Rozprawy doktorskie na temat „Airway (Medicine) - Inflammation”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 27 najlepszych rozpraw doktorskich naukowych na temat „Airway (Medicine) - Inflammation”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj rozprawy doktorskie z różnych dziedzin i twórz odpowiednie bibliografie.
Fitch, Patrick Stephen. "A study of airway inflammation in childhood asthma". Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326411.
Pełny tekst źródłaIp, Sau-man Mary. "A pathophysiologic study of airway inflammation in bronchiectasis". [Hong Kong : University of Hong Kong], 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13793895.
Pełny tekst źródłaRatnawati, Ratnawati Prince of Wale Hospital Clinical School UNSW. "Exhaled nitric oxide in asthmatic airway inflammation". Awarded by:University of New South Wales. Prince of Wale Hospital Clinical School, 2006. http://handle.unsw.edu.au/1959.4/25729.
Pełny tekst źródła葉秀文 i Sau-man Mary Ip. "A pathophysiologic study of airway inflammation in bronchiectasis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1991. http://hub.hku.hk/bib/B31981434.
Pełny tekst źródłaMcKay, Anne. "The role of immune mediators in airway inflammation". Thesis, University of Glasgow, 2004. http://theses.gla.ac.uk/4828/.
Pełny tekst źródłaLaing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma /". Connect to this title, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0097.
Pełny tekst źródłaZheng, 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.
Pełny tekst źródłaLaing, Ingrid A. "Candidate gene approach to investigating airway inflammation and asthma". University of Western Australia. School of Paediatrics and Child Health, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0097.
Pełny tekst źródłaReader, Brenda Faye. "Social Stress Induces Immunoenhancement During Allergic Airway Inflammation and Infection". The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1385475903.
Pełny tekst źródłaStolarski, Bartosz. "The role of IL 33/ST2 pathway in innate immune response in airway inflammation". Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2961/.
Pełny tekst źródłaHaji, Sadeghi Mahboobeh. "The emerging role of the eosinophil and its measurement in chronic cough : airway inflammation in chronic cough". Thesis, University of Hull, 2017. http://hydra.hull.ac.uk/resources/hull:16543.
Pełny tekst źródłaPourazar, Jamshid. "Activation of epithelial signal transduction pathways, cytokine production and airway inflammation following diesel exhaust exposure". Doctoral thesis, Umeå : Department of Public Health and Clinical Medicine, Umeå University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-795.
Pełny tekst źródłaBehndig, Annelie. "Airway antioxidant responses to oxidative air pollution and vitamin supplementation". Doctoral thesis, Umeå universitet, Folkhälsa och klinisk medicin, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-742.
Pełny tekst źródłaCameron, Euan John. "Effects of azithromycin on asthma control, airway inflammation and bacterial colonisation in smokers with asthma : a randomised control trial". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4575/.
Pełny tekst źródłaLee, Allan G. L. "Is chronic nonspecific inflammation of the airway essential for the development of obliterative bronchiolitis after lung transplantation?" Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23909.
Pełny tekst źródłaInadequate immunosuppression of lung allografts leads to severe vascular changes consistent with chronic vascular rejection but fails to induce airway inflammation and OB. The addition of a nonspecific foreign irritant was necessary to induce diffuse airway inflammation and OB in our animal model. This suggests that a co-factor inducing airway inflammation, such as deposited foreign particles or infections, is likely necessary for the development of OB after lung transplantation. Cytokine expression reveals a link between the observed influx of airway inflammatory cells and IL-8. While bFGF is associated more with the proliferative phases of airway and vascular injury. These markers however are not predictive of either rejection or OB, due to the expression of both these markers in all three study groups. (Abstract shortened by UMI.)
Nutku, Turkan Esra. "Role of IL-12 and IL-18 in regulation of eosinophil function in allergic airway inflammation". Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85633.
