Дисертації з теми "ST2 expression in asthma"
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Bradding, Peter. "Cytokine expression in allergic mucosal inflammation." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295929.
Повний текст джерелаOsman, Mustafa. "The expression of asthma in relation to sex and sex steroids from birth to adulthood." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25474.
Повний текст джерелаStinson, Sally Elizabeth. "Exploring the expression and function of CRTh2 in asthma." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/31996.
Повний текст джерелаSeymour, Michelle L. "Expression of eicosanoid pathway enzymes in inflammatory cells." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310699.
Повний текст джерелаKuitert, Lieske Meta Elizabeth. "Eicosanoid synthetic enzymes : aspects of regulation and expression in asthma." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248441.
Повний текст джерелаKonstantinidis, Athanasios. "Genetics and airway expression of interleukin-13 receptors in asthma." Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418599.
Повний текст джерелаCowburn, Andrew Stephen. "Regulation of eicosanoid enzyme expression in inflammatory leukocytes in asthma." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266655.
Повний текст джерелаLacson, Ronilda, Michael Mbagwu, Hisham Yousif, and Lucila Ohno-Machado. "Assessing the quality of annotations in asthma gene expression experiments." BioMed Central, 2010. http://hdl.handle.net/10150/610165.
Повний текст джерелаTuttle, Camilla Susannah Laura. "The expression of HAT and HDAC enzymes in asthma airways." Thesis, Queensland University of Technology, 2013. https://eprints.qut.edu.au/62873/1/Camilla_Tuttle_Thesis.pdf.
Повний текст джерелаHillaby, Caroline Wendy. "Expression of phosphodiesterase isoenzymes in inflammatory cells in allergic airway disease." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370062.
Повний текст джерелаVasavda, Nisha. "Steroid dependent asthma : gene expression changes in T-lymphocytes and functional consequences." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405899.
Повний текст джерелаTajiri, Tomoko. "Association of Eosinophilic Inflammation with FKBP51 Expression in Sputum Cells in Asthma." Kyoto University, 2014. http://hdl.handle.net/2433/185195.
Повний текст джерелаGlare, Eric M. 1965. "The application of competitive PCR technology to asthma research." Monash University, Dept. of Medicine, 2001. http://arrow.monash.edu.au/hdl/1959.1/7975.
Повний текст джерелаSaunders, Michael Anthony. "The expression, regulation and functional role of cyclooxygenase isoforms in human airway cells." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300789.
Повний текст джерелаStandring, Peter. "Class II Human Leukocyte Antigen gene polymorphisms, cell surface expression and immunoglobulin E mediated disease." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262910.
Повний текст джерелаAl-Ramli, Wisam. "Expression of Th-17 related cytokines (IL-17A and F) in severe asthma." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95068.
Повний текст джерелаLe processus inflammatoire et le remodelage des voies respiratoires sont typiquement liés à la pathologie de l'asthme réfractaire. Bien que l'asthme réfractaire n'affecte que 10% des asthmatiques, ce sous-groupe de patients est caractérisé par une plus grande morbidité, mortalité ainsi qu'un besoin disproportionné des services des soins de santé. Il semble que l'asthme réfractaire utilise un mécanisme d'inflammation distinct de celui associé à l'asthme léger et modéré. Il y a une augmentation de l'infiltration des neutrophiles, une régulation positive de l'IL-8 ainsi qu'une dérégulation des cytokines Th-2. Les cytokines IL-17A et F sont pro-inflammatoires, pro-fibrotiques et sont principalement produites par les cellules Th-17. Ces cytokines peuvent agir sur plusieurs types de cellules afin d'induire la production de cytokines, chémokines et métalloprotéinases. De plus, ces deux cytokines jouent un rôle prédominant dans l'activité des neutrophiles. Nous faisons l'hypothèse que l'IL-17A et F sont exprimées dans les voies respiratoires des asthmatiques et qu'elles sont augmentées dans l'asthme réfractaire. Cette étude a pour but d'investiguer l'expression de l'IL-17A et F sur biopsies provenant d'asthmatiques réfractaires et d'en faire la comparaison à celles provenant d'asthmatiques légers, modérés ainsi que de sujets sains et de relier cette expression à celle de l'IL-8 et de la neutrophilie. L'expression des ARNm et des protéines de l'IL-17A et F a été évaluée sur biopsies par immunocytochimie et real-time PCR'. Il a été démontré que l'expression de l'IL-17A et F est augmentée dans les voies aériennes des asthmatiques réfractaires en comparaison aux asthmatiques légers et sujets sains. L'IL-17A est principalement exprimée par les cellules mononucléaires des tissus des régions sous-épithéliales parmi les grappes de cellules inflammatoires. L'IL-17F n'est pas uniquement exprimée par les cellules inflammatoi
Di, Candia Leonarda. "The expression and function of RAGE and HMGB1 in airway structural cells in asthma." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32339.
Повний текст джерелаLéguillette, Renaud. "Expression of smooth muscle myosin heavy chain isoforms in asthma and their molecular mechanics." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103169.
Повний текст джерелаI then quantified the expression of SM-B and several other contractile protein genes in endobronchial biopsies from normal and asthmatic subjects. SM-B, myosin light chain kinase (MLCK), which is responsible for myosin activation, and transgelin, a ubiquitously expressed actin binding protein but whose function is unknown, were overexpressed in the asthmatic biopsies. The increased SM-B expression and myosin activation, due to the increased MLCK expression, both contribute to the increased rate of shortening of the asthmatic airway SM. In addition, I showed that beyond its enzymatic effects, MLCK mechanically enhances numax. The binding of SM22 to actin, however, did not alter numax.
