subject:(Inflammatory bowel disease)

1. TIGHE, DONAL. Optimal use of immunomodulator and biological therapy in Inflammatory Bowel Disease.

Degree: School of Medicine. Discipline of Clinical Medicine, 2017, Trinity College Dublin

► Loss of response (LOR) to anti-TNFa therapy is a significant problem, and leads to increased hospitalisation rates, surgical intervention, and steroid dependency. Loss of response… (more)

▼ Loss of response (LOR) to anti-TNFa therapy is a significant problem, and leads to increased hospitalisation rates, surgical intervention, and steroid dependency. Loss of response is multifactorial. However there is an increasing awareness that immunogenicity has a significant role to play in this process. Immunogenicity against anti-TNFa leads to antibody formation. Antibodies against anti-TNFa lead to faster drug clearance, as well as blocking drug activity. This culminates in a reduction in anti-TNFa trough levels and loss of response. Therapeutic drug monitoring (TDM) allows anti-TNFa trough and antibody levels, to be measured and doses adjusted or treatment switched, to help overcome loss of response and improve outcomes. This thesis aimed to explore the impact of loss of response to anti-TNFa, and accurately identify predictors of loss of response. In addition to investigate the role of therapeutic drug monitoring, in assessing and overcoming loss of response. The main laboratory aspect of this thesis concerned the use of ELISA techniques, to accurately measure anti-TNFa trough and antibody levels. In brief a sandwich ELISA technique was used to detect anti-TNFa trough (infliximab & adalimumab) and antibody levels. ELISA microplates were coated with human TNFa. Horse radish peroxidise conjugated goat anti-human IgG Fc fragment antibody was added to serum samples, followed by diluted antibody. Substrate Solution tetramethylbenzidine (TMB) was added to each well, followed by the addition of stop solution. Drug concentrations in serum samples were determined using a standard curve generated from absorbance readings of infliximab or adalimumab. One arm of this thesis looked at a retrospective cohort study, which confirmed the impact of loss of response to anti-TNFa therapy, with an overall LOR rate of 42.5% for a cohort on maintenance treatment one year after commencing therapy. In addition this iv retrospective cohort study identified a number of key predictors of LOR, such as smoking, prior anti-TNFa therapy, as well as the protective benefits of combination therapy. Furthermore the link with biochemical response was confirmed, with a CRP <5 mg/L at the end of induction therapy being a significant predictor of clinical response. The potential and usefulness of TDM was also explored in further detail. A retrospective study looked at the role of role of measuring anti-TNFa trough and antibody levels in a stand-alone fashion. Analysis did not identify a relationship, but there was evidence that patients with low trough levels, and loss of response, had higher biochemical markers of disease activity. Therefore further work was undertaken to establish a role for TDM at the key time-points of end of induction therapy, and during an assessment for secondary loss of response. A prospective study looked at the role of TDM during induction therapy. There was a clear link between higher anti-TNFa trough levels at the end of induction with clinical response rates. For infliximab, mean trough levels in responders were… Advisors/Committee Members: McNamara, Deirdre.

Subjects/Keywords: Inflammatory Bowel Disease

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APA (6^th Edition):

TIGHE, D. (2017). Optimal use of immunomodulator and biological therapy in Inflammatory Bowel Disease. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/81873

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

Chicago Manual of Style (16^th Edition):

TIGHE, DONAL. “Optimal use of immunomodulator and biological therapy in Inflammatory Bowel Disease.” 2017. Thesis, Trinity College Dublin. Accessed November 17, 2019. http://hdl.handle.net/2262/81873.

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

MLA Handbook (7^th Edition):

TIGHE, DONAL. “Optimal use of immunomodulator and biological therapy in Inflammatory Bowel Disease.” 2017. Web. 17 Nov 2019.

Vancouver:

TIGHE D. Optimal use of immunomodulator and biological therapy in Inflammatory Bowel Disease. [Internet] [Thesis]. Trinity College Dublin; 2017. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/2262/81873.

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

Council of Science Editors:

TIGHE D. Optimal use of immunomodulator and biological therapy in Inflammatory Bowel Disease. [Thesis]. Trinity College Dublin; 2017. Available from: http://hdl.handle.net/2262/81873

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

University of Georgia

2. Knight, Eva Bonney Reed. Adherence in pediatric Inflammatory Bowel Disease: the role of child and family factors.

Degree: MS, Psychology, 2010, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/knight_eva_b_201005_ms

► Objective: To examine correlates and predictors of adolescent and parent reported adherence to prescription and over-the-counter (OTC) medications in a pediatric Inflammatory Bowel Disease sample… (more)

Subjects/Keywords: Adherence; Inflammatory Bowel Disease; Adolescence

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APA (6^th Edition):

Knight, E. B. R. (2010). Adherence in pediatric Inflammatory Bowel Disease: the role of child and family factors. (Masters Thesis). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/knight_eva_b_201005_ms

Chicago Manual of Style (16^th Edition):

Knight, Eva Bonney Reed. “Adherence in pediatric Inflammatory Bowel Disease: the role of child and family factors.” 2010. Masters Thesis, University of Georgia. Accessed November 17, 2019. http://purl.galileo.usg.edu/uga_etd/knight_eva_b_201005_ms.

MLA Handbook (7^th Edition):

Knight, Eva Bonney Reed. “Adherence in pediatric Inflammatory Bowel Disease: the role of child and family factors.” 2010. Web. 17 Nov 2019.

Vancouver:

Knight EBR. Adherence in pediatric Inflammatory Bowel Disease: the role of child and family factors. [Internet] [Masters thesis]. University of Georgia; 2010. [cited 2019 Nov 17]. Available from: http://purl.galileo.usg.edu/uga_etd/knight_eva_b_201005_ms.

Council of Science Editors:

Knight EBR. Adherence in pediatric Inflammatory Bowel Disease: the role of child and family factors. [Masters Thesis]. University of Georgia; 2010. Available from: http://purl.galileo.usg.edu/uga_etd/knight_eva_b_201005_ms

Penn State University

3. BANERJEE, SANJITA. MEPRIN METALLOPROTEASES MODULATE INTESTINAL HOST RESPONSE.

Degree: PhD, Biochemistry and Molecular Biology, 2008, Penn State University

URL: https://etda.libraries.psu.edu/catalog/8216

► Meprins, zinc metalloproteases of the astacin family, are composed of two independently expressed subunits meprin alpha and beta which associate to form homo and heter-oligomers,… (more)

▼ Meprins, zinc metalloproteases of the astacin family, are composed of two independently expressed subunits meprin alpha and beta which associate to form homo and heter-oligomers, termed meprin A and B. Meprin isoforms are enriched in human as well as rodent intestine. They have also been reported in kidney, leukocytes, lung and skin. Considerable research has been conducted regarding the in vitro functions of these proteases, however the physiological roles of these proteases are unknown. Generation of meprin beta, alpha and alpha-beta knock-out mice were steps towards filling this void. This work reports the general characterization of the meprin alpha knock-out mouse and investigates the role of meprin proteases in the mouse intestine using a model of colitis. Several polymorphisms have been identified in the human meprin alpha gene that significantly correlate with ulcerative colitis and Crohn’s disease, which make this mouse model relevant to the human pathology. Human and rodent intestines have high but non-uniform meprin expression and hence allow one to study the contributions of different meprin isoforms. To understand the role of meprin A, colitis was induced in wild-type and meprin alpha knock-out mice by dextran sulfate sodium administration. Meprin alpha knock-out mice showed greater susceptibility to injury and had a phenotype of heightened inflammation as evidenced by different markers of inflammation at macroscopic as well as molecular level. Further investigations showed a role for mucosal meprin A in the process of tissue repair. To understand the phenotype of increased inflammation, meprin interaction with immune-mediators was studied at greater detail. This led to the first known documentation of an in vivo interaction of meprins with an immune-mediator, interleukin–18. Subsequent experiments using meprin alpha-beta knock-out mice elucidated the contribution of meprin B in the phenotype in this model of inflammatory bowel disease. These experiments collectively demonstrated a novel function of meprins in immuno-modulation. This thesis furthers our knowledge about the roles of meprin metalloproteases in the rodent intestine and also elucidates the importance of proper distribution of meprin isoforms.

Subjects/Keywords: MEPRIN; INFLAMMATORY BOWEL DISEASE

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APA (6^th Edition):

BANERJEE, S. (2008). MEPRIN METALLOPROTEASES MODULATE INTESTINAL HOST RESPONSE. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/8216

Chicago Manual of Style (16^th Edition):

BANERJEE, SANJITA. “MEPRIN METALLOPROTEASES MODULATE INTESTINAL HOST RESPONSE.” 2008. Doctoral Dissertation, Penn State University. Accessed November 17, 2019. https://etda.libraries.psu.edu/catalog/8216.

MLA Handbook (7^th Edition):

BANERJEE, SANJITA. “MEPRIN METALLOPROTEASES MODULATE INTESTINAL HOST RESPONSE.” 2008. Web. 17 Nov 2019.

