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Tesis sobre el tema "Lungs Inflammation"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 27 de enero de 2023

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1

McLennan, Geoffrey. "Oxygen toxicity and radiation injury to the pulmonary system." Title page, index and forward only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phm164.pdf.

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Bibliography: leaves 168-184. The work in this study encompasses oxygen free radical related inflammation in the peripheral lung and in lung cells. Animal and human studies have been used. Methods include cell culture with function studies, protein chemistry, animal and human physiology, and cell and lung structure through histopathology, and various forms of electron microscopy. The work resulting from this thesis has formed an important basis for understanding acute and chronic lung injury.

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2

Corsino, Betsy Ann 1962. "THE PULMONARY RESPONSE INDUCED BY GLASS FIBERS (INFLAMMATION, SILICOSIS, MURINE MODEL)." Thesis, The University of Arizona, 1986. http://hdl.handle.net/10150/291468.

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3

Dokka, Sujatha. "IL-10 gene therapy for the treatment of pulmonary inflammation." Morgantown, W. Va. : [West Virginia University Libraries], 2000. http://etd.wvu.edu/templates/showETD.cfm?recnum=1421.

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Thesis (Ph. D.)--West Virginia University, 2000.<br>Title from document title page. Document formatted into pages; contains ix, 132 p. : ill. (some col.) Vita. Includes abstract. Includes bibliographical references.

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4

Finlay, Alison. "Kinetics of pulmonary eosinophilia in a mouse model." Thesis, University of York, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245971.

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5

Karandashova, Sophia. "The Role of Ceramide in Neutrophil Elastase Induced Inflammation in the Lungs." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5468.

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Alterations to sphingolipid metabolism are associated with increased pulmonary inflammation, but the impact of inflammatory mediators, such as neutrophil elastase (NE), on airway sphingolipid homeostasis remains unknown. NE is a protease associated CF lung disease progression, and can be found in up to micromolar concentrations in patient airways. While sphingolipids have been investigated in the context of CF, the focus has been on loss of cystic fibrosis transmembrane conductance regulator (CFTR) function. Here, we present a novel observation: oropharyngeal aspiration of NE increases airway

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6

McDaniel, Dylan K. "Characterization of Biomedical and Incidental Nanoparticles in the Lungs and Their Effects on Health." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/86128.

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Nanomaterials are defined as any material with at least one external dimension less than 100 nm. Recently, nanomaterials have become more common in medicine, technology, and engineering. One reason for their increased interest is due to nanomaterials having unique properties that allow them to interact effectively with biological systems. In terms of drug delivery, the lungs are a highly desirable site to administer therapeutic nanoparticles. Indeed, inflammatory diseases such as asthma and emphysema could potentially benefit from nanoparticle-mediated delivery. However, the lungs are also in

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7

Zheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.

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8

Lewis, Joshua B. "Alterations in Tight Junctional Proteins and Their Effects on Pulmonary Inflammation." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6308.

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The lungs represent one of the earliest interfaces for pathogens and noxious stimuli to interact with the body. As such, careful maintenance of the permeability barrier is vital in providing homeostasis within the lung. Essential to maintaining this barrier is the tight junction, which primarily acts as a paracellular seal and regulator of ionic transport, but also contributes to establishing cell polarity, cell-to-cell integrity, and regulating cell proliferation and differentiation. The loss of these tight junctions has been documented to result in alterations in inflammation, and ultimat

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9

Lau, Kwok-wai, and 劉國威. "The involvement of serotoninergic system in cigarette smoke-induced oxidative stress and inflammation: relevantto chronic obstructive pulmonary disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47869616.

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Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD) with chronic airway inflammation as a key feature. Currently, no effective treatment can reduce the protracted inflammation in the lung of COPD. Further research on the inflammatory mechanisms would therefore be important in determining new potential therapeutic targets in COPD. Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter that plays an important role in pulmonary functions and inflammatory responses. The serotoninergic system including serotonin trans

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10

McNamara, Tracy Renee. "Chlamydia pneumoniae and airways inflammation : an investigation of the host cell-pathogen relationship /." Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phm4791.pdf.

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11

Minucci, Sarah B. "Mathematical Models of the Inflammatory Response in the Lungs." VCU Scholars Compass, 2017. https://scholarscompass.vcu.edu/etd/5191.