Finally, I addressed the mechanisms behind the unique capacity of SM to maintain force at low energy cost, namely the latch-state. This property is mostly observed in SM-A containing, tonic muscle. Using a laser trap, I measured the binding force of unphosphorylated (non-active) SM-A and SM-B myosin isoforms and found that they can both attach to actin and maintain force. I also measured numax at different MgADP concentrations and found that SM-A has a greater affinity for MgADP. Because MgADP must be released before myosin can detach from actin, these results suggest that the SMA isoform remains attached longer to actin, allowing it to get into the latch-state. These findings explain the greater propensity of tonic muscle to get into the latch-state.
Naseer, Tanveer 1971. "In vivo expression of interleukin-12 and interleukin-13 in the pathogenesis of asthma." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23925.
Повний текст джерелаWicks, James. "The expression and regulation of ADAM33, a novel asthma susceptibility gene, during myofibrolast differentiation." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432038.
Повний текст джерелаFarahani, Mosavar. "Regulation of histamine Hâ†1-receptor coupling and expression in cultured human airway smooth muscle cells." Thesis, University of Nottingham, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263099.
Повний текст джерелаScott, Mark George Hunter. "Control of cyclic AMP-mediated and ß₂ adrenergic receptor gene expression in cultured human airway smooth muscle cells." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324123.
Повний текст джерелаJosephs, Lynn K. "A longitudinal study of bronchial responsiveness and its relationship to the clinical expression of asthma." Thesis, University of Southampton, 1992. https://eprints.soton.ac.uk/370379/.
Повний текст джерелаCarney, Katharine W. "Expression patterns and functional roles of amphiregulin in murine CD4+ T cells." Thesis, Royal Veterinary College (University of London), 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669191.
Повний текст джерелаFlorsheim, Esther Borges. "Mecanismos envolvidos na indução da inflamação alérgica pulmonar pela serino protease subtilisina." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-12122014-161448/.
Повний текст джерелаOccupational asthma is the most common form of pulmonary disease related to work. Most of occupational asthma cases reported are strictly correlated with proteases exposure. Serine protease subtilisin was widely used in the detergent industry during the 60s, which resulted in increased incidence of occupational asthma. We aimed to develop and characterize a murine model of occupational asthma using subtilisin as allergen. Briefly, sensitization and challenge with subtilisin triggered lung allergic inflammation, as accessed by eosinophilic influx to the airways, mucus production, and increased levels of type II cytokines. Subtilisin induced total IgE and airway hyperactivity. Allergic responses to subtilisin were dependent on its serine protease activity, protease-activated receptor (PAR)-2, IL-33 receptor ST2, IL-1R, and Myd88 signaling. Together, these data establish a new murine model of occupational asthma induced by subtilisin and provide the main molecular mechanisms responsible for allergic inflammation.
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.
Повний текст джерелаRedington, Anthony Edward. "Fibrogenic mediators in atopic asthma : expression of endothelin, transforming growth factor-beta and basic fibroblast growth factor." Thesis, University of Southampton, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242665.
Повний текст джерелаErickson, Nancy Ann [Verfasser]. "Expression Analyses of CLCA Members in the Feline Respiratory Tract – Biomolecules in Feline Asthma? / Nancy Ann Erickson." Berlin : Freie Universität Berlin, 2021. http://d-nb.info/1240230397/34.
Повний текст джерелаJoubert, Philippe. "Expression and function of chemokine receptors on airway smooth muscle cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103385.
Повний текст джерелаFor the first time, this work describes the expression of chemokine receptors by ASMC. We have shown that eotaxin, an important chemokine in asthma, induces migration of ASMC through the activation of CCR3. Although CCR3 expression is not regulated by Th2 cytokines in vitro, ASMC isolated from asthmatic patients expressed intrinsically higher levels of the surface receptor when compared to controls. We also describe the expression of CCR1 by ASMC, a receptor involved in airway remodelling in an animal model of asthma. We reported the expression of CCR1 mRNA in biopsies obtained from mild, moderate and severe asthmatics and showed that mild group express the highest level of CCR1. We also confirmed that ASMC express the receptor in vivo and showed that stimulation of this receptor with its ligands induces intra-cellular calcium mobilization, which confirms its functionality. Regulation of CCR1 on ASMC was also assessed using proinflammatory, Th1 and Th2 cytokines. We found that TNF-alpha and to a lesser extent, IFN-gamma, upregulated CCR1 mRNA and protein expression, while Th2 cytokines had no effect. The effect of these two cytokines was totally suppressed by either dexamethasone or mithramycin.
Collectively, our results demonstrate the expression of functional C-C chemokine receptors by ASMC. Interestingly, we have shown that CCR3 activation mediates ASMC migration and provides a new possible mechanism for the increased smooth muscle mass observed in asthmatic patients. Although the exact function of the CCR1 expressed by ASMC is unknown, our results suggest an involvement in asthma pathogenesis, possibly through airway remodelling.
Carvalho, Liliana Sofia Machado de. "Expression of cyclooxygenase enzymes and prostaglandin E2 receptors in inflammatory airway diseases." Master's thesis, Faculdade de Ciências e Tecnologia, 2011. http://hdl.handle.net/10362/6347.