Vancouver:

BANERJEE S. MEPRIN METALLOPROTEASES MODULATE INTESTINAL HOST RESPONSE. [Internet] [Doctoral dissertation]. Penn State University; 2008. [cited 2019 Nov 17]. Available from: https://etda.libraries.psu.edu/catalog/8216.

Council of Science Editors:

BANERJEE S. MEPRIN METALLOPROTEASES MODULATE INTESTINAL HOST RESPONSE. [Doctoral Dissertation]. Penn State University; 2008. Available from: https://etda.libraries.psu.edu/catalog/8216

Cornell University

4. Craven, Melanie. Comparative Analysis Of Host-Bacterial Interactions In The Gastrointestinal Tract .

Degree: 2011, Cornell University

URL: http://hdl.handle.net/1813/33572

► Technological advances in culture-independent methods using high throughput DNA sequencing have revolutionized our understanding of gastrointestinal (GI) microbiology. Our ability to now characterize the intestinal… (more)

▼ Technological advances in culture-independent methods using high throughput DNA sequencing have revolutionized our understanding of gastrointestinal (GI) microbiology. Our ability to now characterize the intestinal microbiome (IM) in incredible depth affords insight into the dynamic interrelationships of bacteria with the other pathomechanisms underlying inflammatory bowel diseases (IBD), i.e. genetics, immune dysregulation, and environmental triggers. This work explores these complex interactions in a murine model of Crohn‟s Disease (CD) and canine IBD. In C57BL/6 mice, we reveal that T. gondii and indomethacin-induced ileitis induce a microbial shift termed „dysbiosis,‟ comprising reduced microbial diversity and a global shift from >95% Gram+ (Firmicutes) to >95% Gramspecies (Proteobacteria), which recapitulates the IM of ileal CD. Gramproliferation also appears permissive to intramucosal invasion by the emerging pathogen, Adherent Invasive E. coli (AIEC). By manipulating genetic susceptibility to CD (NOD2-/-) and severity of ileitis (CCR2-/- and anti-TNF[alpha]mAb), we show that dysbiosis is the common end-point of acute ileitis, driven by inflammation rather than genotype or trigger. We postulate that failure to reverse dysbiosis stimulates chronic microbial-driven inflammation in CD. Unlike other GI pathology, e.g. Helicobacter-induced gastric ulceration, the evidence for a specific pathogen in CD is controversial, though growing evidence implicates AIEC. Pathogenicity of AIEC is highlighted by their firm association with Granulomatous colitis (GC) of Boxer dogs. We strengthen the evidence for a direct causal relationship by documenting intramucosally invasive E. coli in 17 GC cases. Further, GC remission correlates with E. coli sensitivity to enrofloxacin, whereas antimicrobial-resistant E. coli are associated with poor outcome. By genome-wide association study, we uncover for the first time parallels between GC and the colitis of human Chronic Granulomatous Disease (CGD), pointing to a potential role for AIEC in CGD pathogenesis. In idiopathic canine IBD, we demonstrate dysbiosis characterized by Bacteroidales depletion and increased Gram- diversity. We highlight potentially distinguishing features of the IM in IBD that warrant further evaluation as potential predictors of treatment response. In protein-losing enteropathy of Yorkshire Terriers, we document a severe, often fatal IBD, associated with sterile, multifocal crypt abscesses. Since we uncover no evidence of a bacterial etiology, we conclude that a familial morphogenetic disorder may be responsible. Advisors/Committee Members: Denkers, Eric Young (committeeMember), McDonough, Sean P (committeeMember).

Subjects/Keywords: Dysbiosis; inflammatory bowel disease

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APA (6^th Edition):

Craven, M. (2011). Comparative Analysis Of Host-Bacterial Interactions In The Gastrointestinal Tract . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/33572

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

Chicago Manual of Style (16^th Edition):

Craven, Melanie. “Comparative Analysis Of Host-Bacterial Interactions In The Gastrointestinal Tract .” 2011. Thesis, Cornell University. Accessed November 17, 2019. http://hdl.handle.net/1813/33572.

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

MLA Handbook (7^th Edition):

Craven, Melanie. “Comparative Analysis Of Host-Bacterial Interactions In The Gastrointestinal Tract .” 2011. Web. 17 Nov 2019.

Vancouver:

Craven M. Comparative Analysis Of Host-Bacterial Interactions In The Gastrointestinal Tract . [Internet] [Thesis]. Cornell University; 2011. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1813/33572.

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

Council of Science Editors:

Craven M. Comparative Analysis Of Host-Bacterial Interactions In The Gastrointestinal Tract . [Thesis]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/33572

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

University of Manitoba

5. Chaity, Nazia. Genetics And Disease Associations Of Organic Cation Transporters With IBD – Special Emphasis On Genetic And Functional Studies Of SLC22A23.

Degree: Human Nutritional Sciences, 2015, University of Manitoba

URL: http://hdl.handle.net/1993/30788

► Inflammatory bowel disease (IBD) is a chronic disease which steadily increases worldwide with the highest prevalence in Canada. Genetic susceptibility is considered to be an… (more)

Subjects/Keywords: IBD- Inflammatory Bowel Disease; SLC22A23

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APA (6^th Edition):

Chaity, N. (2015). Genetics And Disease Associations Of Organic Cation Transporters With IBD – Special Emphasis On Genetic And Functional Studies Of SLC22A23. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/30788

Chicago Manual of Style (16^th Edition):

Chaity, Nazia. “Genetics And Disease Associations Of Organic Cation Transporters With IBD – Special Emphasis On Genetic And Functional Studies Of SLC22A23.” 2015. Masters Thesis, University of Manitoba. Accessed November 17, 2019. http://hdl.handle.net/1993/30788.

MLA Handbook (7^th Edition):

Chaity, Nazia. “Genetics And Disease Associations Of Organic Cation Transporters With IBD – Special Emphasis On Genetic And Functional Studies Of SLC22A23.” 2015. Web. 17 Nov 2019.

Vancouver:

Chaity N. Genetics And Disease Associations Of Organic Cation Transporters With IBD – Special Emphasis On Genetic And Functional Studies Of SLC22A23. [Internet] [Masters thesis]. University of Manitoba; 2015. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1993/30788.

Council of Science Editors:

Chaity N. Genetics And Disease Associations Of Organic Cation Transporters With IBD – Special Emphasis On Genetic And Functional Studies Of SLC22A23. [Masters Thesis]. University of Manitoba; 2015. Available from: http://hdl.handle.net/1993/30788

University of New South Wales

6. Corte, Crispin. Improving the utility of colonoscopy in colorectal neoplasia and inflammatory bowel disease.

Degree: Clinical School - South Western Sydney, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55311 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37103/SOURCE02?view=true

► Background: Colorectal cancer is a common and commonly lethal disease. Colonoscopy is the gold standard for detection of colorectal cancer (CRC) and its precursor lesions,… (more)

▼ Background: Colorectal cancer is a common and commonly lethal disease. Colonoscopy is the gold standard for detection of colorectal cancer (CRC) and its precursor lesions, as well as for evaluation of colonic mucosa for diagnosis and assessment of inflammatory bowel disease (IBD). Australia has amongst the highest rates of colonsocopy per capita of any country. The utility of colonoscopy can be improved in a number of areas.This thesis examines a number of facets of colonoscopy to improve utility; improved methods of triage of colonoscopy, improving polyp detection using pharmacological methods, improving accuracy in assessing IBD during colonoscopy and minimising complications and physical harm at colonoscopy. Methods: Numerous studies were undertaken. A prospective cohort study including 645 patients was used to examine the Asia Pacific Colorectal Screening Score (APCS) in triage of colonoscopy. A randomized double blind placebo controlled trial including 608 patients was used to examine hyoscine butylbromide induced spasmolysis to improve polyp detection at colonoscopy. A retrospective cohort study was used to examine 93 patients with acute severe colitis (ASC) and the ulcerative colitis endoscopic index of severity (UCEIS) to correlate this with treatment outcomes. A meta-analysis was undertaken of previous studies of prophylactic measures to reduce post polypectomy haemorrhage (PPH). Results: The APCS is highly predictive of significant colonoscopic findings (RR 17.1 (95% CI 2.4-123; p=0.0001), and being underweight was protective of similar findings (OR 0.085, 0.011-0.625; p=0.015). Polyp detection was significantly improved (0.91 vs 0.70, p=0.044) by administering hyoscine butylbromide. UCEIS was correlated with outcomes of ASC and was highly predictive of the need for rescue therapy with biologic agents, colectomy and readmission (UCEIS 5 (3-8) vs 4 (3-7); p=0.0035). Meta-analysis demonstrated significant reductions in PPH with prophylactic measures, and an associate cost-benefit analysis confirmed cost saving with prophylaxis (RR for PPH with adrenaline vs placebo 0.28 (0.14-0.57, p<0.0001), NNT 12.3, cost to prevent one PPH USD1368.)Conclusion: Numerous advances can now be recommended to improve the utility, triage, appropriate use, accuracy of reporting, yield of pathology, and prevention of complications. These measures would serve to make colonoscopy a safer, more cost effective and more useful diagnostic and therapeutic tool. Advisors/Committee Members: Leong, Rupert, Clinical School - South Western Sydney, Faculty of Medicine, UNSW, Selby, Warwick, University of Sydney - Central Clinical School.