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Inflammation in the lungs can occur for many reasons, from bacterial infections to stretch by mechanical ventilation. In this work we compare and contrast various mathematical models for lung injuries in the categories of acute infection, latent versus active infection, and particulate inhalation. We focus on systems of ordinary differential equations (ODEs), agent-based models (ABMs), and Boolean networks. Each type of model provides different insight into the immune response to damage in the lungs. This knowledge includes a better understanding of the complex dynamics of immune cells, protei

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12

Henry, Clémence. "Caractérisation du rôle du canal calcique TRPV4 dans la réponse inflammatoire pulmonaire : implication dans la mucoviscidose." Thesis, Tours, 2014. http://www.theses.fr/2014TOUR4037.

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La mucoviscidose est une maladie génétique dont l’atteinte respiratoire est responsable de 90 % de la morbidité et de la mortalité et est caractérisée par une infection chronique et une inflammation persistante. Cette inflammation non contrôlée participe de manière importante à la dégradation du tissu pulmonaire. Malgré les progrès récents, les thérapies actuelles ne permettent pas un traitement efficace de l’atteinte respiratoire. Il est donc indispensable d’identifier de nouveaux mécanismes moléculaires et cellulaires impliqués dans l’inflammation pulmonaire. Dans ce but, nous nous sommes in

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13

Carroll, Mark. "A stereological study assessing the validity of using endobronchial biopsies to assess mast cell density in the central and peripheral bronchial tree." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2009.0005.

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[Tuncated abstract] There has been longstanding concern over whether endobronchial biopsies adequately represent inflammation throughout the bronchial tree in diseases such as asthma, despite the endobronchial biopsy technique having been used frequently to assess airway inflammation in research settings. There has also been ongoing debate about whether endobronchial biopsies should be assessed by new, unbiased, three-dimensional (3D) stereological techniques instead of traditional, two-dimensional (2D) non-stereological techniques. Therefore, the aims of this study were: (i) to investigate wh

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14

Ruiz, Karina Fernandes. "Efeito do DMTI-II, um inibidor de Kunitz isolado das sementes de Dimorphandra molli na resposta inflamatória pulmonar alérgica em ratos." [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308917.

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Orientador: Edson Antunes<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Medicas<br>Made available in DSpace on 2018-08-16T20:02:44Z (GMT). No. of bitstreams: 1 Ruiz_KarinaFernandes_M.pdf: 791032 bytes, checksum: 0730a107f795b476b046410752e6a5e3 (MD5) Previous issue date: 2010<br>Resumo: DMTI-II é um inibidor de serinoproteinase do tipo Kunitz, isolado a partir das sementes de Dimorphandra mollis, uma árvore da família Leguminosae-Mimosoidea, com ampla distribuição nas regiões do cerrado brasileiro e popularmente conhecida por causar toxicidade em gados

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15

Vanderstocken, Gilles. "Caractérisation du rôle des nucléotides extracellulaires et du récepteur purinergique P2Y2 dans la physiopathologie des maladies pulmonaires inflammatoires." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209591.

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Amongst respiratory diseases, inflammatory lung diseases constitute a major part of public <p>health problem. As a consequence, investigating the immune mechanisms that contribute to <p>the pathogenesis of these diseases is essential to identify candidate targets for the <p>development of new therapeutic drugs. Furthermore, over the past 20 years, the growing awareness <p>that purinergic signalling events shape the immune and inflammatory responses to infection and <p>allergic reactions warranted the development of animal models to assess their importance in vivo in <p>acute lung injury and ch

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16

Cooper, Racheal L. "An Applied Mathematics Approach to Modeling Inflammation: Hematopoietic Bone Marrow Stem Cells, Systemic Estrogen and Wound Healing and Gas Exchange in the Lungs and Body." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/4312.

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Mathematical models apply to a multitude physiological processes and are used to make predictions and analyze outcomes of these processes. Specifically, in the medical field, a mathematical model uses a set of initial conditions that represents a physiological state as input and a set of parameter values are used to describe the interaction between variables being modeled. These models are used to analyze possible outcomes, and assist physicians in choosing the most appropriate treatment options for a particular situation. We aim to use mathematical modeling to analyze the dynamics of processe

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17

Marwick, John Alexander. "The impact of cigarette smoke on cell survival and inflammation in rat lungs : the role of oxidative stress and VEGF/KDR signalling and its implications in COPD." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/24912.