Повний текст джерелаAspirin-intolerant asthma (AIA) is a syndrome where the interplay between cyclooxygenase (COX) and lipoxygenase (LOX) pathways is evident and is characterized by several abnormalities in the regulation and biosynthesis of eicosanoid mediators and eicosanoid receptors. Several observations indicate the presence of a complex change in the arachidonic acid (AA) metabolism in patients who suffer from AIA. However, previous studies showed some discrepant results when upper and lower airways were analyzed, and there are no clear explanations for this. The inflammatory responses in upper airways are often associated with the presence of nasal polyps, structures never seen in the lower airways. In this study, upper and lower airways were compared, in order to verify if the multiple factors of the COX pathway are differentially regulated considering both respiratory tracts. To perform the experiments, fibroblasts from nasal mucosa (NM) and bronchial mucosa (BM) of non-asthmatic subjects undergoing corrective surgery and fibrobronchoscopy, respectively, (control group) were compared with NM, nasal polyp (NP), and BM fibroblasts isolated from non-asthmatic and AIA patients suffering from chronic rhinosinusitis (CRS) with NP. The data presented in this investigation suggest that in lower airways, the presence of aspirin intolerance does not seem to alter the expression of COX enzymes or the production of prostaglandin (PG) E2. Considering the expression of the EP receptors, the data suggest significant differences through fibroblasts from upper airways tissues. The differences observed between upper and lower airways combined with others verified in previous studies might contribute to the pathogenesis of nasal polyposis.
Byström, Jonas. "Eosinophil Cationic Protein : Expression Levels and Polymorphisms." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2059.
Повний текст джерелаThe eosinophil cationic protein (ECP) is usually associated with the eosinophil granulocyte. In this thesis the presence and production of this protein has been studied in two other cells. The circulating monocyte was found to contain ECP mRNA and small amounts of ECP, one thousand times less than that found in the eosinophil. The production decreased by differentiation of the myelomonoblastic cell line U937 into a macrophage phenotype. Submucosal lung macrophages did not stain for ECP and alveolar macrophages did not contain ECP mRNA. The circulating neutrophil contains ECP at a level hundred fold less than the eosinophil. We found that the protein is located to the primary granules of the neutrophil but could detect no ECP mRNA in the cell. It was shown in vitro that the protein was taken up by the cell and partly transported to the primary granules. The uptake did not seem to be receptor mediated. Upon stimulation of the neutrophils, ECP previously taken up, was re-secreted.
The ECP protein is heterogeneous both to molecular characteristics and to function. To evaluate if a genetic component is involved, the ECP gene was analysed in 70 individuals. Three single nucleotide polymorphisms (SNP´s) were found, denoted 277(C>T), 434(G>C) and 562(G>C). The two first were located to the mature peptide-coding region and would change the amino acids, arg45cys and arg97thr. The prevalence of the most common SNP, 434, was evaluated in two eosinophil-related diseases, allergy/asthma and Hodgkin Lymphoma (HL). Forty-three HL patients were evaluated and it was found that the 434GG was significantly more prevalent in patients having nodular sclerosis (NS) as compared to other histologies (p=0.03). Erythrocyte sedimentation rate was also related to the 434GG genotype (p=0.009). In 209 medical students 434GG was more common (p=0.002) in those who indicated allergy. The genotype was unrelated to the production of IgE antibodies to allergens. In analysis of 76 subjects with asthma it was found that the 434GG genotype was significantly more common among allergic asthmatics (p=0.04). Asthma and HL-NS are characterized by fibrosis and eosinophils and ECP has been suggested in fibrosis development.
Hadaway, Matthew. "Effect of induced airway inflammation in asthma : the expression of trefoil factors, secretoglobins and genes involved in histone acetylation." Thesis, Queensland University of Technology, 2012. https://eprints.qut.edu.au/62168/1/Matthew_Hadaway_Thesis.pdf.
Повний текст джерелаKaragiannidis, Christian. "Activin A und TGF-[beta]1 [TGF-Beta-1] bei Asthma bronchiale: differentielle Expression und gemeinsame Funktionen sowie deren Regulation durch Glukokortikoide." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=974673056.
Повний текст джерелаHaitchi, Hans Michael. "The expression and function of the asthma susceptibility gene, a Disintegrin and Metalloprotease (ADAM) 33, in airways of normal and asthmatic subjects and in developing lungs." Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/380396/.
Повний текст джерелаBerenchtein, Beatriz. "A INFLUÊNCIA DO STRESS NA EXPRESSÃO CLÍNICA DA ASMA INFANTIL." Universidade Metodista de São Paulo, 2004. http://tede.metodista.br/jspui/handle/tede/1449.
Повний текст джерелаAsthma is the most frequent chronic disease in childhood and stress is considered one of the triggering and aggravating agents of bronchospasm in this patients. The aim of this work was investigate the influence of stress in the clinical expression of asthma and your association with the asthma attacks in children. The asthmatic children answered to a stress scale (LIPP E LUCARELLI, 1998) and their parents answered some questions about the frequency of symptoms and asthma attacks, sleep disturbance, school absenteeism, physical exercises limitations, frequency of use of medicines, their behavior during their child asthma attacks, the triggering agents of crises, their socio-economic status and education level. The results showed that the asthmatic children were more stressed than those from the control group, specially the children with severe asthma. Also, stress can intensify frequency of asthma attacks, physical exercises limitations, school absences and sleep disturbance. The children that had been diagnosed for a long period were less stressed. The results from this study suggest that stress can precipitate or exacerbate asthma attacks. That shows necessity of more researches to refine the knowledge about this subject.