Subjects/Keywords: Gastroenterology; Inflammatory Bowel Disease; Colonoscopy

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APA (6^th Edition):

Corte, C. (2015). Improving the utility of colonoscopy in colorectal neoplasia and inflammatory bowel disease. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55311 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37103/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Corte, Crispin. “Improving the utility of colonoscopy in colorectal neoplasia and inflammatory bowel disease.” 2015. Doctoral Dissertation, University of New South Wales. Accessed November 17, 2019. http://handle.unsw.edu.au/1959.4/55311 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37103/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Corte, Crispin. “Improving the utility of colonoscopy in colorectal neoplasia and inflammatory bowel disease.” 2015. Web. 17 Nov 2019.

Vancouver:

Corte C. Improving the utility of colonoscopy in colorectal neoplasia and inflammatory bowel disease. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2019 Nov 17]. Available from: http://handle.unsw.edu.au/1959.4/55311 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37103/SOURCE02?view=true.

Council of Science Editors:

Corte C. Improving the utility of colonoscopy in colorectal neoplasia and inflammatory bowel disease. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55311 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:37103/SOURCE02?view=true

University of New South Wales

7. Lee, Hoyul. Elucidation of enteric virulence of Campylobacter concisus.

Degree: Biotechnology & Biomolecular Sciences, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55659 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38333/SOURCE02?view=true

► Campylobacter concisus is a Gram-negative mobile oral bacterium that has been shown to be associatedwith human inflammatory bowel disease. Various experiments were conducted in this… (more)

▼ Campylobacter concisus is a Gram-negative mobile oral bacterium that has been shown to be associatedwith human inflammatory bowel disease. Various experiments were conducted in this PhD project, aiming toelucidate the enteric virulence of C. concisus.The growth of oral C. concisus strains under different atmospheric conditions was examined. It was foundthat 92 % of strains grew under anaerobic conditions without H2. However, none of the strains grew undermicroaerobic conditions without H2. The presence H2 greatly increased the growth of C. concisus underanaerobic conditions and enabled C. concisus to grow under microaerobic conditions. The H2 had no effectson the expression of a number of putative virulence factors in C. concisus.The effects of formate and fumarate, on the production of H2S in oral C. concisus were investigated.Supplementation of formate and fumarate significantly increased the positivity of H2S production. Inaddition, the fumarate significantly increased C. concisus growth.Bioinformatics analysis was conducted to search for potential virulence factors encoded by prophages.Four prophage elements were identified in the genome of C. concisus strain 13826 with putative attachmentsites overlapping with tRNA. Each prophage elements contained a novel Xer phage integrase. It was foundthat CON_phi2 prophage encodes a Zot protein, and CON_phi3 encodes a Zot-like protein. Moreover, thephylogenetic analysis showed the horizontal gene transfer between Campylobacter species.Monoclonal antibody to C. concisus Zot was produced and verified. The impact of bile on the expressionof Zot was examined. It was found that a full length and a cleaved fragment of Zot were released from C.concisus in the presence of ox bile.Whether C. concisus strains affect actin in the intestinal epithelial cell line, Caco2 cells, was examined.Some C. concisus strains significantly reduced the levels of β-actin and caused the redistribution of F-actin inCaco2 cells.These findings show that the enteric virulence of C. concisus is determined by bacterial, host andenvironmental factors. Advisors/Committee Members: Zhang, Li, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.

Subjects/Keywords: Campylobacter concisus; Inflammatory bowel disease

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APA (6^th Edition):

Lee, H. (2015). Elucidation of enteric virulence of Campylobacter concisus. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55659 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38333/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Lee, Hoyul. “Elucidation of enteric virulence of Campylobacter concisus.” 2015. Doctoral Dissertation, University of New South Wales. Accessed November 17, 2019. http://handle.unsw.edu.au/1959.4/55659 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38333/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Lee, Hoyul. “Elucidation of enteric virulence of Campylobacter concisus.” 2015. Web. 17 Nov 2019.

Vancouver:

Lee H. Elucidation of enteric virulence of Campylobacter concisus. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2019 Nov 17]. Available from: http://handle.unsw.edu.au/1959.4/55659 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38333/SOURCE02?view=true.

Council of Science Editors:

Lee H. Elucidation of enteric virulence of Campylobacter concisus. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55659 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38333/SOURCE02?view=true

University of Toronto

8. Rahman, Adam. Self-screening for malnutrition risk in outpatient inflammatory bowel disease patients using the Malnutrition Universal Screening Tool.

Degree: 2016, University of Toronto

URL: http://hdl.handle.net/1807/79606

►

Background: Malnutrition is under-recognized in patients with inflammatory bowel disease (IBD). Aims To determine if patient can self-screen nutritional risk using the Malnutrition Universal Screening… (more)

Subjects/Keywords: Inflammatory Bowel Disease; Malnutrition; 0566

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APA (6^th Edition):

Rahman, A. (2016). Self-screening for malnutrition risk in outpatient inflammatory bowel disease patients using the Malnutrition Universal Screening Tool. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/79606

Chicago Manual of Style (16^th Edition):

Rahman, Adam. “Self-screening for malnutrition risk in outpatient inflammatory bowel disease patients using the Malnutrition Universal Screening Tool.” 2016. Masters Thesis, University of Toronto. Accessed November 17, 2019. http://hdl.handle.net/1807/79606.

MLA Handbook (7^th Edition):

Rahman, Adam. “Self-screening for malnutrition risk in outpatient inflammatory bowel disease patients using the Malnutrition Universal Screening Tool.” 2016. Web. 17 Nov 2019.

Vancouver:

Rahman A. Self-screening for malnutrition risk in outpatient inflammatory bowel disease patients using the Malnutrition Universal Screening Tool. [Internet] [Masters thesis]. University of Toronto; 2016. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1807/79606.

Council of Science Editors:

Rahman A. Self-screening for malnutrition risk in outpatient inflammatory bowel disease patients using the Malnutrition Universal Screening Tool. [Masters Thesis]. University of Toronto; 2016. Available from: http://hdl.handle.net/1807/79606

University of Guelph

9. Strauss, Jaclyn. Investigating a role for Fusobacterium nucleatum in Inflammatory Bowel Disease .

Degree: 2011, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/2965

► Inflammatory Bowel Disease (IBD) is an umbrella term used to describe a group of chronic, relapsing/remitting disorders of the gastrointestinal tract (GIT). While the precise… (more)

Subjects/Keywords: Fusobacterium nucleatum; Inflammatory Bowel Disease

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APA (6^th Edition):

Strauss, J. (2011). Investigating a role for Fusobacterium nucleatum in Inflammatory Bowel Disease . (Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/2965

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

Chicago Manual of Style (16^th Edition):

Strauss, Jaclyn. “Investigating a role for Fusobacterium nucleatum in Inflammatory Bowel Disease .” 2011. Thesis, University of Guelph. Accessed November 17, 2019. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/2965.

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

MLA Handbook (7^th Edition):

Strauss, Jaclyn. “Investigating a role for Fusobacterium nucleatum in Inflammatory Bowel Disease .” 2011. Web. 17 Nov 2019.

Vancouver:

Strauss J. Investigating a role for Fusobacterium nucleatum in Inflammatory Bowel Disease . [Internet] [Thesis]. University of Guelph; 2011. [cited 2019 Nov 17]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/2965.

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

Council of Science Editors:

Strauss J. Investigating a role for Fusobacterium nucleatum in Inflammatory Bowel Disease . [Thesis]. University of Guelph; 2011. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/2965

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

Queens University

10. Diener, Jessica Ann. Everyone poops but no one wants to talk about it: The lived experiences of young people with inflammatory bowel disease .