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A decrease in both VEGF and KDR was observed in rat lungs exposed to cigarette smoke as well as disruption to the other components of their signalling complex, neurophilin-1 and glycpican-1. Impaired survival signalling in rat lungs exposed to cigarette smoke was also demonstrated. These changes were mirrored in both smokers and COPD lungs, indicating that these changes may play a role in cigarette smoke induced COPD. Cigarette smoke-triggered inflammation in COPD may be maintained by a mechanism involving enhanced pro-inflammatory gene transcription. The balance between histone acetylation an

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18

Fallata, Ghaith Mohammed. "Association of gut luminal metabolites and allergic responses." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1515185113264117.

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19

Saleh, Yara. "Etude de la pathogénicité pulmonaire des polluants atmosphériques nanoparticulaires." Thesis, Lille 2, 2019. http://www.theses.fr/2019LIL2S014.

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Introduction : Des études épidémiologiques montrent que les polluants atmosphériques particulaires augmentent le risque de morbidité et de mortalité liées à des maladies respiratoires. La toxicité des particules dépend de leur composition chimique, leur conférant des propriétés mutagènes et/ou cancérogènes, mais également de leur granulométrie qui va conditionner leur pénétration et rétention dans les voies respiratoires.Les particules fines (PF<2,5μm) et surtout les particules ultrafines (PUF<0,1μm) peuvent ainsi atteindre les voies aériennes les plus profondes où leur épuration s’effec

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20

Haegens, Astrid. "Role of Myeloperoxidase in lung inflammation." Maastricht : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=11652.

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21

Nelson, Kevin Joseph. "MICRORNA REGULATION OF VENTILATOR INDUCED LUNG INJURY AND PRESSURE-INDUCED LUNG INFLAMMATION." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1462276463.

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22

Shoemark, Amelia. "Non invasive measurement of lung inflammation in bronchiectasis." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509803.

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23

Lai, Cheryl Chuk-Ke. "Therapeutic manipulation of inflammation in exacerbated lung disease." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/61486.

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It is well known that existing and prior inflammatory events in the lung can adversely affect subsequent inflammatory events even though the inciting antigen might be different. For example, viral infections can enhance secondary bacterial infections and also the symptoms of asthma causing increased morbidity and mortality. Understanding changes in the lung micro-environment that lead to altered lung responsiveness is important given the increasing incidence in allergic diseases and the emergence of pandemic influenza strains. Elucidating the molecular mechanisms of these prolonged alterations

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24

Farghaly, Hanan. "Pharmacological targets for gene therapy in lung inflammation." Thesis, University of Bath, 2008. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500756.

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Interleukin-13 (IL-13) has been implicated as a critical inducer of a number of features of allergy and asthma including the induction of nonspecific airway hyperresponsiveness (AHR), eosinophilic inflammatory response, eotaxin production, excess mucus formation, and fibrosis. Determining the mechanism(s) of AHR, a hallmark of asthma, is crucial to our understanding of both the pathogenesis and successful treatment of asthma. After carrying out initial experiments to determine the effect of IL-13-induced AHR on murine and rat tracheal rings, mice tissues were chosen for subsequent experiments

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25

Rodriguez, Ihsan. "Well-being and Inflammation in Interstitial Lung Disease." The Ohio State University, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1619031719578262.

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26

Larsson, Emelie Olivia. "Immune to brain communication in allergic lung inflammation." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/355709/.

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Asthma, a chronic TH2-mediated inflammatory disease of the airways, is the most common form of allergy in the Western world, affecting 300 million people worldwide. Epidemiological studies have shown that asthma is associated with mood disorders, such as anxiety and depression, and numerous experiments have reported that asthma induces functional changes in neuronal fibres of the peripheral nervous system (PNS), which innervate the brain. It is unknown, however, how allergic lung inflammation impacts on the central nervous system (CNS). The ability for peripheral inflammation to impact on the

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27

Blohmke, Christoph Johannes. "Innate immunity and inflammation in cystic fibrosis lung disease." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34559.

