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Relevant bibliographies by topics / Pulmonary infection

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Academic literature on the topic 'Pulmonary infection'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 April 2023

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Journal articles on the topic "Pulmonary infection"

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Cáceres, José. "Pulmonary infection." European Journal of Radiology 51, no. 2 (August 2004): 101. http://dx.doi.org/10.1016/j.ejrad.2004.03.006.

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Allie, S. Rameeza, and Troy D. Randall. "Pulmonary immunity to viruses." Clinical Science 131, no. 14 (June 30, 2017): 1737–62. http://dx.doi.org/10.1042/cs20160259.

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Mucosal surfaces, such as the respiratory epithelium, are directly exposed to the external environment and therefore, are highly susceptible to viral infection. As a result, the respiratory tract has evolved a variety of innate and adaptive immune defenses in order to prevent viral infection or promote the rapid destruction of infected cells and facilitate the clearance of the infecting virus. Successful adaptive immune responses often lead to a functional state of immune memory, in which memory lymphocytes and circulating antibodies entirely prevent or lessen the severity of subsequent infections with the same virus. This is also the goal of vaccination, although it is difficult to vaccinate in a way that mimics respiratory infection. Consequently, some vaccines lead to robust systemic immune responses, but relatively poor mucosal immune responses that protect the respiratory tract. In addition, adaptive immunity is not without its drawbacks, as overly robust inflammatory responses may lead to lung damage and impair gas exchange or exacerbate other conditions, such as asthma or chronic obstructive pulmonary disease (COPD). Thus, immune responses to respiratory viral infections must be strong enough to eliminate infection, but also have mechanisms to limit damage and promote tissue repair in order to maintain pulmonary homeostasis. Here, we will discuss the components of the adaptive immune system that defend the host against respiratory viral infections.

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MATO, S. "Pulmonary infections in children with HIV infection." Seminars in Respiratory Infections 17, no. 1 (March 2002): 33–46. http://dx.doi.org/10.1053/srin.2002.31685.

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Li, Meng, and Wanqing Liao. "Pulmonary Cryptococcocal Infection." Current Respiratory Medicine Reviews 8, no. 5 (November 1, 2012): 365–69. http://dx.doi.org/10.2174/157339812803832511.

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Sottile, Frank D., Donald S. Prough, Anthony G. Gristina, David J. Gower, Cherri D. Hobgood, Lawrence X. Webb, Thomas J. Marrie, and J. William Costerton. "NOSOCOMIAL PULMONARY INFECTION." Critical Care Medicine 13, no. 4 (April 1985): 300. http://dx.doi.org/10.1097/00003246-198504000-00063.

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SOTTILE, FRANK D., THOMAS J. MARRIE, DONALD S. PROUGH, CHERRI D. HOBGOOD, DAVID J. GOWER, LAWRENCE X. WEBB, J. WILLIAM COSTERTON, and ANTHONY G. GRISTINA. "Nosocomial pulmonary infection." Critical Care Medicine 14, no. 4 (April 1986): 265–70. http://dx.doi.org/10.1097/00003246-198604000-00001.

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Finegold, Sydney M. "Anaerobic Pulmonary Infection." Hospital Practice 24, no. 5 (May 15, 1989): 103–33. http://dx.doi.org/10.1080/21548331.1989.11703715.

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Chen, Kuan-Yu, Shiann-Chin Ko, Po-Ren Hsueh, Kwen-Tay Luh, and Pan-Chyr Yang. "Pulmonary Fungal Infection." Chest 120, no. 1 (July 2001): 177–84. http://dx.doi.org/10.1378/chest.120.1.177.

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Lin, Jiejian, and Richard J. Hamill. "Coccidioidomycosis pulmonary infection." Current Infectious Disease Reports 3, no. 3 (June 2001): 274–78. http://dx.doi.org/10.1007/s11908-001-0030-7.

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Liu, Allen T., Lil J. Miedzinski, Eric Vallieres, David C. Rayner, and Dale C. Lien. "Pulmonary Alveolar Proteinosis in an AIDS Patient without Concurrent Pulmonary Infection." Canadian Respiratory Journal 2, no. 3 (1995): 183–86. http://dx.doi.org/10.1155/1995/958415.