Degree: Kinesiology and Health Studies, 2011, Queens University

URL: http://hdl.handle.net/1974/6638

► Crohn’s disease and Colitis, the two most common Inflammatory Bowel Diseases (IBD), are on the rise among young people. IBD symptoms include severe abdominal pain… (more)

▼ Crohn’s disease and Colitis, the two most common Inflammatory Bowel Diseases (IBD), are on the rise among young people. IBD symptoms include severe abdominal pain and frequent bowel movements, which can result in major dietary restrictions and delays in growth. IBD can also limit people’s physical activity, eating habits, and activities that are distant from a bathroom. Having IBD can be both limiting and embarrassing but little research has investigated the social and emotional implications of these diseases from a qualitative approach. Existing research fails to identify how stigma and dominant IBD discourses affect the lived experiences of people with IBD, young people in particular. IBD can create additional challenges for adolescents because it is perceived to threaten their normal development into healthy adults. The purpose of this project is to investigate how being young complicates the already difficult experience of being ill. I conducted interviews with three young people and a discursive analysis of official IBD resources for adolescents and found almost no descriptions of the actual experience of illness. Participants who engaged in photo-elicited interviews minimized the physical and emotional repercussions of having IBD. Informational resources designed for youth failed to address the severe physical and emotional pain of Crohn’s and Colitis. Instead, the available resources provided saccharine and arguably unrealistic depictions of IBD that deny young people a forum to express their own struggles. I compare my analysis of the interviews and IBD resources with my own experience and experiences presented in a zine. Analysis of both the interviews and the IBD resources reveals that young people with IBD can experience an embodied disappearance. Their bodies are smaller and weak, they retreat from social situations to avoid embarrassment, and their emotions are denied because they have no forums to be expressive. Finally, young people can experience a compounded disappearance because they are treated not for who they are but for what they should become. I argue that enabling young people the opportunity to speak candidly about the social conditions that contribute to their struggles could help them better understand, negotiate, and express their illness experiences

Subjects/Keywords: Youth; Inflammatory Bowel Disease

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APA (6^th Edition):

Diener, J. A. (2011). Everyone poops but no one wants to talk about it: The lived experiences of young people with inflammatory bowel disease . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/6638

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

Chicago Manual of Style (16^th Edition):

Diener, Jessica Ann. “Everyone poops but no one wants to talk about it: The lived experiences of young people with inflammatory bowel disease .” 2011. Thesis, Queens University. Accessed November 17, 2019. http://hdl.handle.net/1974/6638.

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

MLA Handbook (7^th Edition):

Diener, Jessica Ann. “Everyone poops but no one wants to talk about it: The lived experiences of young people with inflammatory bowel disease .” 2011. Web. 17 Nov 2019.

Vancouver:

Diener JA. Everyone poops but no one wants to talk about it: The lived experiences of young people with inflammatory bowel disease . [Internet] [Thesis]. Queens University; 2011. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1974/6638.

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

Council of Science Editors:

Diener JA. Everyone poops but no one wants to talk about it: The lived experiences of young people with inflammatory bowel disease . [Thesis]. Queens University; 2011. Available from: http://hdl.handle.net/1974/6638

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

University of Alberta

11. El-Matary, Wael. Celiac disease in children with inflammatory bowel disease: a prospective cohort study.

Degree: MS, School Public Health Sciences, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/r781wg113

► The aim of this work was to examine any possible IBD activity-related variations in immunoglobulin A (IgA) anti-tissue transglutaminase (tTG) levels in children with IBD.… (more)

Subjects/Keywords: children; inflammatory bowel disease; celiac disease

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APA (6^th Edition):

El-Matary, W. (2012). Celiac disease in children with inflammatory bowel disease: a prospective cohort study. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/r781wg113

Chicago Manual of Style (16^th Edition):

El-Matary, Wael. “Celiac disease in children with inflammatory bowel disease: a prospective cohort study.” 2012. Masters Thesis, University of Alberta. Accessed November 17, 2019. https://era.library.ualberta.ca/files/r781wg113.

MLA Handbook (7^th Edition):

El-Matary, Wael. “Celiac disease in children with inflammatory bowel disease: a prospective cohort study.” 2012. Web. 17 Nov 2019.

Vancouver:

El-Matary W. Celiac disease in children with inflammatory bowel disease: a prospective cohort study. [Internet] [Masters thesis]. University of Alberta; 2012. [cited 2019 Nov 17]. Available from: https://era.library.ualberta.ca/files/r781wg113.

Council of Science Editors:

El-Matary W. Celiac disease in children with inflammatory bowel disease: a prospective cohort study. [Masters Thesis]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/r781wg113

University of Georgia

12. Gil, Armande. Repressive adaptive style, disease severity, and psychological functioning of adolescents with inflammatory bowel diseases.

Degree: PhD, Educational Psychology, 2006, University of Georgia

URL: http://purl.galileo.usg.edu/uga_etd/gil_armande_200608_phd

► The impact of a repressive adaptive style on disease status, self-reports of psychological functioning, self-reports of quality of life, and disease severity indices was examined… (more)

Subjects/Keywords: Inflammatory Bowel Disease

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APA (6^th Edition):

Gil, A. (2006). Repressive adaptive style, disease severity, and psychological functioning of adolescents with inflammatory bowel diseases. (Doctoral Dissertation). University of Georgia. Retrieved from http://purl.galileo.usg.edu/uga_etd/gil_armande_200608_phd

Chicago Manual of Style (16^th Edition):

Gil, Armande. “Repressive adaptive style, disease severity, and psychological functioning of adolescents with inflammatory bowel diseases.” 2006. Doctoral Dissertation, University of Georgia. Accessed November 17, 2019. http://purl.galileo.usg.edu/uga_etd/gil_armande_200608_phd.

MLA Handbook (7^th Edition):

Gil, Armande. “Repressive adaptive style, disease severity, and psychological functioning of adolescents with inflammatory bowel diseases.” 2006. Web. 17 Nov 2019.

Vancouver:

Gil A. Repressive adaptive style, disease severity, and psychological functioning of adolescents with inflammatory bowel diseases. [Internet] [Doctoral dissertation]. University of Georgia; 2006. [cited 2019 Nov 17]. Available from: http://purl.galileo.usg.edu/uga_etd/gil_armande_200608_phd.

Council of Science Editors:

Gil A. Repressive adaptive style, disease severity, and psychological functioning of adolescents with inflammatory bowel diseases. [Doctoral Dissertation]. University of Georgia; 2006. Available from: http://purl.galileo.usg.edu/uga_etd/gil_armande_200608_phd

Texas A&M University

13. Heilmann, Romy Monika. Evaluation of Canine S100A12 and sRAGE as Novel Disease.

Degree: 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/155105

► Inflammatory bowel disease (IBD) is a common condition in dogs that is challenging to diagnose. A dysregulated innate immunity plays a major role in its… (more)

▼ Inflammatory bowel disease (IBD) is a common condition in dogs that is challenging to diagnose. A dysregulated innate immunity plays a major role in its pathogenesis, and surrogate inflammatory markers that reflect disease severity would be clinically useful. S100A12, a damage-associated molecular pattern molecule, is involved in phagocyte activation. S100A12 binds to the receptor of advanced glycation end products (RAGE), a pattern-recognition receptor, and results in human studies suggest a role of S100A12 and RAGE in chronic inflammation. Soluble RAGE (sRAGE), a decoy receptor, functions as an anti-inflammatory molecule. S100A12 and RAGE/sRAGE have not been studied in canine IBD. Canine S100A12 has not been purified, and while an immunoassay for measurement of S100A12 in humans is available, human antibodies do not cross-react with canine S100A12 (cS100A12). Canine RAGE has been cloned and characterized. The aims of this project were to purify and partially characterize cS100A12, to develop and analytically validate an immunoassay for cS100A12, and to determine the relationship between cS100A12 and systemic sRAGE concentrations and clinical, endoscopic, and histologic disease severity in dogs with IBD. Markers of gastrointestinal inflammation were also evaluated in dogs with acute hemorrhagic diarrhea syndrome (AHDS). Canine S100A12 was successfully purified from canine whole blood, and a competitive liquid-phase radioimmunoassay was developed and analytically validated. Fecal cS100A12 concentrations were shown to be increased in dogs with IBD and were associated with clinical disease activity, the severity of endoscopic lesions, and the severity of colonic inflammation. Serum sRAGE concentrations were decreased in dogs with IBD, but were not correlated with disease severity, cS100A12 concentrations, or outcome. Dogs that were euthanized had higher fecal cS100A12 concentrations than dogs that were alive at the end of the study, and serum sRAGE concentrations increased only in IBD dogs with complete clinical remission. A significant but transient increase in fecal cS100A12 was also seen in dogs with AHDS. Fecal cS100A12 may be clinically useful as a biomarker of inflammation in dogs with IBD, and the sRAGE/RAGE axis appears to be altered in canine IBD. Lack of correlation between sRAGE and cS100A12 is consistent with sRAGE being a non-specific decoy receptor. Advisors/Committee Members: Steiner, J?rg M (advisor), Suchodolski, Jan S (advisor), Pool, Roy (committee member), Jergens, Albert E (committee member), Allenspach, Karin (committee member).

Subjects/Keywords: S100A12; sRAGE; calgranulin; canine; inflammatory bowel disease

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APA (6^th Edition):

Heilmann, R. M. (2015). Evaluation of Canine S100A12 and sRAGE as Novel Disease. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/155105

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

Chicago Manual of Style (16^th Edition):

Heilmann, Romy Monika. “Evaluation of Canine S100A12 and sRAGE as Novel Disease.” 2015. Thesis, Texas A&M University. Accessed November 17, 2019. http://hdl.handle.net/1969.1/155105.