Pełny tekst źródłaThe general aim of this study was to determine the effect of IL-12 and IL-18 on eosinophil functions. Results from this thesis demonstrate that eosinophils express functional receptors for IL-12 and IL-18. Acting alone or in synergy, IL-12 and IL-18 induced eosinophil apoptosis, in vitro. The apoptotic effect of IL-12 was reversed by IL-5, suggesting that IL-5 and IL-12 have counter-regulatory effects on eosinophil survival. Our regulation studies demonstrated that Phorbol-Myristate-Acetate (PMA) induced optimal expression of IL-18 and IL-12 receptors by eosinophils. IL-18 receptor expression by eosinophils was markedly increased following stimulation with interferon (IFN)-gamma, Tumor Necrosis Factor (TNF), or IL-12. Up-regulation of IL-18 receptor upon IL-12 stimulation was particularly important, which may explain IL-12 and IL-18 synergy on eosinophil apoptosis. We also investigated IL-12 and IL-18 expression by eosinophils. Eosinophils did not express IL-18. However, there was constitutive IL-12 expression by eosinophils. Release of IL-12 was also confirmed in eosinophil supernatants, which suggested an autocrine mechanism of IL-12 action on eosinophils.
Extending our understanding of the role of IL-12 and IL-18 in allergic inflammation, we have defined a novel pathway by which IL-12 and/or IL-18 may actually regulate eosinophils functions, and exert an inhibitory effect on eosinophil survival. Our findings provide critical new insights into mechanisms regulating eosinophil survival. To gain an even more detailed understanding of regulatory signals mediating eosinophil survival, we need to define the mechanisms involved in IL-12 and IL-18 signalling. We have just begun to identify the molecules involved, and these include IL-12 and IL-18 receptors. Activation via IL-12 and/or IL-18 receptor-mediated mechanisms may provide a novel strategy for reducing the numbers or inhibiting the function of these cells in allergic diseases or other diseases characterized by increased numbers of, or mediators from, eosinophils.
Sehlstedt, Maria. "Respiratory effects of particulate matter air pollution : studies on diesel exhaust, road tunnel, subway and wood smoke exposure in human subjects". Doctoral thesis, Umeå universitet, Lungmedicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-39568.
Pełny tekst źródłaCarroll, 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.
Pełny tekst źródłaLund, Sandy Tecklenburg. "Comparative and synergistic effects of fish oil supplementation and a leukotriene receptor antagonist on exercise-induced bronchoconstriction and airway inflammation in subjects with asthma". [Bloomington, Ind.] : Indiana University, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3380103.
Pełny tekst źródłaTitle from PDF t.p. (viewed on Jul 19, 2010). Source: Dissertation Abstracts International, Volume: 70-12, Section: B, page: 7486. Adviser: Timothy D. Mickleborough.
Flores, Chiari Nydia. "Cost of Treatment of Asthma Attacks in a Tertiary Level Healthcare Hospital in Panama". Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4671.
Pełny tekst źródłaBajoriūnienė, Ieva. "17-o tipo T limfocitų pagalbininkų vaidmuo sergant alergine astma". Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2014. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2014~D_20140904_150025-10728.
Pełny tekst źródłaAllergic asthma is a chronic inflammatory disease of the airways associated with the response of predominant type 2 helper T lymphocytes to an inhaled allergen. However, differences in inflammation and clinical symptoms of this disease not always can be explained by this mechanism. Recent animal model studies have shown the importance of type 17 helper T lymphocytes (Th17) in the development of allergic asthma. The role of these cells in causing allergen-induced airway inflammation as well as systemic inflammatory response in human is still not well defined. Therefore, we investigated the peripheral blood Th17 lymphocyte response to inhaled Dermatophagoides pteronyssinus (D. pteronyssinu) allergen in patients with allergic asthma. The present study has shown that patients with allergic asthma have a higher percentage of peripheral blood Th17 lymphocytes and elevated serum as well as induced sputum interleukin-17 levels compared with healthy subjects. Moreover, all studied allergic asthma patients, especially with early- and late-phase asthmatic reaction, showed an enhanced airway and systemic Th17 lymphocyte response 7 h and 24 h after bronchial challenge. We documented an enhanced local and systemic Th17 lymphocyte response to inhaled D. pteronyssinus in association with late-phase allergen-induced airway inflammation in patients with allergic asthma.
Downey, D. G. "Airways inflammation in cystic fibrosis". Thesis, Queen's University Belfast, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269047.