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Patients with acquired immunodeficiency syndrome (AIDS) are potentially at increased risk for developing secondary pulmonary alveolar proteinosis because of underlying immunosuppression and frequent opportunistic lung infections. This condition. however, has been diagnosed uncommonly in these patients and, with the exception of one previously reported case. only in the presence of concurrent pulmonary infection. The case of a 35-year-old male with AIDS who was found on open lung biopsy to have pulmonary alveolar proteinosis without evidence of associated lung infection is presented.

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Dissertations / Theses on the topic "Pulmonary infection"

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Moriarty, T. F. M. "Pulmonary infection in cystic fibrosis : microbiology and antibiotic treatment at the site of infection." Thesis, Queen's University Belfast, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432522.

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Field, Tyler Robert. "Anaerobic pulmonary infection in cystic fibrosis : detection, characterisation and treatment." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479420.

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McManus, T. E. "Viral infection and associated inflammation in chronic obstructive pulmonary disease." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426766.

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Keir, Pamela Alexandra. "Early responses in the pulmonary phase of Nippostrongylus brasiliensis infection." Thesis, Edinburgh Napier University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270301.

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Wilkinson, Thomas Michael Alan. "The role of airway infection in chronic obstructive pulmonary disease." Thesis, Queen Mary, University of London, 2006. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1897.

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This. thesis examines the role of respiratory bacterial and viral infection in the natural history of Chronic Obstructive Pulmonary Disease. The rationale for this study is basedu pon previous data demonstratingt hat airway bacterial colonisationi s common in stable COPD and that bacterial and viral pathogens are commonly detected at exacerbations. The methodsu sed have involved the careful characterisationa nd clinical follow up of a cohort of patients with moderate to severe COPD in the stable state and at exacerbation. Sampling of airway and systemic compartments enabled the detection of respiratory pathogens and quantification of inflammation. Comparisons between clinical indices and evidence of infection were performed to determine the relationships between bacterial and viral infections and disease outcomes including lung function decline and exacerbation severity. The findings confirmed that lower airway bacterial colonisation is common in stable COPD and is associated with airway inflammation. They demonstrated for the first time a relationship between the degree of bacterial carriage and the rate of disease progression. This study has also described novel evidence for persistence of respiratorys yncytial virus in the lower airway and associationsw ith inflammation and lung function decline and impaired anti-viral immune responsesT. he combined role of human rhinoviral and bacterial infection at exacerbation has been studied and factors influencing responsesto exacerbationt herapy determinedw ith the importance of early initiation of treatment identified. The findings in this thesis indicate that both viral and bacterial pathogens may play an important role in the natural history of COPD and are therefore targets for potentially novel interventions. This work suggests that viral and bacterial infections and their interactions play an important role in modulating airway inflammation in stable disease and at exacerbation thus impacting on both disease progression and exacerbation severity. This work has provided a rationale for future investigation into the mechanisms underlying susceptibility to infection in this important disease.

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Robert, Camille. "Evaluation du potentiel thérapeutique d'un mannodendrimère anti-inflammatoire dans un modèle murin d'infection par Francisella tularensis." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30299/document.