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

MLA Handbook (7^th Edition):

Heilmann, Romy Monika. “Evaluation of Canine S100A12 and sRAGE as Novel Disease.” 2015. Web. 17 Nov 2019.

Vancouver:

Heilmann RM. Evaluation of Canine S100A12 and sRAGE as Novel Disease. [Internet] [Thesis]. Texas A&M University; 2015. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1969.1/155105.

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

Council of Science Editors:

Heilmann RM. Evaluation of Canine S100A12 and sRAGE as Novel Disease. [Thesis]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/155105

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

University of Cincinnati

14. Ciresi, Michael R. Relationship between Dietary Intake of Fatty Acids and Disease Activity in Pediatric Inflammatory Bowel Disease Patients.

Degree: MS, Allied Health Sciences: Nutrition, 2012, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1328201550

► Background. Crohn'¿¿¿¿¿¿¿s disease (CD) and ulcerative colitis (UC), collectively known as inflammatory bowel disease (IBD), are chronic illnesses that affect predominately the gastrointestinal tract. The… (more)

▼ Background. Crohn'¿¿¿¿¿¿¿s disease (CD) and ulcerative colitis (UC), collectively known as inflammatory bowel disease (IBD), are chronic illnesses that affect predominately the gastrointestinal tract. The pathogenesis and etiology remain unclear but the importance of environmental factors, in particular diet, is evidenced by the increased incidence rates of the recent decades that genetic inheritance cannot account for. In particular, the quantity of fatty acid consumption has been consistently linked with IBD risk. While several studies have investigated the connections between diet, etiology, signs and symptoms associated with IBD, very few have explored the relationship between disease state and specific fatty acid intake in the pediatric IBD population. Methods. In this cross-sectional study, 100 pediatric patients from Cincinnati Children's Hospital and the Hospital for Sick Children in Toronto with diagnosed IBD (73 with Crohn's disease (CD) and 27 with ulcerative colitis (UC)) were included. Three-day diet records were collected from the patients for the assessment of their dietary intake. The abbreviated Pediatric Crohn's Disease Activity Index (PCDAI), the abbreviated Ulcerative Colitis Activity Index (PUCAI), and markers of inflammation (lipopolysaccharide binding protein (LBP) and S100A12) were used to assess disease severity. A logistic regression analysis was carried out to correlate disease severity with the dietary intake of specific fatty acids and total dietary intake. Results.Total caloric, saturated fat (SFA), and monounsaturated fat (MUFA) intake were negatively associated (p<0.05) with PCDAI scores in CD alone. The individual SFAs butyric, caproic, caprylic, capric, lauric, myristic, palmitic, margaric, and stearic also were also negatively associated with disease activity scores in CD group. However, no significant associations were observed between the major types of fatty acids and markers of inflammation. Margaric acid was the only fatty acid significantly associated (p<0.05) with the markers of inflammation, as it was positively correlated with S100A12. Discussion. Our analysis indicates that both total fatty acid intake and total caloric intake were inversely associated with disease activity. A change in habitual dietary intake is the most likely explanation for this negatively associated trend. Relapsed patients consumed significantly lesser amounts of fatty acids and calories than patients who were in remission. The importance of this relationship should not be disregarded since pediatric IBD patients are at a high risk for growth failure, delayed puberty, anemia, osteoporosis, and other medical conditions. This study adds reason for the importance of follow-ups with nutrition professionals and gastroenterologists during remission and active states in order for pediatric IBD patients to maintain a healthy nutritional status. Advisors/Committee Members: Falciglia, Graciela (Committee Chair).

Subjects/Keywords: Nutrition; Inflammatory bowel disease; Saturated fat

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APA (6^th Edition):

Ciresi, M. R. (2012). Relationship between Dietary Intake of Fatty Acids and Disease Activity in Pediatric Inflammatory Bowel Disease Patients. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1328201550

Chicago Manual of Style (16^th Edition):

Ciresi, Michael R. “Relationship between Dietary Intake of Fatty Acids and Disease Activity in Pediatric Inflammatory Bowel Disease Patients.” 2012. Masters Thesis, University of Cincinnati. Accessed November 17, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1328201550.

MLA Handbook (7^th Edition):

Ciresi, Michael R. “Relationship between Dietary Intake of Fatty Acids and Disease Activity in Pediatric Inflammatory Bowel Disease Patients.” 2012. Web. 17 Nov 2019.

Vancouver:

Ciresi MR. Relationship between Dietary Intake of Fatty Acids and Disease Activity in Pediatric Inflammatory Bowel Disease Patients. [Internet] [Masters thesis]. University of Cincinnati; 2012. [cited 2019 Nov 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1328201550.

Council of Science Editors:

Ciresi MR. Relationship between Dietary Intake of Fatty Acids and Disease Activity in Pediatric Inflammatory Bowel Disease Patients. [Masters Thesis]. University of Cincinnati; 2012. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1328201550

University of Edinburgh

15. Limbergen, Johan Emiel van. Identification of novel genetic determinants in the high prevalence early-onset inflammatory bowel disease population in Scotland.

Degree: PhD, 2010, University of Edinburgh

URL: http://hdl.handle.net/1842/4470

► Background & aims: The inflammatory bowel diseases (IBD), Crohn‟s disease (CD) and ulcerative colitis (UC), are common causes of chronic gastrointestinal morbidity, affecting up to… (more)

▼ Background & aims: The inflammatory bowel diseases (IBD), Crohn‟s disease (CD) and ulcerative colitis (UC), are common causes of chronic gastrointestinal morbidity, affecting up to 1 in 250 of the general population in Northern Europe. Up to 25% of IBD is diagnosed during childhood or adolescence. The aims for this thesis were to study the epidemiology, natural history and novel genetic determinants of childhood onset IBD in Scotland. Methods: The existing repository of childhood onset and adult onset IBD patients, established at the Western General Hospital in Edinburgh, was used and expanded. Thus, anatomical location and behaviour of disease were assessed in 416 childhood onset (276 CD, 99 UC, 41 IBDU diagnosed before 17th birthday) and 1297 adult patients (596 CD, 701 UC) using the Montreal classification. Additional phenotypic (at diagnosis and at regular follow-up intervals) and epidemiological data were gathered. In this cohort, genotyping of germline variants in putative susceptibility genes (NOD1/CARD4, IL23R, ATG16L1, IRGM, FLG) was performed to enable single variant and haplotype-tagging association studies. Genotypic data of population-matched healthy controls were obtained locally (n=342) and from the Wellcome Trust Case Control Consortium (n=2937). Results: Compared with adults, childhood-onset CD was characterized by a more extensive, “panenteric” phenotype (ileocolonic plus upper GI; p<0.0001 OR23.3; 95% CI (13.4–40.6) with less isolated ileal (p<0.0001 OR 0.06 (0.03–0.1) or colonic disease (p<0.0001, OR 0.3 (0.2–0.5)). In 39%, the anatomic extent increased within 2 years. UC was also more extensive in children at diagnosis vs adults (p<0.0001 OR 5.1 (2.7–9.4)). In population-matched and age, sex and postcode-matched case-control analysis, childhood onset IBD and CD was associated with asthma (p<0.0001 OR 1.7 (1.3-2.1) and (p=0.005 OR 2.5 (1.3-4.8), respectively). Inherited variation of NOD1/CARD4 was not a strong determinant of disease susceptibility in the Scottish population (both in single marker and haplotype-tagging studies, all p>0.05 after Bonferroni correction). We found that the allelic frequency of rs11209026*A located within the IL23R gene, differed significantly between IBD/CD cases and controls (p=0.01 OR 0.51(0.3-0.9) and p=0.04 OR 0.5 (0.3-0.98)). Using a gene-wide haplotype-tagging strategy, we demonstrated that the multiple association signals of the IL23R locus are independent of rs11209026 in childhood onset IBD and CD. In Scottish children, the effect of germline variation of ATG16L1 and IRGM on CD susceptibility was relatively small (OR< 1.4), and appeared less than in adult disease. Genotype–phenotype analysis demonstrated an association of pure ileal disease with the ATG16L1 rs2241880G-allele (p=0.02 OR 1.3 (1.03–1.7)). Using binary logistic regression analysis, we confirmed the effect of rs2241880 genotype (GG) on ileal disease versus colonic disease (p=0.03 OR 2.4 (1.05–5.6)). Null alleles of the epithelial barrier protein FLG have no important effect on IBD susceptibility…

Subjects/Keywords: 616.042; genetics; pediatric gastroenterology; inflammatory bowel disease

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APA (6^th Edition):

Limbergen, J. E. v. (2010). Identification of novel genetic determinants in the high prevalence early-onset inflammatory bowel disease population in Scotland. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/4470

Chicago Manual of Style (16^th Edition):

Limbergen, Johan Emiel van. “Identification of novel genetic determinants in the high prevalence early-onset inflammatory bowel disease population in Scotland.” 2010. Doctoral Dissertation, University of Edinburgh. Accessed November 17, 2019. http://hdl.handle.net/1842/4470.

