology of COPD (Progress in Inflammation Research). Birkhäuser Basel, 2004.

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25

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

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26

Montuschi, Paolo. New Perspectives in Monitoring Lung Inflammation: Analysis of Exhaled Breath Condensate. Taylor & Francis Group, 2004.

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27

Montuschi, Paolo. New Perspectives in Monitoring Lung Inflammation: Analysis of Exhaled Breath Condensate. Taylor & Francis Group, 2004.

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28

Montuschi, Paolo. New Perspectives in Monitoring Lung Inflammation: Analysis of Exhaled Breath Condensate. Taylor & Francis Group, 2004.

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29

New perspectives in monitoring lung inflammation: Analysis of exhaled breath condensate. Boca Raton, FL: CRC Press, 2006.

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30

Montuschi, Paolo. New Perspectives in Monitoring Lung Inflammation: Analysis of Exhaled Breath Condensate. Taylor & Francis Group, 2004.

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31

Montuschi, Paolo. New Perspectives in Monitoring Lung Inflammation: Analysis of Exhaled Breath Condensate. Taylor & Francis Group, 2004.

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32

Acute Lung Injury: From Inflammation to Repair (Biomedical and Health Research). Ios Pr Inc, 2001.

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33

A, Persson C. G., ed. Inflammatory indices in chronic bronchitis. Basel: Birkhäuser, 1990.

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34

1942-, Church Martin y Robinson Clive 1958-, eds. Eicosanoids in inflammatory conditions of the lung, skin, and joints. Lancaster: MTP Press, 1988.

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35

Ray, Abhijit y Punit Kumar Srivastave. Obstructive Airway Diseases. Taylor & Francis Group, 2011.

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36

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

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37

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

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38

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

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39

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

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40

Ong, Kian Chung, ed. Lung Inflammation. InTech, 2014. http://dx.doi.org/10.5772/57068.

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41

Adlam, David. Pericardial disease. Editado por Patrick Davey y David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0109.

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Resumen
The pericardium forms a continuous sac around the heart, analogous to the pleura surrounding the lungs, and the peritoneum surrounding the abdominal viscera. Between the parietal and visceral layers of the serous pericardium is the pericardial space, which normally contains a small volume of pericardial fluid. The clinical spectrum of pericardial diseases can be divided into: pericarditis, caused by acute inflammation; pericardial effusion, or fluid accumulation in the pericardial space, leading to tamponade; and constrictive pericarditis, caused by chronic infiltration or inflammation leading to pericardial constriction.
42

Wick, Mark R. y Henry D. Tazelaar. Neoplastic Mimics in Thoracic and Cardiovascular Pathology. Springer Publishing Company, Incorporated, 2013.

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43

Wick, Mark R. y Henry D. Tazelaar. Neoplastic Mimics in Thoracic and Cardiovascular Pathology. Springer Publishing Company, Incorporated, 2013.

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44

Wiffen, Philip, Marc Mitchell, Melanie Snelling y Nicola Stoner. Therapy-related issues: musculoskeletal diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0025.

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Rheumatoid arthritis 548Gout 556Rheumatoid arthritis (RA) is an autoimmune disease which causes joints lined with synovium to become inflamed, swollen, stiff, and painful, and leads to joint erosion. It is a multisystem disorder which can affect many organs including the eyes, lungs, heart, and blood vessels. The aim of treatment is to decrease pain and inflammation, prevent joint damage, and ultimately induce remission of disease....
45

Blend, Doctor Herry. Ketoconazole: Perfect Guide for Most Effective Antifungal Treatment That Completely Cures Jock Itch, Athlete's Foot, Ringworm, Painful Inflammation, Lungs or Skin Diseases and Other Fungal Diseases. Lulu Press, Inc., 2018.

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46

Klepikov, Igor. Didactics of Acute Lung Inflammation. Cambridge Scholars Publishing, 2022.

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47

Kriemler, Susi, Thomas Radtke y Helge Hebestreit. Exercise, physical activity, and cystic fibrosis. Editado por Neil Armstrong y 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 exercise training in CF on exercise capacity, decline of pulmonary function, and health-related quality of life, the observed effects are encouraging and exercise should be implemented in all patient care. More research is needed to understand pathophysiological mechanisms of exercise limitations and to find optimal exercise modalities to slow down disease progression, predict long-term adherence, and improve health-related quality of life.
48

Balhara, Kamna S., Basem F. Khishfe y 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) management; aggressive fluid resuscitation; early administration of broad-spectrum antibiotics; and early goal-directed therapy and severe sepsis resuscitation bundle. Diagnosis can be challenging in pediatric and geriatric populations.
49

Lynn, William S. Inflammatory Cells & Lung Disease. Taylor & Francis Group, 2020.

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50

Kriemler, Susi. Exercise, physical activity, and cystic fibrosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0033.

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Cystic fibrosis (CF) is the most common genetic autosomal recessive disease of the Caucasian race, generally leading to death in early adulthood.1 The frequency of the gene carrier (heterozygote) is 1:20–25 in Caucasian populations, 1:2000 in African-Americans, and practically non-existent in Asian populations. The disease occurs in about 1 in every 2500 life births of the white population. Mean survival has risen from 8.4 years in 1969 to 32 years in 2000 due to improvements in treatment. The genetic defect causes a pathological electrolyte transport through the cell membranes by a defective chloride channel membrane transport protein [cystic fibrosis transmembrane conductance regulator (CFTR)]. With respect to the function, this affects mainly the exocrine glands of secretory cells, sinuses, lungs, pancreas, liver, and the reproductive tract of the human body leading to a highly viscous, water-depleted secretion. The secretion cannot leave the glands and in consequence causes local inflammation and destruction of various organs. The main symptoms include chronic inflammatory pulmonary disease with a progressive loss of lung function, exocrine and sometimes endocrine pancreas insufficiency, and an excessive salt loss through the sweat glands.1 A summary of the signs and symptoms of CF will be given with a special emphasis on the effect of exercise performance and capacity.
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