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Francisella tularensis est une bactérie intracellulaire à Gram négatif et l'un des agents les plus infectieux connu à l'heure actuelle, en particulier par voie respiratoire. L'inhalation d'une dizaine de bactéries suffit à provoquer une maladie mortelle : la tularémie pulmonaire. Sa facilité de dissémination par aérosols, ainsi que le caractère létal de cette pathologie, ont contribué à considérer F. tularensis comme une arme biologique potentielle. La tularémie pulmonaire est une infection aigue qui s'accompagne d'une réponse immunitaire inadaptée. F. tularensis infecte en premier lieu les cellules phagocytaires, notamment les macrophages. Alors que ces derniers sont des acteurs majeurs de la défense contre les agents infectieux, de nombreux mécanismes d'échappement permettent à F. tularensis d'éviter ou de résister aux réponses de l'hôte et ainsi de se multiplier et de disséminer dans l'organisme. Ainsi, après un retard initial dans la mise en place de la réponse immunitaire, la présence d'un grand nombre de bactéries et de signaux de danger libérés par les cellules infectées, conduisent au déclenchement d'une réponse inflammatoire excessive. Celle-ci se caractérise par une tempête cytokinique provoquant un recrutement massif de cellules immunitaires, en particulier de neutrophiles, dans les tissus infectés. Les dommages tissulaires associés à cette réponse inflammatoire sont en grande partie responsable de la mortalité associée aux infections pulmonaires par F. tularensis. La tularémie est actuellement traitée par antibiothérapie. Malheureusement, l'absence de symptômes spécifiques de cette maladie rend le diagnostic difficile et, par conséquent, retarde la prescription du traitement adapté. Or, l'efficacité des antibiotiques est considérablement réduite par cette administration tardive. De nouvelles stratégies thérapeutiques sont donc nécessaires pour remplacer ou compléter l'antibiothérapie. Dans ce contexte, nous avons cherché à déterminer si la modulation de la réponse inflammatoire excessive induite par F. tularensis pouvait être bénéfique pour l'hôte infecté et ainsi être utilisée comme thérapie accessoire. L'objectif de mon travail de thèse était d'évaluer les propriétés anti-inflammatoires et le potentiel bénéfice thérapeutique du mannodendrimère 3T (M3T), un composé synthétisé par l'équipe de J. Nigou, dans un modèle murin d'infection pulmonaire par F. tularensis. Le M3T, conçu pour mimer les propriétés anti-inflammatoires d'un glycolipide de la paroi de Mycobacterium tuberculosis, a précédemment montré un effet inhibiteur sur la production de cytokines pro-inflammatoires et le recrutement de neutrophiles dans un modèle murin d'inflammation pulmonaire aigue induite par le LPS. La souche F. novicida, provoquant chez la souris une pathologie similaire à une infection pulmonaire par F. tularensis, a été utilisée comme souche de substitution dans ces travaux. In vitro, nous avons montré que le M3T inhibe la production de cytokines pro-inflammatoires induite par F. novicida dans des macrophages et cellules dendritiques humaines. D'un point de vue mécanistique, l'ensemble des données suggère que le M3T inhibe la réponse inflammatoire induite par F. novicida via le récepteur TLR2, en activant une voie de signalisation dépendante du récepteur DC-SIGN. In vivo, le M3T a été administré par injection intraveineuse 6 h post-infection, puis quotidiennement pendant 3 jours, en combinaison avec un traitement antibiotique sous-optimal
Francisella tularensis is an intracellular Gram negative bacterium and the causative agent of tularemia. It is one of the most infectious agents known to date. Infection by the respiratory route leads to the deadly pulmonary form of tularemia. For these reasons, F. tularensis has been considered for years as a potential biological weapon. Pulmonary tularemia is characterized by an acute infection and a defect in immune responses. Particularly, the innate immune system plays a central role in F. tularensis infection and pathology. Macrophages, key cells of the innate immune system, are the main target for F. tularensis. This bacterium has evolved many strategies to escape host defenses that allow it to replicate within the cells and then disseminate into the whole organism. At this systemic stage, bacteria, along with alarm signals from infected cells, are recognized by innate immune receptors, triggering an inappropriate inflammatory response. The latter is characterized by a cytokine storm leading to a massive recruitment of immune cells, particularly neutrophils, in infected tissue. Tissue damages caused by this inflammation are a major cause of mortality associated with F. tularensis infections. Today, the treatment of tularemia is based on antibiotherapy. However, no specific symptoms can be assigned to pulmonary tularemia making its diagnosis difficult. This delays the administration of an appropriate antibiotiotherapy whose efficacy is therefore decreased. Thus, new therapeutic strategies are needed to replace or complement antibiotics. In this context, we investigated whether reducing the excessive inflammation induced by F. tularensis could be beneficial for the host and be considered as an adjunctive host- directed therapy. The aim of my work was to evaluate the anti-inflammatory properties and the therapeutic potential of mannodendrimer 3T (M3T), a synthetic coumpond designed in the team, in a mouse model of pulmonary infection by F. tularensis. M3T was previously designed to mimic the anti-inflammatory traits of a specific glycolipid from Mycobacterium tuberculosis. It was previously shown to inhibit the production of pro-inflammatory cytokines and neutrophils recruitment in a mouse model of LPS-induced pulmonary inflammation. Here, we used F. novicida as a surrogate for F. tularensis since it induces an identical inflammatory pathology. In vitro, M3T was found to inhibit the production of pro-inflammatory cytokines in human macrophages and dendritic cells infected by F. novicida. M3T modulates inflammatory response triggered by F. novicida via TLR2 most likely by the activation of a DC-SIGN-dependant pathway. In vivo, M3T was administered 6 h post-infection and then, daily for 3 days, by intraveinous injection and combined with a suboptimal antibiotic. This combination increases the survival rate of mice infected with F. novicida as compared to mice treated with antibiotic alone. M3T treatment has no impact on bacterial burden but seems to reduce tissue damages as observed by histological analyses of lungs, liver and spleen of infected mice. Altogether, our data demonstrate that M3T administration provides a therapeutic benefit in a mouse model of pulmonary infection by F. novicida. On a more general perspective our results suggest that targeting inflammation can be considered as an adjunctive treatment in acute pulmonary infections