MLA Handbook (7^th Edition):

Limbergen, Johan Emiel van. “Identification of novel genetic determinants in the high prevalence early-onset inflammatory bowel disease population in Scotland.” 2010. Web. 17 Nov 2019.

Vancouver:

Limbergen JEv. Identification of novel genetic determinants in the high prevalence early-onset inflammatory bowel disease population in Scotland. [Internet] [Doctoral dissertation]. University of Edinburgh; 2010. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1842/4470.

Council of Science Editors:

Limbergen JEv. Identification of novel genetic determinants in the high prevalence early-onset inflammatory bowel disease population in Scotland. [Doctoral Dissertation]. University of Edinburgh; 2010. Available from: http://hdl.handle.net/1842/4470

University of Edinburgh

16. Phillips, Anne Mairead. Investigation of the phenotypic and genotypic determinants of disease susceptibility and progression in Crohn's Disease.

Degree: PhD, 2011, University of Edinburgh

URL: http://hdl.handle.net/1842/9473

► The inflammatory bowel diseases (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the gastrointestinal tract. Their aetiology is not… (more)

Subjects/Keywords: 616.3; Crohn's disease; inflammatory bowel diseases

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APA (6^th Edition):

Phillips, A. M. (2011). Investigation of the phenotypic and genotypic determinants of disease susceptibility and progression in Crohn's Disease. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/9473

Chicago Manual of Style (16^th Edition):

Phillips, Anne Mairead. “Investigation of the phenotypic and genotypic determinants of disease susceptibility and progression in Crohn's Disease.” 2011. Doctoral Dissertation, University of Edinburgh. Accessed November 17, 2019. http://hdl.handle.net/1842/9473.

MLA Handbook (7^th Edition):

Phillips, Anne Mairead. “Investigation of the phenotypic and genotypic determinants of disease susceptibility and progression in Crohn's Disease.” 2011. Web. 17 Nov 2019.

Vancouver:

Phillips AM. Investigation of the phenotypic and genotypic determinants of disease susceptibility and progression in Crohn's Disease. [Internet] [Doctoral dissertation]. University of Edinburgh; 2011. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1842/9473.

Council of Science Editors:

Phillips AM. Investigation of the phenotypic and genotypic determinants of disease susceptibility and progression in Crohn's Disease. [Doctoral Dissertation]. University of Edinburgh; 2011. Available from: http://hdl.handle.net/1842/9473

Case Western Reserve University

17. Meisch, Jeffrey P. Human ß-defensin 3 peptide is increased and redistributed in Crohn’s ileitis.

Degree: MSs, Pathology, 2010, Case Western Reserve University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=case1270735950

► Epithelial cell-derived antimicrobial peptides (AMPs) maintain a sterile environment in intestinal crypts, limiting colonization and invasion of commensal microbiota. Decreases in AMP expression are proposed… (more)

Subjects/Keywords: Inflammatory Bowel Disease; antimicrobial peptides, hBD-3

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APA (6^th Edition):

Meisch, J. P. (2010). Human ß-defensin 3 peptide is increased and redistributed in Crohn’s ileitis. (Masters Thesis). Case Western Reserve University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=case1270735950

Chicago Manual of Style (16^th Edition):

Meisch, Jeffrey P. “Human ß-defensin 3 peptide is increased and redistributed in Crohn’s ileitis.” 2010. Masters Thesis, Case Western Reserve University. Accessed November 17, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1270735950.

MLA Handbook (7^th Edition):

Meisch, Jeffrey P. “Human ß-defensin 3 peptide is increased and redistributed in Crohn’s ileitis.” 2010. Web. 17 Nov 2019.

Vancouver:

Meisch JP. Human ß-defensin 3 peptide is increased and redistributed in Crohn’s ileitis. [Internet] [Masters thesis]. Case Western Reserve University; 2010. [cited 2019 Nov 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1270735950.

Council of Science Editors:

Meisch JP. Human ß-defensin 3 peptide is increased and redistributed in Crohn’s ileitis. [Masters Thesis]. Case Western Reserve University; 2010. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=case1270735950

University of Cincinnati

18. Minar, Phillip. Validation of Neutrophil CD64 Blood Biomarkers to Detect Mucosal Inflammation in Pediatric Crohn’s Disease.

Degree: MS, Medicine: Clinical and Translational Research, 2017, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1515508268721564

► Background: In a pilot study, neutrophil CD64 surface expression was significantly elevated in newly diagnosed, pediatric-onset Crohn’s disease. We aimed to test the CD64 biomarkers… (more)

Subjects/Keywords: Surgery; pediatrics; inflammatory bowel disease; biomarkers; CD64

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APA (6^th Edition):

Minar, P. (2017). Validation of Neutrophil CD64 Blood Biomarkers to Detect Mucosal Inflammation in Pediatric Crohn’s Disease. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1515508268721564

Chicago Manual of Style (16^th Edition):

Minar, Phillip. “Validation of Neutrophil CD64 Blood Biomarkers to Detect Mucosal Inflammation in Pediatric Crohn’s Disease.” 2017. Masters Thesis, University of Cincinnati. Accessed November 17, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1515508268721564.

MLA Handbook (7^th Edition):

Minar, Phillip. “Validation of Neutrophil CD64 Blood Biomarkers to Detect Mucosal Inflammation in Pediatric Crohn’s Disease.” 2017. Web. 17 Nov 2019.

Vancouver:

Minar P. Validation of Neutrophil CD64 Blood Biomarkers to Detect Mucosal Inflammation in Pediatric Crohn’s Disease. [Internet] [Masters thesis]. University of Cincinnati; 2017. [cited 2019 Nov 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1515508268721564.

Council of Science Editors:

Minar P. Validation of Neutrophil CD64 Blood Biomarkers to Detect Mucosal Inflammation in Pediatric Crohn’s Disease. [Masters Thesis]. University of Cincinnati; 2017. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1515508268721564

University of Debrecen

19. Njikam Chamna, Laurence. Pharmacological treatment of inflammatory bowel disease .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/218641

► Pharmacological therapy of inflammatory bowel disease with their potential side effect. Supportive therapy and surgical treatment methods.Epidemiology , etiology and pathogenesis. Complication in pregnant women.… (more)

Subjects/Keywords: Inflammatory bowel disease

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APA (6^th Edition):

Njikam Chamna, L. (n.d.). Pharmacological treatment of inflammatory bowel disease . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/218641

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Njikam Chamna, Laurence. “Pharmacological treatment of inflammatory bowel disease .” Thesis, University of Debrecen. Accessed November 17, 2019. http://hdl.handle.net/2437/218641.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Njikam Chamna, Laurence. “Pharmacological treatment of inflammatory bowel disease .” Web. 17 Nov 2019.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Njikam Chamna L. Pharmacological treatment of inflammatory bowel disease . [Internet] [Thesis]. University of Debrecen; [cited 2019 Nov 17]. Available from: http://hdl.handle.net/2437/218641.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Njikam Chamna L. Pharmacological treatment of inflammatory bowel disease . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/218641

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Debrecen

20. Hatlestad, Maren Rytilahti. Biological Therapy In Inflammatory Bowel Disease .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/229598

► Inflammatory bowel disease (IBD) represents a group of chronic disorders of the gastrointestinal tract, subdivided into Crohns disease (CD) and ulcerative colitis (UC). Although the… (more)

Subjects/Keywords: inflammatory bowel disease

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APA (6^th Edition):

Hatlestad, M. R. (n.d.). Biological Therapy In Inflammatory Bowel Disease . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/229598

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hatlestad, Maren Rytilahti. “Biological Therapy In Inflammatory Bowel Disease .” Thesis, University of Debrecen. Accessed November 17, 2019. http://hdl.handle.net/2437/229598.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hatlestad, Maren Rytilahti. “Biological Therapy In Inflammatory Bowel Disease .” Web. 17 Nov 2019.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Hatlestad MR. Biological Therapy In Inflammatory Bowel Disease . [Internet] [Thesis]. University of Debrecen; [cited 2019 Nov 17]. Available from: http://hdl.handle.net/2437/229598.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Hatlestad MR. Biological Therapy In Inflammatory Bowel Disease . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/229598

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Debrecen

21. Srour, Nicolas Nihad. Pharmacotherapy of inflammatoy bowel disease .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/233624

► this thesis deals with the pharmacological therapy of Crohn's disease and Ulcerative colitis , explaining the main pathological findings and the corresponding treatment , the… (more)

Subjects/Keywords: inflammatory bowel disease

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

APA (6^th Edition):

Srour, N. N. (n.d.). Pharmacotherapy of inflammatoy bowel disease . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/233624