Pełny tekst źródłaGouveia, Ana Cláudia Carvalho. "Avaliação do efeito do Mycobacterium bovis BCG sobre a resposta imunológica em modelo murino de alergia pulmonar". Universidade Federal de Juiz de Fora, 2012. https://repositorio.ufjf.br/jspui/handle/ufjf/1561.
Pełny tekst źródłaApproved for entry into archive by Adriana Oliveira (adriana.oliveira@ufjf.edu.br) on 2016-06-28T14:35:33Z (GMT) No. of bitstreams: 1 anaclaudiacarvalhogouveia.pdf: 2060044 bytes, checksum: a2757483182ff953fdffbf86f346380b (MD5)
Made available in DSpace on 2016-06-28T14:35:33Z (GMT). No. of bitstreams: 1 anaclaudiacarvalhogouveia.pdf: 2060044 bytes, checksum: a2757483182ff953fdffbf86f346380b (MD5) Previous issue date: 2012-08-30
FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais
A asma alérgica é uma doença inflamatória crônica das vias aéreas, caracterizada por uma resposta de hipersensibilidade imediata, obstrução brônquica, inflamação pulmonar e níveis elevados de IgE. A doença é mediada principalmente por uma resposta imunológica alérgeno-específica tipo Th2. Nas últimas décadas, a prevalência da asma alérgica tem aumentado significativamente, sobretudo nos países desenvolvidos. A Hipótese da Higiene atribui este aumento a uma menor exposição a determinados microrganismos durante a infância, quando o amadurecimento adequado do sistema imunológico requer estímulos que induzam respostas imunológicas de perfil Th1, fundamentais para o equilíbrio de respostas Th2 exacerbadas. Diversos trabalhos epidemiológicos parecem comprovar esta hipótese, evidenciando a existência de uma relação inversa entre o contato com microrganismos indutores de uma resposta Th1 e o desenvolvimento de asma alérgica. Paralelamente, estudos em modelos murinos constataram que o tratamento com Mycobacterium bovis BCG (BCG) reduz respostas Th2 alérgenoespecíficas. No entanto, os mecanismos pelos quais a micobactéria inibe o desenvolvimento da resposta alérgica são ainda pouco conhecidos. Este estudo avaliou o efeito da administração do BCG sobre a resposta imunológica ocorrida na alergia pulmonar em camundongos BALB/c previamente sensibilizados e desafiados com OVA. Vinte e quatro horas após o último desafio, o sangue e o lavado broncoalveolar foram coletados para análises de imunoglobulinas e contagem de células, respectivamente. Adicionalmente, os pulmões foram submetidos à análise histológica, avaliação da atividade de EPO e dosagens de citocinas e quimiocinas, assim como avaliação da expressão de CTLA-4, Foxp3 e IL-10 por citometria de fluxo. Os resultados obtidos indicam que o tratamento com BCG melhorou o processo alérgico através da redução dos principais parâmetros relacionados à resposta Th2, como o infiltrado eosinofílico pulmonar, a atividade de EPO, IL-4, IL-13, CCL11, além de IgE e IgG1 específicas anti-OVA. Por outro lado, a administração da micobactéria aumentou os níveis de IFN-γ, IL-10 e TGF-β, além das expressões de Foxp3 e CTLA-4 pelos linfócitos T CD4+. Paralelamente, houve um aumento na produção de IL-10 pelos linfócitos T CD8+. Esses dados sugerem que, além da indução de uma resposta imune Th1, a ação imunomoduladora do BCG está relacionada também à indução de mecanismos reguladores.