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Nixon, Lisette Sheena. "Neutrophil function in patients with cystic fibrosis and chronic pulmonary infection." Thesis, Cardiff University, 2003. http://orca.cf.ac.uk/54082/.

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The thesis investigates reasons for a failure of neutrophils to clear pulmonary bacterial infection in cystic fibrosis (CF). Patients with CF experience bacterial colonization of the lungs associated with progressive lung injury and poor prognosis. Neutrophil responsiveness in vitro was determined in patients with CF at different clinical states, and compared to healthy subjects. Neutrophils from the patients were able to phagocytose and kill Pseudomonas aeruginosa effectively, but the presence of sputum sol reduced intracellular killing. Superoxide generation and elastase release in response to fMLP were shown to be reduced in neutrophils from patients with an exacerbation of respiratory symptoms. This was not observed when the cells were stimulated with PMA, which acts intracellularly, rather than through cell surface receptors. There was no difference in the down-regulation of cell surface L-selectin and up-regulation of CD11b in response to fMLP suggesting no alteration in number or function of the fMLP receptors. There was increased adherence to nylon columns by neutrophils from patients with CF. Infection resulted in a greater proportion of band neutrophils, and this correlated with the reduced superoxide generation and elastase release, although it was not possible to separate the band forms to prove this conclusively. Alterations in circulating lipid and fatty acid composition inpatients could potentially affect neutrophil membrane composition and fluidity and therefore signal processing or release of products. The reason for the observed reduced responsiveness appears to be multifactorial. Band cell number post receptor signalling and/or receptor desensitization may result in the observed reduced responsiveness, which returns towards healthy subject levels after treatment of an exacerbation, is likely to be the result of chronic infection.

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Tomlinson, G. S. "Inflammatory responses by monocytes and macrophages in pulmonary sarcoidosis and infection." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1344095/.

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Inflammatory responses by macrophages are essential for host defense, but also underpin the pathogenesis of numerous diseases. I adopted a systems biology approach using transcriptional profiling to investigate monocyte and macrophage inflammatory responses in relation to pulmonary sarcoidosis and infection, to compare alveolar macrophages (AM) and monocyte derived macrophages (MDM), and to probe integrated innate and adaptive immunological responses within the tuberculin skin test (TST). In sarcoidosis I established the importance of prostaglandin endoperoxide synthase (PTGS)2 promoter haplotypes in determining susceptibility to disease across two genetically dissimilar ethnic groups, UK Whites and Afro-Caribbeans, but found no functional effect of promoter haplotype on PTGS2 gene expression, in mononuclear phagocytic cells. In contrast to the widely held view that AM have an anti-inflammatory bias, I show that freshly isolated AM have a striking pro-inflammatory profile that may confound the study of their responses to innate immune stimulation. In human immunodeficiency virus (HIV)/Mycobacterium tuberculosis (Mtb) co-infection I show that HIV-1 infection of macrophages leads to augmented inflammatory responses to Mtb, accompanied by enhanced viral replication, due to deficient induction of anti-inflammatory IL10, via attenuation in mitogen activated protein kinase (MAPK) signalling pathways downstream of TLR2 and dectin-1. These changes were not evident in HIV-1/Streptococcus pneumoniae co-infected macrophages, and the specificity of the effect in Mtb co-infection was mirrored by lower IL10 and higher pro-inflammatory IL1β in HIV-infected patients with pulmonary tuberculosis compared with non-tuberculous infection. Finally, I show that the TST is characterised by Th1 polarised and cytotoxic T cell responses. Distinct innate immune and IFNγ-stimulated gene expression signatures under NFκB and STAT1 transcriptional control and highly enriched for chemokines and MHC class II molecules, provide a mechanism for paracrine amplification of inflammatory responses in the TST. Strikingly, identical responses of lower magnitude were also detectable in clinically negative TST subjects.