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Inflammatory lung disease is the major life-limiting factor of cystic fibrosis (CF) and occurs through a self-sustaining cycle of airway obstruction, infection and inflammation. Although there is no consensus regarding the pathways responsible for the excessive inflammation, reducing lung-damaging pro-inflammatory responses are likely to be beneficial for CF patients. Using CF (IB3-1) and non-CF control (C38) respiratory cells, the host-pathogen interaction between the airway epithelium and the common CF pathogens P. aeruginosa and B. cepacia was investigated. Using purified Toll-like receptor

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28

McClean, K. M. "Nutrition, Inflammation and Lung Function in Middle-Aged Men." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527847.

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29

Clayton, Andrew Alan. "Linking lung inflammation and chloride secretion in cystic fibrosis." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433982.

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30

Phillips, Gary John. "The role of inflammation in hyperoxia-induced lung injury." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295865.

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31

Sundaram, Kruthika. "Expression And Function Of Human IkappaBzeta In Lung Inflammation." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1436224271.

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32

Lyonga, Daphne E. "The regulation of lung homeostasis and influenza-associated inflammation." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/7127.

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Alveolar macrophages are the main cell population in the naïve airway and are held in a state of tight regulation by several suppressive mechanisms. One would expect them to display a regulatory phenotype but here we show that at homeostasis they express markers of alternative activation such as YM1 and mannose receptor (MR) but not resistin-like molecule (RELM)-α. We show also that these markers are differentially regulated during influenza infection on macrophage populations in the lungs and airways. We hypothesised that removing the suppressive effects of IL-10 using an IL-10R blocking anti

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33

Lucas, Christopher David. "Modulation of inflammatory cell apoptosis in infection-associated inflammation." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/17874.

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Neutrophils are a central component of the innate immune system, whose major role is to defend the host against invading microorganisms. As such they are integral players in the process of inflammation, the response of vascular tissues to injury. They are frequently the first immune cells recruited from the systemic circulation into a site of tissue injury or infection where they themselves play a key antimicrobial role. Direct killing of microbes can be accomplished by phagocytosis, degranulation, production of reactive oxygen species (ROS) or the release of DNA and antimicrobial peptides int

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34

Pariollaud, Marie. "Role of REV-ERBα in the regulation of lung inflammation". Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/role-of-reverbalpha-in-the-regulation-of-lung-inflammation(140db598-4670-4605-8c8e-f589fec33e69).html.

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The clock-controlled nuclear receptor REV-ERBα has emerged as a critical regulator of multiple pathways involved in metabolism, development and immunity. Recent evidence has highlighted a major role for the clock in epithelial cells regulating lung inflammation, mediated by control of neutrophil chemokine expression. In this thesis, I examined the role of REV-ERBα in pulmonary immunity, using in-vivo gene targeting and nebulised lipopolysaccharide (LPS), a model for gram-negative bacterial infection, ex-vivo cell biology approaches and in vitro cell models. Initial studies of Rev-Erbα knock-ou

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35

Jonasson, Sofia. "Lung mechanics and airway inflammation in murine models of asthma." Doctoral thesis, Uppsala universitet, Klinisk fysiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-107061.

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Allergic asthma is an inflammatory disease of the airways and is characterized by eosinophilic inflammation and increased airway reactivity. In the studies presented in this thesis, lung mechanics and measurements of airway reactivity were assessed in anaesthetized tracheostomized mice by using an animal ventilator (flexiVent®). A forced oscillation technique makes it possible to measure of both airway and tissue mechanics with a potential to distinguish between central and peripheral airways. The results of the experiments on lung mechanics imply that it is important to understand how altered

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36

Dakin, Carolyn Women's &amp Children's Health Faculty of Medicine UNSW. "Infection and inflammation in children with cystic fibrosis lung disease." Awarded by:University of New South Wales. Women's & Children's Health, 2009. http://handle.unsw.edu.au/1959.4/44624.