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Srour, Nicolas Nihad. “Pharmacotherapy of inflammatoy bowel disease .” Thesis, University of Debrecen. Accessed November 17, 2019. http://hdl.handle.net/2437/233624.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Srour, Nicolas Nihad. “Pharmacotherapy of inflammatoy bowel disease .” Web. 17 Nov 2019.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Srour NN. Pharmacotherapy of inflammatoy bowel disease . [Internet] [Thesis]. University of Debrecen; [cited 2019 Nov 17]. Available from: http://hdl.handle.net/2437/233624.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Srour NN. Pharmacotherapy of inflammatoy bowel disease . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/233624

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Ottawa

22. Deeke, Shelley. Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease .

Degree: 2019, University of Ottawa

URL: http://hdl.handle.net/10393/38660

► Background: Reliable biomarkers are needed to evade the risk of injury, invasiveness and discomfort of endoscopies, which are required for inflammatory bowel disease (IBD) diagnosis… (more)

▼ Background: Reliable biomarkers are needed to evade the risk of injury, invasiveness and discomfort of endoscopies, which are required for inflammatory bowel disease (IBD) diagnosis and extent of disease assessment in ulcerative colitis (UC) patients. The need for biomarkers is accentuated in children, wherein the most frequently used IBD biomarker yields low specificity. Proteomics of clinical samples or their enriched components is a means to evaluate and identify alterations in proteins reflective of disease, with the potential for use as biomarkers and for providing insight on disease pathogenesis. Methods: Proteins were isolated from the intestinal mucosal-luminal interface (MLI), collected from the ascending and descending colon of pediatric treatment-naive patients. The intestinal MLI proteomes of 42 IBD and 18 control patients were analyzed by high resolution mass spectrometry (HRMS). Multivariate analysis and receiver operating characteristics curves were performed to develop protein biomarker panels to discriminate IBD from control, and for UC extent of disease. ELISAs were used to assess a subset of biomarker candidates in stool samples from an independent pediatric cohort (n=24). Extracellular vesicles (EVs) were isolated by ultracentrifugation from the intestinal MLI of 11 IBD and seven control patients, and analyzed by electron microscopy, nanoparticle tracking analysis and HRMS. Results: A biomarker panel of four proteins classified patients as either controls or active IBD with 97.5% accuracy. A second biomarker panel correctly classified 100% of UC patients as presenting with pancolitis or non-pancolitis. The differential protein expression of two biomarker candidates (catalase and leukotriene A-4 hydrolase) identified from the intestinal MLI was comparable in stool samples. Comparison of EV proteomes isolated from IBD patients and controls identified differential expression of processes related to host defense and immunity. Conclusions: Proteomic analysis of clinical samples identified differentially expressed proteins that can classify IBD patients from non-IBD controls and distinguish UC patients with pancolitis from those without pancolitis; proteins identified in intestinal aspirates displayed consistent differential expression in stool. Furthermore enrichment of EVs from the intestinal MLI indicates that these may contribute to the dysregulated host response against the intestinal microbiota which is observed in IBD.

Subjects/Keywords: Biomarkers; Proteomics; Inflammatory bowel disease; ulcerative colitis

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APA (6^th Edition):

Deeke, S. (2019). Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/38660

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

Chicago Manual of Style (16^th Edition):

Deeke, Shelley. “Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease .” 2019. Thesis, University of Ottawa. Accessed November 17, 2019. http://hdl.handle.net/10393/38660.

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

MLA Handbook (7^th Edition):

Deeke, Shelley. “Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease .” 2019. Web. 17 Nov 2019.

Vancouver:

Deeke S. Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease . [Internet] [Thesis]. University of Ottawa; 2019. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/10393/38660.

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

Council of Science Editors:

Deeke S. Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease . [Thesis]. University of Ottawa; 2019. Available from: http://hdl.handle.net/10393/38660

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

University of Tasmania

23. Basheer, WF. Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model.

Degree: 2018, University of Tasmania

URL: https://eprints.utas.edu.au/28689/1/Basheer_whole_thesis.pdf ; Basheer, WF ORCID: 0000-0002-7403-0398 <https://orcid.org/0000-0002-7403-0398> 2018 , 'Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model', PhD thesis, University of Tasmania.

► Inflammatory bowel disease (IBD) is an immunological imbalance of the gut, characterised by chronic inflammation involving the mucosal lining of the colon. IBD presents in… (more)

▼ Inflammatory bowel disease (IBD) is an immunological imbalance of the gut, characterised by chronic inflammation involving the mucosal lining of the colon. IBD presents in two forms: Crohn’s disease (CD) and ulcerative colitis (UC). The increasing global incidence of IBD has necessitated a better understanding of the underlying mechanism of disease progression, and while its aetiology remains obscure, current literature suggests that both genetic susceptibility and environmental aspects have an influence on the course of IBD. Murine models have led to a number of discoveries in IBD pathogenesis. Amongst the many mouse models developed, the Winnie mouse model of colitis closely resembles the condition of human colitis in terms of both symptoms and immunology. A number of studies have reported that Winnie mice are a preclinical resource for better understanding IBD pathogenesis. An emerging mechanism for the pathogenicity of IBD development includes a dysregulated chemokine system. In particular, the CCR6-CCL20 axis has been implicated due to its major role in regulating T cell homeostasis in the intestine. The current literature regarding CCR6-CCL20 is inconclusive as to the exact role of CCR6. The aim of this study was to introduce CCR6 deficiency in the Winnie spontaneous colitis model in order to further elucidate the functional role of CCR6 in colitis and characterise clinical, histopathological and immunological changes. In this present study, the hypothesis was that the genetic ablation of the Ccr6 gene would exacerbate intestinal inflammation. Winnie mice were backcrossed with Ccr6(^-/-) mice to generate Winnie mice with a Ccr6 deficiency. Winnie x Ccr6(^-/-) mice developed normally and did not have any developmental abnormalities. At around 8–12 weeks of age, the Winnie x Ccr6(^-/-) mice were clinically assessed, and no significant differences were noted between Winnie and Winnie x Ccr6(^-/-) mice with regard to body weight. There was, however, a significant increase in the colon weight/body weight ratio (±0.026 mg/g), with Winnie x Ccr6(^-/-) mice revealing a significant increase in colon weight by body weight ratio compared to control mice (WT and Ccr6(^-/-) mice) of a similar magnitude to the expected Winnie-only phenotype. Histopathological examination of proximal and distal colonic sections showed no obvious inflammatory changes in the control mice (WT grade-0 and Ccr6(^-/-) grade-0). Winnie mice demonstrated the expected amount of inflammation in the distal colonic segment (grade-6). Surprisingly, there was a differential distribution of inflammation in Winnie x Ccr6(^-/-) mice, where the proximal colon revealed significant inflammation (grade-8) while there was mild inflammation (grade-4) in the distal colon. Immuno-phenotyping of splenocytes and colonic lymphocytes did not reveal any significant changes in the functions of T regulatory cells. To identify the differential regulation in Winnie x Ccr6(^-/-) mice, we cultured ex…

Subjects/Keywords: role; Chemokine receptor; inflammatory bowel disease

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APA (6^th Edition):

Basheer, W. (2018). Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/28689/1/Basheer_whole_thesis.pdf ; Basheer, WF ORCID: 0000-0002-7403-0398 <https://orcid.org/0000-0002-7403-0398> 2018 , 'Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model', PhD thesis, University of Tasmania.

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

Chicago Manual of Style (16^th Edition):

Basheer, WF. “Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model.” 2018. Thesis, University of Tasmania. Accessed November 17, 2019. https://eprints.utas.edu.au/28689/1/Basheer_whole_thesis.pdf ; Basheer, WF ORCID: 0000-0002-7403-0398 <https://orcid.org/0000-0002-7403-0398> 2018 , 'Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model', PhD thesis, University of Tasmania..

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

MLA Handbook (7^th Edition):

Basheer, WF. “Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model.” 2018. Web. 17 Nov 2019.

Vancouver:

Basheer W. Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model. [Internet] [Thesis]. University of Tasmania; 2018. [cited 2019 Nov 17]. Available from: https://eprints.utas.edu.au/28689/1/Basheer_whole_thesis.pdf ; Basheer, WF ORCID: 0000-0002-7403-0398 <https://orcid.org/0000-0002-7403-0398> 2018 , 'Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model', PhD thesis, University of Tasmania..

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

Council of Science Editors:

Basheer W. Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model. [Thesis]. University of Tasmania; 2018. Available from: https://eprints.utas.edu.au/28689/1/Basheer_whole_thesis.pdf ; Basheer, WF ORCID: 0000-0002-7403-0398 <https://orcid.org/0000-0002-7403-0398> 2018 , 'Genetic ablation of CCR6 confers differential exacerbation in a spontaneous colitis model', PhD thesis, University of Tasmania.

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

Queen Mary, University of London

24. Sanders, Theodore James. Production of retinoic acid by antigen presenting cells in the healthy and inflamed human intestine.