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Chidgey, Sharon Michelle. "Airway function, inflammation and pulmonary histopathology following parainfluenza-3 virus infection." Thesis, Cardiff University, 2007. http://orca.cf.ac.uk/55663/.

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Human parainfluenza viruses (PIV) 1, 2, 3 and 4 (A and B) cause approximately 39-40% of all acute respiratory infections in infants and children for which there is no effective therapy. Firstly, this thesis was aimed at ascertaining a suitable guinea pig model of PIV-3 infection by determining the most efficient route of virus application. Secondly, to ascertain if a temporal association may be established during the time course of infection (Day 1-40) by measuring the following parameters: body weight, rectal temperature, airway function (sGaw), airways reactivity to inhaled histamine, inflammatory cell infiltration to the lungs measured by bronchoalveolar lavage, wet lung weights, inflammatory markers (nitric oxide and total protein levels), lung histological analysis and recovery of the virus from bronchoalveolar lavage fluid and lung tissue. Further to this, experiments were also designed to determine the impact of the glucocorticoid, dexsamethasone (in vivo and in vitro) and the phosphodiesterase inhibitor, rolipram (in vivo). Lastly, this study ascertained the effect of pre-sensitisation with antigen on the responses of antigen in PIV-3 infected guinea pigs. These investigations have shown guinea pigs to be a suitable model for PIV-3 infection and intranasal inoculation is the most efficient route of virus application. In addition, these investigations also established a temporal association between the time course of PIV-3 infection including airway reactivity to histamine, airway function (sGBW), airways reactivity to inhaled histamine, inflammatory cell infiltration, wet lung weights, inflammatory markers (nitric oxide and total protein levels), pulmonary histopathology and recovery of the virus from bronchoalveolar lavage fluid and lung tissue. Pre-treatment of PIV-3 infected guinea pigs with the glucocorticoid, dexamethasone and the phosphodiesterase inhibitor, rolipram (in vitro) ameliorated the inflammatory response and airway hyperreactivity. Unlike rolipram, dexamethasone also reduced viral titre (in vivo and in vitro), supporting a role for the anti-viral effects of dexamethasone. The anti-inflammatory effects of dexamethasone are well known and it has been speculated by other authors which maybe caused by decreased viral receptors on the epithelial cells via inhibition of intracellular adhesion molecule-1 expression. Finally, in this study PTV-3 infection, enhanced the effect of pre-allergen sensitisation, which may arise from increased permeability of the airway mucosa to allergens, due to damage of the respiratory epithelium and increased recruitment of dendritic cells. In summary, this thesis has established a clearly defined efficacy of dexamethasone use in the treatment of PIV-3 infection.

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Tsuyuguchi, Kazunari. "Effect of estrogen on Mycobacterium avium complex pulmonary infection in mice." Kyoto University, 2001. http://hdl.handle.net/2433/150522.

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Books on the topic "Pulmonary infection"

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Pokorski, Mieczyslaw, ed. Pulmonary Infection. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17458-7.

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Pokorski, Mieczyslaw, ed. Pulmonary Infection and Inflammation. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44485-7.

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Chadwick, Derek J., and Jamie Goode, eds. Innate Immunity to Pulmonary Infection. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470035399.

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Derek, Chadwick, Goode Jamie, and Novartis Foundation, eds. Innate immunity to pulmonary infection. Chichester: John Wiley, 2006.

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Symposium on Innate Immunity to Pulmonary Infection (2005 University of Cape Town, Medical School). Innate Immunity to Pulmonary Infection. New York: John Wiley & Sons, Ltd., 2007.

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Pulmonary complications of HIV infection. Philadelphia: W.B. Saunders, 1996.

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A, White Dorothy, and Stover Diane E, eds. Pulmonary complications of HIV infection. Philadelphia: Saunders, 1996.

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Agust, Carlos, and Antoni Torres, eds. Pulmonary Infection in the Immunocompromised Patient. Chichester, UK: John Wiley & Sons, Ltd, 2009. http://dx.doi.org/10.1002/9780470714171.

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Carlos, Agustí, and Torres Martí A, eds. Pulmonary infection in the immuno-compromised patient: Strategies for management. Chichester, West Sussex, UK: John Wiley & Sons, 2009.