Atopic asthma is a chronic respiratory disease characterized by airway hyperresponsiveness, reversible airway obstruction, lung inflammation, and high levels of allergen-specific IgE, driven by allergen-specific Th2 cells. The increasing prevalence of allergic diseases, particularly in industrialized countries, has led to the hygiene hypothesis, which states that the newborn infant’s immune system is skewed toward Th2 responses and needs timely and appropriate environmental stimulus to create a balanced immune response. Supporting this hypothesis, epidemiological and experimental evidence has shown an inverse correlation between Th1-induced microbial infections and atopic asthma. Similarly, some animal studies have demonstrated that exposure to Mycobacterium tuberculosis or to environmental mycobacteria is able to protect against the development of allergic responses. However the exact mechanism underlying this inhibition still remains poorly understood. This study aimed to evaluate the ability of BCG to suppress an established allergic response in a mouse model of OVA-induced airway inflammation. To achieve this, OVA sensitized and challenged BALB/c mice were twice treated with BCG via nasal and 21 days after the first treatment, mice were rechallenged with OVA. Twenty-four hours after the last challenge, blood samples were collected to detect anti-OVA immunoglobulin isotypes, and bronchoalveolar lavage (BAL) was harvested for cell count. Additionally, lungs were collected for histological analysis, detection of EPO activity and measurement of cytokines and chemokines. The expression of CTLA-4, Foxp3 and IL-10 was also determined in lung tissue by flow cytometry. The data indicated that BCG treatment was able to inhibit an established allergic Th2-response by decreasing the allergen-induced eosinophilic inflammation, EPO activity, levels of IL-4, IL-13, CCL11 and serum levels of IgE and IgG1. Mycobacteria treatment increased lung levels of IFN-γ, IL-10 and TGF-β, and expressions of Foxp3 and CTLA-4 in CD4+T cells. Additionally, an increased production of IL-10 by CD8+ T cells was observed, even though no detectable changes in CD4+IL-10+ was noticed. Altogether, these results suggest that the mechanism underlying the down-regulatory effects of BCG on OVA-induced airway inflammation appear to be associated with the induction of both Th1 and T regulatory immune responses.
Byrnes, Catherine Ann. "Non-invasive method of measuring airway inflammation : exhaled nitric oxide". 2008. http://hdl.handle.net/2292/5558.
Pełny tekst źródłaCockeran, Riana. "Effects of sub-lethal concentrations of pneumolysin on the proinflammatory activities of human neutrophils in vitro". Thesis, 2003. http://hdl.handle.net/2263/28021.
Pełny tekst źródłaThesis (DPhil)--University of Pretoria, 2005.
Immunology
unrestricted
Mwanthi, Muithi. "PAK1's regulation of eosinophil migration and implications for asthmatic inflammation". Thesis, 2013. http://hdl.handle.net/1805/3786.
Pełny tekst źródłaMore than 300 million people world-wide suffer from breathlessness, wheezing, chest tightness, and coughing characteristic of chronic bronchial asthma, the global incidence of which is on the rise. Allergen-sensitization and challenge elicits pulmonary expression of chemoattractants that promote a chronic eosinophil-rich infiltrate. Eosinophils are increasingly recognized as important myeloid effectors in chronic inflammation characteristic of asthma, although few eosinophil molecular signaling pathways have successfully been targeted in asthma therapy. p21 activated kinases (PAKs), members of the Ste-20 family of serine/threonine kinases, act as molecular switches in cytoskeletal-dependent processes involved in cellular motility. We hypothesized that PAK1 modulated eosinophil infiltration in an allergic airway disease (AAD) murine model. In this model, Pak1 deficient mice developed reduced inflammatory AAD responses in vivo with notable decreases in eosinophil infiltration in the lungs and broncho-alveolar lavage fluids (BALF). To test the importance of PAK1 in hematopoietic cells in AAD we used complementary bone marrow transplant experiments that demonstrated decreased eosinophil inflammation in hosts transplanted with Pak1 deficient bone marrow. In in vitro studies, we show that eotaxin-signaling through PAK1 facilitated eotaxin-mediated eosinophil migration. Ablating PAK1 expression by genetic deletion in hematopoietic progenitors or siRNA treatment in derived human eosinophils impaired eotaxin-mediated eosinophil migration, while ectopic PAK1 expression promoted this migration. Together these data suggest a key role for PAK1 in the development of atopic eosinophil inflammation and eotaxin-mediated eosinophil migration.
Taylor, Janet Lynley. "An analysis of polyphenolic blackcurrant (Ribes nigrum) extracts for the potential to modulate allergic airway inflammation : a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Nutritional Science at Massey University, Palmerston North, New Zealand". 2009. http://hdl.handle.net/10179/1212.
Pełny tekst źródła