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The purpose of this study was to examine the relationships between inflammation, infection and lung function in cystic fibrosis during the evolution of lung disease in childhood and early adolescence. The developmental stages of childhood and the progression of lung disease together affected the methods and techniques used in the study, with the consequence that the work for this thesis fell naturally into two parts. The first part concerned the study of early lung disease in infants and young children who were unable to expectorate or to cooperate with lung function testing. In the second par

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37

Yang, Fu. "Role and regulation of 11β-hydroxysteroid dehydrogenase in lung inflammation". Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4828.

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Glucocorticoids are steroid hormones that have potent anti-inflammatory actions. Endogenous glucocorticoid action is modulated by 11β-hydroxysteroid dehydrogenase (11β-HSD) which catalyses the interconversion of active glucocorticoids (cortisol, corticosterone) and intrinsically inert forms (cortisone, 11-dehydrocorticosterone). There are 2 isozymes; 11β-HSD type 1 regenerates active glucocorticoids in vivo whereas 11β-HSD type 2 inactivates glucocorticoids. Although 11β-HSD1 is highly expressed in the lung, its role there has been little explored. In this study, the expression and localizatio

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38

Koch, Andrea. "Clinical Aspects of Inflammation in Non-small Cell Lung Cancer." Doctoral thesis, Linköpings universitet, Internmedicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-68749.

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Lung cancer is the most common cause of cancer death worldwide, with about 1.2 million deaths every year. In Sweden, about 3500 new cases are diagnosed every year. The majority of patients presents with advanced non-small cell lung cancer (NSCLC) and is treated with palliative intent. Standard treatment in these patients in performance status 0-2 is combination chemotherapy. Radiotherapy may be added for palliative purposes. Median survival time with such treatment is 6-10 months. New treatment strategies are urgently needed. There is growing evidence for a link between cancer and inflammation

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39

Brown, Sarah. "Mechanisms of resolution of inflammation in paediatric neutrophilic lung disease." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/56921.

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Many paediatric airway diseases are characterised by persistent neutrophilic inflammation, which can lead to damage to the airways and lung parenchyma. One possible mechanism for the persistence of neutrophilic inflammation is failure of the normal active resolution of the inflammatory process. There is limited published literature on the role of inflammatory resolution in paediatric inflammatory lung disease. It is possible that targeting inflammatory resolution mechanisms and the ability to “switch off” inflammation may provide therapeutic targets in the future for these diseases. This thesi

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40

Barr, Laura Caroline. "Peripheral blood mononuclear cell depletion for experimental human lung inflammation." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/23705.

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Acute lung injury (ALI) affects a significant proportion of patients requiring critical care and is associated with high morbidity and mortality. Treatment is currently only supportive, with no pharmacological treatment yet shown to definitively improve outcome. There is evidence from murine models of ALI that monocytes play a key role in the development of the neutrophilic lung infiltration characteristic of ALI. Depletion of blood monocytes in mice given intra-tracheal lipopolysaccharide (LPS) significantly reduces pulmonary neutrophil influx, systemic neutrophilia and other markers of lung

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41

MacGregor, Gordon. "Non-invasive markers of inflammation in cystic fibrosis lung disease." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4834.

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Cystic fibrosis (CF) lung disease is characterised by early airways infection and inflammation, chronic suppuration, frequent infective exacerbations and an increased influx of acute, and chronic inflammatory cells. The inflammatory process involves activation of many cell types including neutrophils, macrophages and epithelial cells, and leads ultimately to the development of progressive respiratory failure and death. Accurate assessment of the inflammatory process is a crucial part of disease monitoring and should allow appropriate evaluation of therapeutic interventions so as to maximize co

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42

Singh, Ravinder. "The role of Death Receptor 3 in allergic lung inflammation." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/56963/.

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Death Receptor 3 (DR3) is a death domain containing member of the TNF Receptor Superfamily (TNFRSF), refereeing a range of cellular responses from differentiation and proliferation to cell death, depending upon the context of receptor activation. DR3 has been reported to have a role in many inflammatory diseases, including inflammatory arthritis and inflammatory bowel disease. The aim of this study was to determine the contribution of DR3 in a mouse model of acute and chronic allergic lung inflammation. Mice genetically deficient in the DR3 gene (DR3ko) were resistant to cellular accumulation

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43

Xin, Gang. "The role of TREM proteins in lung homeostasis and inflammation." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/9058.