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Organization), Stop TB Partnership (World Health. A revised framework to address TB-HIV co-infection in the Western Pacific Region. Geneva, Switzerland: World Health Organization, 2008.

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Book chapters on the topic "Pulmonary infection"

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Sobonya, Richard E. "Pneumocystis Infection." In Pulmonary Pathology, 301–13. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4757-3932-9_11.

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Sobonya, Richard E. "Pneumocystis Infection." In Pulmonary Pathology, 475–89. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4757-3935-0_14.

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Kim, Tae Jung, Kyung Hee Lee, Yeon Hyeon Choe, and Kyung Soo Lee. "Pulmonary Infection (Pneumonia)." In Emergency Chest Radiology, 119–41. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-4396-2_8.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Pulmonary Chlamydia Infection." In Encyclopedia of Molecular Mechanisms of Disease, 1762–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_3225.

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Franquet, Tomás, and Johnathan H. Chung. "Imaging of Pulmonary Infection." In IDKD Springer Series, 65–77. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11149-6_7.

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Abbasi, Adeel, Francis DeRoos, José Artur Paiva, J. M. Pereira, Brian G. Harbrecht, Donald P. Levine, Patricia D. Brown, et al. "Clinical Pulmonary Infection Score (CPIS)." In Encyclopedia of Intensive Care Medicine, 567. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3062.

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Gordon, Siamon. "Chair's Introduction." In Innate Immunity to Pulmonary Infection, 1–3. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035399.ch1.

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Brown, Gordon D. "Macrophage Receptors and Innate Immunity: Insights from Dectin-1." In Innate Immunity to Pulmonary Infection, 114–26. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035399.ch10.

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Ryffel, Bernhard, Muazzam Jacobs, Shreemanta Parida, Tania Botha, Dieudonnée Togbe, and Valerie Quesniaux. "Toll-Like Receptors and Control of Mycobacterial Infection in Mice." In Innate Immunity to Pulmonary Infection, 127–41. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035399.ch11.

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Williams, T. J., and C. L. Weller. "Population of Lungs by Mast Cells." In Innate Immunity to Pulmonary Infection, 142–54. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470035399.ch12.

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Conference papers on the topic "Pulmonary infection"

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Andrabi, A., M. Seth, P. Sundar, and K. Aslam. "Pulmonary Nocardiosis Underdiagnosed Respiratory Opportunistic Infection." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7336.

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Burattin, Marco, Jayanta Mukherjee, and Anton Borg. "Haemophagocytic Syndrome Secondary To Pulmonary Infection." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4737.

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Babalık, Aylin, Tülin Kuyucu, Fatma Kutluhan, Hamide Gül Işık, Emine Nur Koç, Gül Erdal Dönmez, Emine Nilgün Ordu, Ahmet Balıkçı, and Orhan Kaya Köksalan. "Pulmonary non-tuberculous mycobacterial infection: 889 cases." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2159.

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Flight, WG, NE Hough, and SJ Chapman. "M6 Outcomes of pulmonary mycobacterium abscessus infection." In British Thoracic Society Winter Meeting 2019, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 4 to 6 December 2019, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2019. http://dx.doi.org/10.1136/thorax-2019-btsabstracts2019.414.

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Henderson, Jason, Sandy Genes, Zachery Young, and Peter Kaplan. "Mycobacterium Riyadhense Causing Pulmonary Infection In Human." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6113.

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Marmor, M., F. K. Hazard, and S. J. Ruoss. "Atypical Presentation of Mycobacterium Abscessus Pulmonary Infection." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2023.

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Jupelli, Madhulika, Shamimunisa Mustafa, Barbara Henson, Steven Seidner, Neal Guentzel, Dale Selby, Guangming Zhong, Ashlesh Murthy, and Bernard Arulanandam. "Pulmonary Chlamydial Infection As Neonates Contributes To Pulmonary Dysfunction As Adults." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6788.

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Rodriguez, W., A. Candelario, Y. Otero-Dominguez, and J. Torres-Palacios. "A Not so Typical Atypical Mycobacterial Infection: Pulmonary Mycobacterial Infection with Mycobacterium Marseillense." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2030.

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Wydro, L., and C. Shapiro. "A Case of Pulmonary Actinomycosis with Endobronchial Involvement, a Rare Pulmonary Infection." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7328.

