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You searched for +publisher:"University of Adelaide" +contributor:("Lester, Susan"). Showing records 1 – 2 of 2 total matches.

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University of Adelaide

1. Lau, Aden Ho Yin. An immunological perspective of the mucosal inflammation in chronic rhinosinusitis – lymphoid neo-organogenesis and humoral immunity.

Degree: 2018, University of Adelaide

Chronic rhinosinusitis (CRS) is defined by the symptomatic inflammation of the nose and paranasal sinuses longer than 12 weeks. These symptoms include nasal discharge, nasal obstruction, facial pain and pressure, leading to a substantial impact on the quality of life of CRS patients. CRS can be phenotypically classified into either CRS without nasal polyps (CRSsNP) or CRS with nasal polyps (CRSwNP), based on the presence of endoscopically visualized nasal polyps in the middle meatus. Interestingly, ectopic accumulations of lymphoid cells are often observed within the nasal polyps of CRSwNP. This raises the question as to whether these aberrant lymphoid cell aggregates play a role in orchestrating the perpetual inflammation in CRS. Studies in the past have identified the increased amount of local class-switched antibodies in nasal polyps, but few studies have investigated the source of these immunoglobulins and utilized specific markers to study the presence of the organized lymphoid structures and their relation to disease severity in the context of CRS. This thesis investigates the significance of organized lymphoid neo-organogenesis in CRS pathogenesis and its effect on humoral immunity within both CRSsNP and CRSwNP patients. Advisors/Committee Members: Vreugde, Sarah (advisor), Lester, Susan (advisor), Rischmueller, Maureen (advisor), School of Medicine (school).

Subjects/Keywords: Research by publication; CRS; inflammation; immunology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Lau, A. H. Y. (2018). An immunological perspective of the mucosal inflammation in chronic rhinosinusitis – lymphoid neo-organogenesis and humoral immunity. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/115371

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Lau, Aden Ho Yin. “An immunological perspective of the mucosal inflammation in chronic rhinosinusitis – lymphoid neo-organogenesis and humoral immunity.” 2018. Thesis, University of Adelaide. Accessed August 22, 2019. http://hdl.handle.net/2440/115371.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Lau, Aden Ho Yin. “An immunological perspective of the mucosal inflammation in chronic rhinosinusitis – lymphoid neo-organogenesis and humoral immunity.” 2018. Web. 22 Aug 2019.

Vancouver:

Lau AHY. An immunological perspective of the mucosal inflammation in chronic rhinosinusitis – lymphoid neo-organogenesis and humoral immunity. [Internet] [Thesis]. University of Adelaide; 2018. [cited 2019 Aug 22]. Available from: http://hdl.handle.net/2440/115371.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lau AHY. An immunological perspective of the mucosal inflammation in chronic rhinosinusitis – lymphoid neo-organogenesis and humoral immunity. [Thesis]. University of Adelaide; 2018. Available from: http://hdl.handle.net/2440/115371

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. Roscioli, Eugene. Inhibitor of apoptosis proteins as regulatory factors in the normal and inflamed airways.

Degree: 2014, University of Adelaide

Asthma is potentiated by complex gene-environment interactions, and characterised by inflammation and degenerative changes to the conducting airways. Current therapeutics targeting the inflammation and bronchoconstriction are restricted to prophylactic effects. The airway epithelium is known to participate in the pathogenesis of asthma, and represents a therapeutic target. Airway epithelial cells (AEC) from asthmatics exhibit apoptotic changes, which correlate with disease-associated factors presented by the epithelium. However, the mechanisms which cause the apoptosis are not well defined. In particular, there has been little study of the role of the family of Inhibitor of Apoptosis Proteins (IAPs) in models of AEC apoptosis. The over-arching hypothesis in this thesis is that anomalies in one or more of the IAPs contribute to inflammation-induced AE apoptosis in asthma. Experiments in this thesis explored the role of XIAP, cIAP1 and cIAP2 in asthma, models of asthma-related inflammation, and genetic susceptibility to asthma. The major methods used in these experiments included cell culture of primary AEC from both asthmatics and controls with/without treatment with IFNγ and TNFα. siRNA knockdown, qPCR, western blotting, immunocytochemistry, functional caspase assays, and genotyping. The major findings of this study are i) surprisingly, primary AECs do not undergo apoptosis after prolonged exposure to the proinflammatory cytokines IFNγ and TNFα ex vivo; ii) rather, IFNγ elicits a proapoptotic state in AECs, evidenced by, partial processing of procaspase-3, the absence of Poly (ADP-ribose) polymerase (PARP) cleavage, an increased Bax:Bcl2 transcript ratio, and the absence of morphological changes associated with apoptosis; iii) both XIAP and cIAP1 were constitutively expressed in AEC, and protein levels were unaffected by cytokine treatment. In contrast cIAP2, initially weakly expressed, was strongly inducible by cytokine treatment; iv) No differences were observed between AEC from asthmatics and controls in terms of either basal IAP gene expression levels or their response to cytokine treatment; v) siRNA-mediated depletion of cIAP2- transcripts allows AEC to progress into apoptosis after extended culture, conditions which also resulted in a decrease in both cIAP1 and Bcl2; vi) genetic polymorphism in the genes encoding, XIAP cIAP1 and cIAP2 do not associate with susceptibility for asthma. However, cIAP1 polymorphism may modulate disease severity within asthmatics. This thesis contributes to the knowledge of IAPs and apoptosis in asthma, and provides evidence that they are important for sustaining AEC survival, and participate within a cooperative of endogenous regulators of apoptosis. There is no evidence of intrinsic dysregulation of IAPs in asthma, yet cIAP1 polymorphism may modulate asthma severity, and IAPs are central in maintaining a proapoptotic state in AECs exposed to asthma related cytokines. Epithelial activation and damage, coupled with non-progression to apoptosis may contribute to fragility of the AE… Advisors/Committee Members: Zalewski, Peter Ernest (advisor), Lester, Susan (advisor), Ruffin, Richard Ernest (advisor), School of Medicine (school).

Subjects/Keywords: apoptosis; asthma; IAP; epithelial; inflammation

…institution without the prior approval of the University of Adelaide and where applicable, any… …recipient ($24,000) for The University of Adelaide postgraduate certificate in… 

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Roscioli, E. (2014). Inhibitor of apoptosis proteins as regulatory factors in the normal and inflamed airways. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/90337

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Roscioli, Eugene. “Inhibitor of apoptosis proteins as regulatory factors in the normal and inflamed airways.” 2014. Thesis, University of Adelaide. Accessed August 22, 2019. http://hdl.handle.net/2440/90337.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Roscioli, Eugene. “Inhibitor of apoptosis proteins as regulatory factors in the normal and inflamed airways.” 2014. Web. 22 Aug 2019.

Vancouver:

Roscioli E. Inhibitor of apoptosis proteins as regulatory factors in the normal and inflamed airways. [Internet] [Thesis]. University of Adelaide; 2014. [cited 2019 Aug 22]. Available from: http://hdl.handle.net/2440/90337.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Roscioli E. Inhibitor of apoptosis proteins as regulatory factors in the normal and inflamed airways. [Thesis]. University of Adelaide; 2014. Available from: http://hdl.handle.net/2440/90337

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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