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The family of Triggering Receptors Expressed on Myeloid Cells (TREM) contain novel activating receptors of the Ig super-family that are expressed on myeloid cells. TREM-1 is a transmembrane glycoprotein expressed on blood neutrophils and a subset of monocytes, but not on lymphocytes or other cell types and is upregulated by bacterial and fungal products. TREM-1 signaling potentiates the outcome of Toll-like Receptor (TLR) signaling. Blockade of TREM-1 prevents experimentally induced septic shock. In addition to the membrane-bound form, a soluble TREM-1 molecule (sTREM-1) exists that regulates

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44

White, Anna-Marie. "The role of tumour necrosis factor α in lung inflammation". Thesis, University of Bath, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362198.

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45

Morla, Shravan. "Glycosaminoglycan Mimetics for the Treatment of Cancer and Lung Inflammation." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5948.

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Glycosaminoglycans (GAGs) are linear polysaccharides whose disaccharide building blocks consist of an amino sugar and either uronic acid or galactose. They are expressed on virtually all mammalian cells, usually covalently attached to proteins, forming proteoglycans. GAGs are highly negatively charged due to an abundance of sulfate and carboxylic acid groups, and are structurally very diverse, with differences arising from chain length, the type of monomeric units, the linkages between each monomeric unit, the position of sulfate groups, and the degree of sulfation. GAGs are known to interact

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46

McNeil, Kathryn Suzanne. "Nitrosative and oxidative stress in Nippostrongylus brasiliensis induced pulmonary inflammation." Thesis, Edinburgh Napier University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312974.

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47

Hedbrant, Alexander. "Cancer and Inflammation : Role of Macrophages and Monocytes." Doctoral thesis, Karlstads universitet, Institutionen för hälsovetenskaper, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-37086.

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Macrophages are cells of the innate immune system that can be found in large quantities in cancer tumors and affect cancer progression by regulating growth and invasiveness of cancer cells. There are two main phenotypes of macrophages denoted M1 and M2. In this thesis, the M1 and M2 phenotype of human macrophages were characterized, and effects of the macrophages on the growth and invasiveness of colon and lung cancer cells were studied. Macrophages of the M1 phenotype, but not the M2 phenotype, inhibited growth of both colon and lung cancer cells, and the inhibition for some of the cancer cel

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Sánchez, Vidaurre Sara. "Non-invasive methods to study lung inflammation in work-related asthma." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96716.

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El asma relacionado con el trabajo (ART) incluye el asma ocupacional (AO) y el asma exacerbado por el trabajo (AET), y representa un problema de salud importante con un negativo impacto socio-económico. El AO se refiere al asma causado de novo por exposición a un agente específico en el lugar de trabajo, y el AET se define como un empeoramiento de un asma preexistente o concomitante agravado por las condiciones de trabajo. Al igual que el asma bronquial, el ART es una enfermedad inflamatoria crónica heterogénea de las vías respiratorias. La inflamación bronquial es un reflejo directo de la e

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Thakur, Sheetal A. "Role of scavenger receptor MARCO in particle uptake and lung inflammation." The University of Montana, 2009. http://etd.lib.umt.edu/theses/available/etd-10302008-102542/.

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Alveolar macrophages (AM) form the first line of defense against chronic inflammation caused by occupational exposure to environmental particulates such as crystalline silica (CSiO2). The chronic inflammatory process triggered by CSiO2 is known to culminate into a fibrotic response called silicosis in the human lungs. Previous studies have indicated the role of membrane glycoproteins called scavenger receptors in binding of environmental particles. The scavenger receptors are classified into different classes (A-H) based on their structure and function. Class A scavenger receptors are critical

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Cornejo, Perales Salomon. "Mechanisms of glucocorticoid responsiveness in the lung during development and inflammation." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116918.

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Glucocorticoids (GCs) are vital hormones involved in lung development and the regulation of the inflammatory/immune response. High inter-individual variability in GC responsiveness exists among patients using steroids as treatment for inflammatory diseases. Evidence suggests that vitamin D (VitD), another player in lung development, improves GC function. Even though progress has been made in the study of steroid insensitivity, the molecular mechanisms are not completely elucidated and the effects of limited GC response during lung development have not been explored. The first objective of the

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