A asma é a doença crônica mais freqüente na infância e o stress é considerado um dos agentes desencadeantes e agravantes do broncoespasmo nesses pacientes. O objetivo deste trabalho foi investigar a influência do stress na expressão clínica da asma e sua associação com as crises em crianças. Para verificar a presença de stress, utilizou-se a Escala de Stress Infantil (LIPP E LUCARELLI, 1998) e por meio de um questionário aplicado aos pais, observou-se freqüência de sintomas e crises de asma, as alterações do sono, o absenteísmo escolar, as limitações à prática de atividade física, a freqüência de uso de broncodilatador, as condutas dos pais durante as crises de asma, os fatores associados ao desencadeamento das crises, o poder aquisitivo e o grau de instrução do chefe da família. Observou-se que as crianças com asma estavam mais estressadas que as crianças do grupo controle, principalmente aquelas com maior gravidade da doença. Os resultados indicam que a presença de stress pode intensificar a freqüência de sintomas da asma, a limitação à atividade física, o absenteísmo escolar e as interrupções do sono. O maior tempo de diagnóstico de asma implicou em menor ocorrência de stress, sugerindo a existência de um fator de adaptação à doença. Conclui-se que o stress é um fator importante no desencadeamento e agravamento das crises de asma nas crianças e observa-se a necessidade de maiores pesquisas na aérea para aprofundar os conhecimentos sobre esse assunto.
Bradley, Jennifer L. "Obesity and Asthma: Adiponectin Receptor 1 (Adipo R1) and Adiponectin Receptor 2 (Adipo R2) are expressed by normal human bronchial epithelial (NHBE) cells at air-liquid interface (ALI) and expression changes with IL-13 stimulation." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4576.
Повний текст джерелаHartley, Judith Ann. "Developing methods for the identification and isolation of dendritic cells from peripheral blood and their application to the study of high affinity IgE receptor (Fc#epsilon#RI) expression by dendritic cells in health and atopic asthma." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285820.
Повний текст джерелаVorsprach, Monique [Verfasser], Marino [Gutachter] Venerito, and Marek [Gutachter] Lommatzsch. "Expression von Cyclooxygenasen (COX-1 und COX-2) und Lipoxygenase (5-LOX) in Nasenpolypen und Bronchialschleimhaut bei Patienten mit Asthma bronchiale, rezidivierender Polyposis nasi und Analgetikainteroleranz : Korrelation mit klinischen und funktionellen Parametern / Monique Vorsprach ; Gutachter: Marino Venerito, Marek Lommatzsch." Magdeburg : Universitätsbibliothek Otto-von-Guericke-Universität, 2020. http://d-nb.info/1220035637/34.
Повний текст джерелаPasanen, A. (Anu). "Genetic susceptibility to childhood bronchiolitis." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526218991.
Повний текст джерелаTiivistelmä Bronkioliitti on viruksen aiheuttama alahengitystieinfektio, joka usein johtaa pienten lasten sairaalahoitoon. Yleisin bronkioliitin aiheuttaja lapsilla on respiratory syncytial -virus (RSV). Perintötekijöiden arvellaan altistavan bronkioliitille, joten uusi tieto altistavista geeneistä voi auttaa ymmärtämään taudin taustalla olevia biologisia mekanismeja. Lapsuusiän bronkioliitin ajatellaan voivan altistaa astmalle, joten bronkioliitin tehokas hoito voi vaikuttaa merkittävästi hengitysterveyteen myös pitkällä aikavälillä. Työssä pyrittiin selvittämään lapsuusajan bronkioliitille altistavia geneettisiä tekijöitä genominlaajuisella assosiaatiokartoituksella, joka toteutettiin suomalais-ruotsalaisessa tapaus-verrokkiväestössä. Löydökset pyrittiin varmentamaan soveltuvilla jatkotutkimuksilla. Lisäksi tarkastelimme astmalle altistavaa CDHR3-geenin polymorfismia viidessä eurooppalaisessa bronkioliittikohortissa käyttäen meta-analyysia. Assosiaatiokartoituksessa havaittiin useita mahdollisia bronkioliittialttiuteen vaikuttavia geenikohtia. Näistä kolme sai tukea hollantilaisessa väestössä tehdyssä assosiaatioanalyysissä, jossa testattiin assosiaatiokartoituksen lupaavimmat löydökset. Yksi altistavista polymorfismeista vaikutti KCND3-geenin ilmentymiseen, ja kaksi muuta olivat geenien välisiä, mahdollisesti geeninsäätelyyn osallistuvia variantteja. Assosiaatiokartoituksen osa-analyysissä NKG2D tunnistettiin mahdolliseksi bronkioliitille altistavaksi geeniksi. NKG2D-immuunireseptorin alentunut ilmentyminen voi tulostemme perusteella altistaa vakavalle bronkioliitille. Meta-analyysissä, jonka tutkimuskohortit olivat peräisin Tanskasta, Suomesta, Ruotsista, Saksasta ja Hollannista, todettiin mahdollinen yhteys CDHR3-geenin polymorfismin ja muun viruksen kuin RSV:n aiheuttaman bronkioliitin välillä. Toteutimme tässä työssä ensimmäisen genominlaajuisen bronkioliittialttiutta koskevan assosiaatiokartoituksen. Assosiaatiokartoituksessa, sitä seuranneissa jatkotutkimuksissa ja meta-analyysissä tunnistimme useita lupaavia alttiusgeenejä, mutta tuloksemme vaativat varmentamista suuremmissa tutkimusväestöissä
Cheng, Fang-Yi, та 鄭芳怡. "Feasibility Study of TSLPR /IL-7Rα Expression for Children with Allergic Asthma". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/zsy3j7.
Повний текст джерелаLee, Tsai-Chun, and 李采純. "The Correlation Between Thymic Stromal Lymphopoietin Receptor Complex Expression and Pediatric Asthma." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/wsc85p.