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Salman, Z., S. Beshay, and Z. Safdar. "Infection-Related Hospitalization in Pulmonary Arterial Hypertension Patients." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5080.

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Reports on the topic "Pulmonary infection"

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Wang, Mingxin, Qian Gao, Chunjiao Zhou, and Zhijian Tan. Risk factors of postoperative pulmonary infection in patients with gastric cancer：A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2021. http://dx.doi.org/10.37766/inplasy2021.5.0057.

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lin, kai, and meng ren. Risk factors for postoperative pulmonary infection in patients with esophageal cancer：A systematic review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0139.

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Feng, XinYu, and YuLan Zeng. Effects of Pseudomonas aeruginosa infection on the prognosis of patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0092.

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Wang, Xiao, Hong Shen, Yujie Liang, Yixin Wang, Meiqi Zhang, and Hongtao Ma. Effects of physical activity interventions for post-COVID-19 patients: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0036.

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Review question / Objective: Coronavirus disease 2019 (COVID-19) is a novel infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which has caused a huge impact in many countries and has attracted great attention from countries around the world. However, since the outbreak of the COVID-19 pandemic, most attention has focused on containing transmission and addressing the surge of critically ill patients in acute care settings. As we enter the second phase of the pandemic, emphasis must evolve to post care of COVID-19 survivors. A variety of persistent symptoms, such as severe fatigue, shortness of breath, and attention disorder have been reported at several months after the onset of the infection. We urgently need to identify safe and effective COVID-19 rehabilitative strategies. Overwhelming evidence exists that physical activity produces short-, middle- and long-term health benefits that prevent, delay, mitigate and even reverse a large number of metabolic, pulmonary and cardiovascular diseases. The purpose of this study was to evaluate the effects of physical activity interventions for rehabilitation of post-covid-19 patient and provide a reliable method and credible evidence to improve the prognosis of post-COVID-19 patients via systematic review and meta-analysis.

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Tang, Jiqin, Gong Zhang, Jinxiao Xing, Ying Yu, and Tao Han. Network Meta-analysis of Heat-clearing and Detoxifying Oral Liquid of Chinese Medicines in Treatment of Children’s Hand-foot-mouth Disease：a protocol for systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0032.

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Review question / Objective: The type of study was clinical randomized controlled trial (RCT). The object of study is the patients with HFMD. There is no limit to gender and race. In the case of clear diagnosis standard, curative effect judgment standard and consistent baseline treatment, the experimental group was treated with pure oral liquid of traditional Chinese medicine(A: Fuganlin oral liquid, B: huangzhihua oral liquid, C: Lanqin oral liquid, D: antiviral oral liquid, E: Huangqin oral liquid, F: Pudilan oral liquid, G: Shuanghuanglian oral liquid.)and the control group was treated with ribavirin or any oral liquid of traditional Chinese medicine. The data were extracted by two researchers independently, cross checked and reviewed according to the pre-determined tables. The data extraction content is (1) Basic information (including the first author, published journal and year, research topic). (2) Relevant information (including number of cases, total number of cases, gender, age, intervention measures, course of treatment of the experimental group and the control group in the literature). (3) Design type and quality evaluation information of the included literature. (4) Outcome measures (effective rate, healing time of oral ulcer, regression time of hand and foot rash, regression time of fever, adverse reactions.). The seven traditional Chinese medicine oral liquids are comparable in clinical practice, but their actual clinical efficacy is lack of evidence-based basis. Therefore, the purpose of this study is to use the network meta-analysis method to integrate the clinical relevant evidence of direct and indirect comparative relationship, to make quantitative comprehensive statistical analysis and sequencing of different oral liquid of traditional Chinese medicine with the same evidence body for the treatment of the disease, and then to explore the advantages and disadvantages of the efficacy and safety of different oral liquid of traditional Chinese medicine to get the best treatment plan, so as to provide reference value and evidence-based medicine evidence for clinical optimization of drug selection. Condition being studied: Hand foot mouth disease (HFMD) is a common infectious disease in pediatrics caused by a variety of enteroviruses. Its clinical manifestations are mainly characterized by persistent fever, hand foot rash, oral herpes, ulcers, etc. Because it is often found in preschool children, its immune system development is not perfect, so it is very vulnerable to infection by pathogens and epidemic diseases, resulting in rapid progress of the disease. A few patients will also have neurogenic pulmonary edema Meningitis, myocarditis and other serious complications even lead to death, so effectively improve the cure rate, shorten the course of disease, prevent the deterioration of the disease as the focus of the study. In recent years, traditional Chinese medicine has played an important role in the research of antiviral treatment. Many clinical practices have confirmed that oral liquid of traditional Chinese medicine can effectively play the role of antiviral and improve the body's immunity.