Повний текст джерела國立虎尾科技大學
生物科技研究所
101
Recent studies found that cytokine thymic stromal lymphopoietin (TSLP) play a very important role and related with allergic inflammatory diseases including atopic dermatitis, rhinitis, and asthma. The TSLP receptor (TSLPR) is a heterodimeric cytokine receptor consisting of the IL-7 receptor alpha chain (IL-7Rα) and a TSLP-specific receptor chain. In our research, our specific aim is focused on the relationship between thymic stromal lymphopoietin receptor complex expression and the severity pediatric asthma. TSLPR chain can express on dendritic cells, T cells, B cells, mast cells, natural killer (NK) cells, eosinophil cells and monocytes. IL-7Rα chain can express on bone marrow lymphoid precursors, pro-B cells, NK cells, naïve and memory CD4+ and CD8+ T cells, dendritic cells, monocytes/macrophages, mast cells and eosinophil cells. T cells, monocytes, dendritic cells, NK cells, mast cells and eosinophil cells can coexpress the TSLPR chain and IL-7Rα chain. In some report, they found that genetic polymorphisms will affect the expression of the TSLPR chain and IL-7Rα chain. The SNP of TSLPR chain is one possible factor correlated with the susceptibility to atopic asthmatic disease. Also, polymorphisms of IL-7Rα chain are associated with allergic asthma susceptibility. One report found that TSLPR expressing cells have potential to modulate expression of the TSLPR when exist in a milieu of proallergic and proinflammatory cytokines and other factors (e.g., allergens, bacterial products, and lipid mediators). This result indicates acquired environmental factors can also affect the expression of the TSLPR. Until now, it is unclear that if the expression of TSLPR complex is correlated with genetic factors or environmental factors or both. In recent study, we found that TSLPR chain and IL-7Rα chain mRNA expression in PBMC layer of the AA (atopic, asthmatic) group children is more significantly higher than NN (non-atopic, non-asthmatic) group children. In another study of Hung et al., stimulation of human THP-1 cell by Der p2 did not affect the expression of TSLPR chain and IL-7Rα chain. The TSLP receptor expression mechanism in other cell types is still need further investigation. We hope that the expression of TSLPR can be applied to the evaluation of the severity of asthma and to be as a disease marker in the future.
"Activation of NF-[kappa]B and p38 MAPK regulating the expression of cytokines, chemokines and adhesion molecules upon the co-culture of human eosinophils and bronchial epithelial cells." Thesis, 2005. http://library.cuhk.edu.hk/record=b6074068.
Повний текст джерелаFreshly isolated eosinophils from human peripheral blood and confluent BEAS-2B cells were co-cultured together in tissue culture plate for a pre-determined time period. Cytokines including interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-10, IL-12p70, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma and chemokines regulated upon activation normal T cell expressed and secreted (RANTES), monokine induced by interferon-gamma (MIG), monocyte chemoattractant protein (MCP)-1, IL-8, and interferon inducible protein (IP)-10 in culture supernatant were evaluated by protein array and quantified by cytometric bead array (CBA) kit of Th1/Th2 cytokines, inflammatory cytokines, and human chemokines using flow cytometry and enzyme linked immunosorbent assay (ELISA) kit.
In order to investigate the immunopathological mechanism in allergic asthma of eosinophils interacting with bronchial epithelium in inflammation site, a in vitro system of co-culture of human bronchial epithelial cells and eosinophils was set up to mimic the inflammatory reaction.
In summary, co-culture of epithelial cells, BEAS-2B cells, and eosinophils could activate NF-kappaB and p38 MAPK signal transduction pathways to induce inflammatory cytokine IL-6, and chemokines IL-8, MCP-1, MIG and IP-10 release in culture supernatant, and up-regulated the expression of surface adhesion molecules ICAM-1, VCAM-1, ICAM-3 and CD49d protein on BEAS-2B, and CD18 and ICAM-3 on eosinophils. (Abstract shortened by UMI.)
In this study, co-culture of a human epithelial cell line, BEAS-2B cells, and peripheral eosinophils was adopted as an in vitro model to investigate the effect of interaction of epithelial cells and eosinophils in airways on pathophysiology of asthma.
Wang Chengbin.
"July 2005."
Advisers: Wai kei Lam; Chun kwok Wong; Yaping Tian.
Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3723.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2005.
Includes bibliographical references (p. 119-134).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract in English and Chinese.
School code: 1307.
Movassagh, Hesamaldin. "Expression of Semaphorin 3E in Asthma and its role in Allergic Airway Disease." 2016. http://hdl.handle.net/1993/31121.
Повний текст джерелаMay 2016
Wu, Wen-Chia, and 吳文嘉. "Relationship between Sialyl Glycan Expression on T Cells and Endophenotypes of Childhood Asthma." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/94597722629521297350.
Повний текст джерела國立臺灣大學
流行病學與預防醫學研究所
104
Background: Asthma is a common chronic inflammatory disease in children. Helper T (Th) cells and regulatory T cells (Tregs) play important role of the pathogenesis of asthma and lead to various endophenotypes. The expression level of functional adhesion molecules, sialyl Lewis x (CD15s) and sialyl 6-sulfo Lewis x (G152) glycan, on memory Th cells are associated with the severity of allergic diseases. The association between the expression level of sialyl glycans and asthma endophenotypes remain unclear and needs further investigation. Methods: Thirty-one asthma patients and nineteen healthy controls aged 6 to 15 were recruited from NTUCH and a clinic in 2015 and 2016. The percentage of glycan-expressing cells among memory Th cells was detected by flow cytometry. The association between the expression of sialyl glycan and several asthma endophenotypes, such as severity, blood eosinophils and serum total IgE level, was investigated. Results: CD15s and G152 glycans on memory Th cells are upregulated in asthma patients compared with healthy controls. The population of suppressive CD15s+ Tregs among CD4+ T cells was significantly lower in the moderate to severe group of asthma. Blood eosinophils and serum total IgE and, as two indicators of the exacerbation of asthma were associated with G152 glycan and G159 glycan respectively. Conclusions:CD15s and G152 glycans were associated with the current status of childhood asthma. Patients expressing the higher level of G152 glycan and less G159 glycan on central helper memory T cells would have higher risk on exacerbation.
Chia-Hsiu and 許家修. "Selective Cysteinyl Leukotriene Receptor Antagonist Modulates Matrix Metalloproteinase Expression in a Mouse Asthma Model." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/74042283014051297734.
Повний текст джерела中山醫學大學
醫學研究所
96
Atopic disease including allergic rhinitis and asthma is common in the world and Taiwan. The disease is generally considered to be caused by interaction of genetic and environmental factors. The incidence of asthma has increased substantially in the last two decades. New medication is developed rapidly in recent years to apply to allergic asthma, since lots of people have investigated about these. However, now existing drugs just offer partial relief of symptoms in such disease. Therefore, the aim of our study was to investigate the complicated mechanism of asthma by different drugs. The more effective drugs to suppress asthmatic airway response are expectantly to be developed. Even we can then reverse the damaged lung tissue after airway remodeling. As we known today, asthma is a repeated chronic inflammatory disease. It is characterized by a complex response of pulmonary eosinophilia, edema, mucus hypersecretion, and airway hyperreactivity. Under the condition of long-term asthma, airway remodeling may develop by goblet cells increased, subepithelial fibrosis, airway smooth muscle mass increased and vascular hyperplasia. These make asthma control more difficult. Many mechanisms, mediators and cytokines, including cysteinyl leukotrienes (CysLTs), are related to these structural changes. To determine the effect of a specific CysLT receptor antagonist on airway inflammation and remodeling, a mouse asthma model was applied. BALB/c mice, after intraperitoneal ovalbumin (OVA) sensitization on Days 0 and 14, were given intranasal OVA on Day 14 and Days 25-27. Randomized treatment groups of sensitized mice were fed a CysLT receptor antagonist singulair (montelukast, MK-476), verlukast (MK-679) or placebo from Days 15-27. Prednisolone is one kind of steroid which is known as efficient anti-inflammatory agent. It is used extensively at clinic for long time. One group of sensitized mice in the study would be fed with prednisolone according to the same feeding protocol as other study groups. The steroid-treated group will act as standard index of treatment efficacy. On Day 28, pulmonary mechanics were determined noninvasively using whole body plethysmography. The mice were then sacrificed; the serum, the bronchoalveolar lavage fluid (BALF) and the lung tissue were obtained for further evaluation of airway inflammation and remodeling. In present study, the OVA-sensitized mice developed a significant airway inflammatory response than control group. The serum IgE level, the percentage of BALF eosinophils, the airway collagen deposition and peribronchial fibrosis were significantly elevated in OVA-sensitized group (P < 0.001 vs. control group). The significant airway inflammatory response in OVA-sensitized mice was inhibited by prednisolone or montelukast (P < 0.01 vs. sensitized group). MK-679, given during airway remodeling, reduced airway inflammation less effectively (P < 0.05 vs. sensitized group) but reversed structural changes more effectively (P < 0.001 vs. sensitized group) than prednisolone. Montelukast also reversed the airway structural changes to significant level as MK-679 (P < 0.001 vs. sensitized group). Here the study also showed that BALF matrix metalloproteinase (MMP)-2 and MMP-9 levels were proportional to the extent of airway remodeling. Airway hyperresponsiveness to methacholine was observed in OVA-sensitized mice (P < 0.01 vs. control group). Airway hyperresponsiveness could be reversed by prednisolone, montelukast and MK-679. However, when the OVA-sensitized mice were challenged with higher dose of methacholine (20mg/ml), only the prednisolone and montelukast reversed airway hyperresponsiveness to significant level (P < 0.05 vs. sensitized group). In conclusion, this study demonstrates that many cytokines participate in airway inflammation and remodeling. The CysLT plays a more important role than other cytokines in chronic allergic airway inflammation. Thus the selective CysLT receptor antagonist inhibits airway remodeling more effectively than prednisolone. Furthermore, the MMP-2 and MMP-9 may be useful for monitoring airway remodeling.
Yasruel, Zivart. "Expression of membrane-anchored and soluble isoforms of interleukin-5 receptor Ü mRNA in bronchial asthma." Thesis, 1996. http://spectrum.library.concordia.ca/6253/1/MM18457.pdf.
Повний текст джерелаRevez, Joana Nunes Mexia Allen 1989. "A new variant in the interleukin-6 receptor (IL-6R) gene increases gene expression and asthma risk." Master's thesis, 2013. http://hdl.handle.net/10451/9449.