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Saldanha, Ian J., Wangnan Cao, Justin M. Broyles, Gaelen P. Adam, Monika Reddy Bhuma, Shivani Mehta, Laura S. Dominici, Andrea L. Pusic, and Ethan M. Balk. Breast Reconstruction After Mastectomy: A Systematic Review and Meta-Analysis. Agency for Healthcare Research and Quality (AHRQ), July 2021. http://dx.doi.org/10.23970/ahrqepccer245.

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Objectives. This systematic review evaluates breast reconstruction options for women after mastectomy for breast cancer (or breast cancer prophylaxis). We addressed six Key Questions (KQs): (1) implant-based reconstruction (IBR) versus autologous reconstruction (AR), (2) timing of IBR and AR in relation to chemotherapy and radiation therapy, (3) comparisons of implant materials, (4) comparisons of anatomic planes for IBR, (5) use versus nonuse of human acellular dermal matrices (ADMs) during IBR, and (6) comparisons of AR flap types. Data sources and review methods. We searched Medline®, Embase®, Cochrane CENTRAL, CINAHL®, and ClinicalTrials.gov from inception to March 23, 2021, to identify comparative and single group studies. We extracted study data into the Systematic Review Data Repository Plus (SRDR+). We assessed the risk of bias and evaluated the strength of evidence (SoE) using standard methods. The protocol was registered in PROSPERO (registration number CRD42020193183). Results. We found 8 randomized controlled trials, 83 nonrandomized comparative studies, and 69 single group studies. Risk of bias was moderate to high for most studies. KQ1: Compared with IBR, AR is probably associated with clinically better patient satisfaction with breasts and sexual well-being but comparable general quality of life and psychosocial well-being (moderate SoE, all outcomes). AR probably poses a greater risk of deep vein thrombosis or pulmonary embolism (moderate SoE), but IBR probably poses a greater risk of reconstructive failure in the long term (1.5 to 4 years) (moderate SoE) and may pose a greater risk of breast seroma (low SoE). KQ 2: Conducting IBR either before or after radiation therapy may result in comparable physical well-being, psychosocial well-being, sexual well-being, and patient satisfaction with breasts (all low SoE), and probably results in comparable risks of implant failure/loss or need for explant surgery (moderate SoE). We found no evidence addressing timing of IBR or AR in relation to chemotherapy or timing of AR in relation to radiation therapy. KQ 3: Silicone and saline implants may result in clinically comparable patient satisfaction with breasts (low SoE). There is insufficient evidence regarding double lumen implants. KQ 4: Whether the implant is placed in the prepectoral or total submuscular plane may not be associated with risk of infections that are not explicitly implant related (low SoE). There is insufficient evidence addressing the comparisons between prepectoral and partial submuscular and between partial and total submuscular planes. KQ 5: The evidence is inconsistent regarding whether human ADM use during IBR impacts physical well-being, psychosocial well-being, or satisfaction with breasts. However, ADM use probably increases the risk of implant failure/loss or need for explant surgery (moderate SoE) and may increase the risk of infections not explicitly implant related (low SoE). Whether or not ADM is used probably is associated with comparable risks of seroma and unplanned repeat surgeries for revision (moderate SoE for both), and possibly necrosis (low SoE). KQ 6: AR with either transverse rectus abdominis (TRAM) or deep inferior epigastric perforator (DIEP) flaps may result in comparable patient satisfaction with breasts (low SoE), but TRAM flaps probably increase the risk of harms to the area of flap harvest (moderate SoE). AR with either DIEP or latissimus dorsi flaps may result in comparable patient satisfaction with breasts (low SoE), but there is insufficient evidence regarding thromboembolic events and no evidence regarding other surgical complications. Conclusion. Evidence regarding surgical breast reconstruction options is largely insufficient or of only low or moderate SoE. New high-quality research is needed, especially for timing of IBR and AR in relation to chemotherapy and radiation therapy, for comparisons of implant materials, and for comparisons of anatomic planes of implant placement.

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