Повний текст джерелаA interleucina-6 (IL-6) é uma citocina envolvida na asma alérgica, que atua nas suas células-alvo através de um recetor constituído por pelo menos duas subunidades membranares: uma glicoproteína de associação ao ligando (IL-6R) e uma glicoproteína transdutora de sinal (gp130). Embora a gp130 se expresse na grande maioria das células, apenas algumas são diretamente estimuladas pela IL-6, porque a expressão da IL-6R membranar (mIL-6R) é limitada a hepatócitos e determinadas células imunes. No entanto, a IL-6R também existe sob forma solúvel (sIL-6R), que tanto pode ser formada por clivagem da mIL-6R, como por splicing alternativo. Uma vez ligada à IL-6, a sIL-6R pode associar-se à gp130, estimulando as células por uma via alternativa, também viável em células que não expressam mIL-6R. A variante rs2228145, no gene IL6R, encontra-se na região que codifica para o local de corte da mIL-6R e é considerada o principal determinante genético dos níveis de sIL-6R, representando cerca de 19% da sua variabilidade. Portadores do alelo de risco têm elevados níveis de sIL-6R e maior risco de asma. No entanto, a percentagem de variação nos níveis de sIL-6R explicada geneticamente é estimada em 70%, muito superior aos 19% supramencionados, pelo que é possível que outras variantes no IL6R, ou próximo deste, também contribuam para a sua variabilidade independentemente da rs2228145, e possivelmente afetem o risco de asma. Para testar esta hipótese, neste estudo (1) efetuámos uma imputação exaustiva de variantes comuns na região do IL6R; (2) testámos a associação entre as variantes obtidas e os níveis de sIL-6R de 360 indivíduos; (3) replicámos o estudo numa amostra independente de 354 indivíduos para as variantes que apresentaram associação mais forte; e (4) testámos a associação das variantes replicadas (a) com os níveis de transcrito do IL6R (em dois estudos independentes; N = 851 e N = 5 191) e (b) com o risco de asma (N = 47 514). Segue-se uma descrição mais pormenorizada de todos estes pontos. Numa primeira fase, medimos em duplicado as concentrações serológicas de sIL-6R de 360 asmáticos já genotipados. Após eliminar variabilidades técnicas, calculámos a média dos níveis corrigidos de sIL-6R para cada indivíduo e normalizámos a distribuição global das medições. Não se verificaram efeitos significativos do sexo ou da idade. Tendo o 1000 Genomes Project como referência, imputámos 452 variantes no IL6R (± 50 kb) dos 360 asmáticos, e testámos a sua associação com os níveis de sIL-6R, bem como a de outras 19 variantes diretamente genotipadas nestes indivíduos. A variante que apresentou maior grau de associação (P = 0.0005) com os níveis de sIL-6R ajustados pelo rs4129267, uma variante correlacionada (r2 = 0.99) com a rs2228145, foi a rs12083537, e a associação manteve-se significativa (P = 0.0496) após correção pelo número de variantes testadas. Três variantes independentes demonstraram estar significativamente associadas com os níveis de sIL-6R ajustados pelas variantes rs4129267 e rs12083537, mas qualquer destas associações deixou de ser significativa depois de corrigir pelo número de variantes testadas. Para confirmar a associação entre a variante rs12083537 e os níveis de sIL-6R, replicámos o estudo de associação em 354 indivíduos não relacionados com os anteriores. Após ajustamento pelos efeitos do rs4129267, detetámos uma associação significativa entre o rs12083537 e os níveis de sIL-6R (P = 0.033), sendo a direção do efeito a mesma que a da análise prévia. Estes resultados confirmam portanto que rs12083537, ou uma variante correlacionada com esta, regula os níveis serológicos de sIL-6R. Depois de combinar as duas amostras onde se efetuaram os estudos de associação (N = 714), o rs12083537 passou a explicar 2.2% da variabilidade dos níveis de sIL-6R ajustados pelo rs4129267 (P = 6x10-5), sendo que antes do ajuste explicava 0.15%. O alelo rs12083537:G reduziu os níveis de sIL-6R de forma semelhante nas três classes genotípicas do rs4129267. Para ajudar a compreender o mecanismo molecular pelo qual o rs12083537 afeta os níveis de sIL-6R, estudámos em seguida os níveis de RNA mensageiro (mRNA) do IL6R num grupo de gémeos adolescentes (N = 851) para determinar se esta variante influenciava os níveis da transcrição. Não foi detetada associação significativa entre o rs12083537 e os níveis de mRNA, quer com uma sonda para a região 3’UTR, quer com uma sonda para o exão 9. Por outro lado, detetámos uma associação significativa entre a variante rs4129267 e os níveis de transcrito do IL6R. Contraintuitivamente, o alelo rs4129267:T, que aumenta os níveis de sIL- 6R, demonstrou associação com baixos níveis de transcrito do IL6R. Para garantir que a ausência de associação entre o rs12083537 e os níveis de mRNA do IL6R não se deveu a baixo poder de deteção da nossa amostra, realizámos uma análise semelhante à anterior num estudo independente e maior (N = 5 191). Neste estudo, após correção pelo número de sondas testadas, não foi detetada uma associação significativa entre a variante e os níveis de mRNA do IL6R. A sonda para a qual a associação foi mais forte é complementar à região 3’UTR (P = 0.0031); o alelo rs12083537:A que aumenta os níveis de sIL-6R esteve associado com uma redução dos níveis de transcrito do IL6R. Por fim, como o alelo rs2228145:C aumenta não só os níveis de sIL-6R mas também o risco de asma, testámos a hipótese de o rs12083537 também ser um fator genético de risco para a asma. A associação entre esta variante e asma foi testada em 47 514 indivíduos de três estudos independentes, dos quais 16 705 eram asmáticos diagnosticados por um médico. O alelo rs12083537:A foi detetado com mais frequência em asmáticos do que nao-asmáticos nos três estudos individuais, sendo a associação global entre o rs12083537 e o risco de asma fraca mas estatisticamente significativa (OR = 1.039, 95% I.C. = 1.002 – 1.078, P = 0.0419). A variante rs12083537 localizada no intrão 1 do IL6R, a 2.9 kb do exão 1, revelou estar significativamente associada com os níveis de sIL-6R independentemente da variante rs4129267, e a associação foi confirmada quando replicámos a análise. A variante localiza-se numa região do gene que, em pelo menos quatro linhas celulares, incluindo fibroblastos pulmonares e queratinócitos, tem elevado grau de metilação (H3K4Me1). Este tipo de modificação de histonas está associada a enhancers e promotores, sendo portanto plausível que o rs12083537 influencie a transcrição do IL6R. No entanto, não foi detetada associação significativa entre o rs12083537 e os níveis de mRNA do IL6R, pelo que o mecanismo de ação da variante permanece por elucidar. Também verificámos que o alelo rs4129267:T, que aumenta os níveis de sIL-6R, está associado a baixos níveis de mRNA do IL6R. As medições para as quais se verificou esta associação foram feitas com uma sonda que se liga ao exão 9, o qual pode ser removido por splicing alternativo. Assim, as medições em causa correspondem apenas aos níveis de mRNA que não sofreu splicing. Tendo em conta que o alelo rs4129267:T está associado a um aumento do splicing do exão 9, é portanto de esperar que os níveis da isoforma que não sofreu splicing diminuam na presença deste alelo. Por fim, verificámos que a variante rs12083537 está significativamente associada com o risco de asma. Com base na nossa análise, cada alelo rs12083537:A aumenta os níveis serológicos de sIL-6R cerca de 2.4 vezes e o risco de asma1.04 vezes. Em conclusão, este estudo demonstra que pelo menos duas variantes genéticas influenciam os níveis serológicos de sIL-6R. Como tal, estudos de resposta clínica ao tocilizumab, um anticorpo monoclonal para o IL-6R já aprovado para o tratamento da artrite reumatoide, devem avaliar a contribuição das diversas variantes que regulam os níveis de sIL-6R. Pontuações de risco genético cumulativo poderão ser úteis para explicar variabilidade na respostas clínica ao tocilizumab.
O principal determinante genético dos níveis de IL-6R solúvel é a variante rs2228145, que se encontra no local de corte da proteína IL-6R. Por cada alelo Ala, os níveis de sIL-6R aumentam por ~20 ng/ml e o risco de asma aumenta 1.09 vezes. No entanto, esta variante não explica a totalidade da componente hereditária dos níveis de sIL-6R. É portanto possível que outras variantes no gene IL6R também contribuam para variações nos níveis de sIL-6R e influenciem o risco de asma. Para testar esta hipótese, imputámos 471 variantes comuns no IL6R e testámos a sua associação com os níveis serológicos de sIL-6R em 360 indivíduos. Uma variante intrónica (rs12083537) apresentou associação com os níveis de sIL-6R independentemente da variante rs4129267 (P = 0.0005). Observámos uma associação significativa e consistente ao replicar o estudo em 354 indivíduos (P = 0.033). Cada cópia do alelo rs12083537:A aumentou os níveis de sIL-6R em 2.4 ng/ml. Na análise dos níveis de mRNA em dois estudos independentes não foram identificadas associações significativas entre a variante rs12083537 e os níveis de transcrição do IL6R. Por outro lado, o alelo rs12083537:A aumentou o risco de asma 1.04 vezes (P = 0.0419) na análise de 16 705 asmáticos e 30 908 controlos. Pontuações de risco genético poderão portanto ser úteis para explicar variabilidade na resposta clínica ao tocilizumab, um anticorpo monoclonal contra o IL-6R.
Chagani, Tabassum. "Apoptosis and expression of Fas (CD95) and Fas ligand (CD95L) in the airways of severe asthma subjects." Thesis, 2001. http://hdl.handle.net/2429/11659.
Повний текст джерелаJin, C., CP Shelburne, G. Li, EN Potts, KJ Riebe, GD Sempowski, WM Foster, and SN Abraham. "Particulate allergens potentiate allergic asthma in mice through sustained IgE-mediated mast cell activation." Thesis, 2011. http://hdl.handle.net/10161/2358.
Повний текст джерелаDissertation
Wang, Chien-Neng, and 王建能. "Study on Shikonin and Brazilin Inhibited Mitogens Induced Th2 Cytokines Expression in Vitro and Airway Inflammation and Hyperresponsiveness in a Murine Model of Asthma." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/20408005427422609396.
Повний текст джерела中國醫藥大學
基礎醫學研究所
98
Asthma patients has dramatically increased during the past decade years. Medicines for asthma such as inhaled corticosteroid, anti-histamine or anti-leukotriene, can rescue the late phase symptom but reappear without taking. Inhalation of corticosteroid showed side effects. Therefore, it needs to develop the drug of asthma. Shikonin and brazilin are two components of Chinese herbal medicines, isolated from Lithospermum erythrorhizon and Caesalpinia sappatin L. Shikonin has been reported to treat macular eruption, measles, sore-throat and burns and brazilin has been used to treat chronic intestinal inflammation, amenorrhea and Enterorrhagia. We choose shikonin and brazilin to investigate the therapeutic effects on allergic asthma in vitro and in vivo. EL4 T cell treated with different doses of shikonin(0.003 μM, 0.01 μM, 0.03 μM, 0.1 μM, 0.3μM)and brazilin(0.1 μM, 0.3 μM, 1 μM, 10 μM, 30 μM)combined with PMA and cAMP to induce T helper 2 (TH2) cytokines release. We analyzed T helper 2 (TH2) cytokines by ELISA and transcription factors mRNA expression by real-time PCR. We also investigated the therapeutic effects of shikonin and brazilin in a murine asthma model. We found that different doses of shikonin and brazilin have no cytotoxicity by trypan-blue exclusion and could dose-dependently reduce TH2 cytokines (IL-4, IL-5) expression and GATA-3 and c-Maf expression. We also found that shikonin and brazilin could inhibit TH2-specific transcription factors mRNA but not TH1 transcription factor (T-bet) mRNA. Shikonin and brazilin inhibited antigen–induced bronchial alveolar fluid (BALF) IL-4, IL-5 and eotaxin expression, reduced eosinophils cells infiltration in BALF and lungs, and airway hyperresoseiveness(AHR). Our study suggested that shikonin can effectively suppressed TH2 cytokines release in vitro and inhibited allergic inflammation and airway hyperresponsiveness in a murine model of asthma. Key words: shikonin, brazilin, type II T helper cell, allergic asthma.