Degree: PhD, 2013, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8648 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667206

► Murine small intestinal CD103+ dendritic cells (DCs) produce retinoic acid (RA) through retinaldehyde dehydrogenase (RALDH) activity, thereby inducing ‘gut-homing’ α4β7 and CCR9 on T cells… (more)

▼ Murine small intestinal CD103+ dendritic cells (DCs) produce retinoic acid (RA) through retinaldehyde dehydrogenase (RALDH) activity, thereby inducing ‘gut-homing’ α4β7 and CCR9 on T cells they activate, enhancing TGF-β-mediated induction of Foxp3+ regulatory T cells and suppressing induction of pro-inflammatory TH17 cells. RALDH activity of CD103+ DCs is reduced in mouse models of inflammatory bowel disease (IBD) but the role of RALDH activity in human intestinal DCs in the pathogenesis of IBD is undefined. This project aimed to determine the influence of inflammation on RALDH activity of antigen presenting cell (APC) subsets including CD103+ DCs within human distal intestinal mucosa. RALDH activity was identified by Aldefluor assay in intestinal DCs (CD103+ and CD103- subsets) alongside ALDH1A2 expression in healthy controls. In contrast with mouse models, RALDH activity was not reduced in CD103+ DCs from IBD patients. An increased frequency of CD14+ macrophages (MФ) of IBD patients displayed ALDH1A1-associated RALDH activity compared with healthy controls. Blood CD14+ monocytes, putative precursors of intestinal CD14+ MФ, of healthy controls and IBD patients displayed ALDH1A1-associated RALDH activity indicating RALDH is systemically acquired by monocytes and upregulated within the mucosa of IBD patients, or alternatively that RALDH+ monocytes are selectively recruited in IBD. In vitro, inhibition of RA receptor-α signalling blocked GM-CSF-mediated differentiation of TNFα-producing pro-inflammatory RALDH+ CD14+ MФ from monocytes, consistent with enhanced RALDH activity of intestinal CD14+ MФ in IBD supporting a pro-inflammatory phenotype. Soluble intestinal mediators including prostaglandin E2 suppressed RALDH activity of MoDCs in vitro, whilst mediators from inflamed IBD mucosa conditioned MoDCs to imprint enhanced levels of α4β7 expression on naive CD4+ T cells independent of RALDH activity. This study provides the first systematic analysis of RALDH activity in human intestinal APCs and indicates important distinctions between mouse models and human IBD.

Subjects/Keywords: 616.3; Medicine; Inflammatory bowel disease; Retinaldehyde dehydrogenase

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APA (6^th Edition):

Sanders, T. J. (2013). Production of retinoic acid by antigen presenting cells in the healthy and inflamed human intestine. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/8648 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667206

Chicago Manual of Style (16^th Edition):

Sanders, Theodore James. “Production of retinoic acid by antigen presenting cells in the healthy and inflamed human intestine.” 2013. Doctoral Dissertation, Queen Mary, University of London. Accessed November 17, 2019. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8648 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667206.

MLA Handbook (7^th Edition):

Sanders, Theodore James. “Production of retinoic acid by antigen presenting cells in the healthy and inflamed human intestine.” 2013. Web. 17 Nov 2019.

Vancouver:

Sanders TJ. Production of retinoic acid by antigen presenting cells in the healthy and inflamed human intestine. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2013. [cited 2019 Nov 17]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8648 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667206.

Council of Science Editors:

Sanders TJ. Production of retinoic acid by antigen presenting cells in the healthy and inflamed human intestine. [Doctoral Dissertation]. Queen Mary, University of London; 2013. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/8648 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667206

25. Wennberg, Jenny. Upplevelser och hanteringsstrategier hos ungdomar med IBD. : en litteraturstudie.

Degree: Faculty of Health and Occupational Studies, 2010, University of Gävle

URL: http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-7896

► The purpose of this study was to describe how adolescents aged 12-18 years with inflammatory bowel disease experience their illness and what coping strategies… (more)

Subjects/Keywords: Inflammatory bowel disease; adolescents; experiences; copingstrategies

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APA (6^th Edition):

Wennberg, J. (2010). Upplevelser och hanteringsstrategier hos ungdomar med IBD. : en litteraturstudie. (Thesis). University of Gävle. Retrieved from http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-7896

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

Chicago Manual of Style (16^th Edition):

Wennberg, Jenny. “Upplevelser och hanteringsstrategier hos ungdomar med IBD. : en litteraturstudie.” 2010. Thesis, University of Gävle. Accessed November 17, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-7896.

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

MLA Handbook (7^th Edition):

Wennberg, Jenny. “Upplevelser och hanteringsstrategier hos ungdomar med IBD. : en litteraturstudie.” 2010. Web. 17 Nov 2019.

Vancouver:

Wennberg J. Upplevelser och hanteringsstrategier hos ungdomar med IBD. : en litteraturstudie. [Internet] [Thesis]. University of Gävle; 2010. [cited 2019 Nov 17]. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-7896.

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

Council of Science Editors:

Wennberg J. Upplevelser och hanteringsstrategier hos ungdomar med IBD. : en litteraturstudie. [Thesis]. University of Gävle; 2010. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-7896

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

University of Melbourne

26. Iyngkaran, Guruparan. Indigenous Australians have a distinctive gut microbial profile compared to Caucasian controls and patients with inflammatory bowel disease.

Degree: 2015, University of Melbourne

URL: http://hdl.handle.net/11343/58623

► The aetiology of inflammatory bowel disease (IBD) is yet unknown but it is thought to occur in a genetically predisposed individual following an environmental trigger.… (more)

▼ The aetiology of inflammatory bowel disease (IBD) is yet unknown but it is thought to occur in a genetically predisposed individual following an environmental trigger. The incidence of IBD has risen rapidly in industrialised nations but remains low in developing countries. In Canada, the incidence of IBD is high in their urban population but extremely low in their Indigenous populations. This has led to the “hygiene hypothesis”, which postulates that a reduced exposure to antigens due to urbanisation may lead to an increase in immune mediated diseases such as IBD. Many studies have shown that patients with active IBD have changes in gut microbiota or “dysbiosis”. My first hypothesis was that IBD is rare in Indigenous Australians (IA). I confirmed this by setting up an IBD database at the Royal Darwin Hospital in the Northern Territory (NT) and by interrogating the hospital records from 2007-2014. The NT has a large Indigenous population with a third of its population being Indigenous. The IBD database revealed that the prevalence of IBD in Indigenous Australians in the NT is 5/100,000 compared to 186/100,000 in the non- Indigenous population. My second hypothesis was that IA have a distinct gut microbial profile that may account for their low incidence of IBD. I utilised 16S amplicon based techniques to study gut microbial profiles in IA, Caucasian controls and IBD patients. Whilst it is difficult to prove causality, I demonstrated that gut microbial profiles of IA are highly abundant in Prevotella sp and lactic acid producing bacteria, and are different from Caucasian controls and IBD patients. The gut microbiota of IA are also enriched in enzymes that are involved in propionate production, a food source for colonocytes. My third hypothesis was that the gut mucosa of IA would have a higher expression of anti-inflammatory cytokines. I showed, through quantitative real-time PCR, that there was a trend in increased expression of Thymic Stromal Lymphopoeitin (TSLP) in IA. TSLP is a cytokine that is involved in preventing helminthic infections and has been shown in mouse models to confer some protection to IBD. Patients with IBD showed a typical pro-inflammatory cytokine expression pattern. My results demonstrate that IA, who have a low incidence of IBD, have a distinctive gut microbial profile and a trend in increase of the cytokine TSLP. This may be directly related to their traditional lifestyle. Testing their gut microbial profiles in mouse models of colitis may reveal if their gut microbiota are truly protective against IBD.

Subjects/Keywords: inflammatory bowel disease; microbiota; indigenous; epidemiology

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

APA (6^th Edition):

Iyngkaran, G. (2015). Indigenous Australians have a distinctive gut microbial profile compared to Caucasian controls and patients with inflammatory bowel disease. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/58623

Chicago Manual of Style (16^th Edition):

Iyngkaran, Guruparan. “Indigenous Australians have a distinctive gut microbial profile compared to Caucasian controls and patients with inflammatory bowel disease.” 2015. Doctoral Dissertation, University of Melbourne. Accessed November 17, 2019. http://hdl.handle.net/11343/58623.

MLA Handbook (7^th Edition):

Iyngkaran, Guruparan. “Indigenous Australians have a distinctive gut microbial profile compared to Caucasian controls and patients with inflammatory bowel disease.” 2015. Web. 17 Nov 2019.

Vancouver:

Iyngkaran G. Indigenous Australians have a distinctive gut microbial profile compared to Caucasian controls and patients with inflammatory bowel disease. [Internet] [Doctoral dissertation]. University of Melbourne; 2015. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/11343/58623.

Council of Science Editors:

Iyngkaran G. Indigenous Australians have a distinctive gut microbial profile compared to Caucasian controls and patients with inflammatory bowel disease. [Doctoral Dissertation]. University of Melbourne; 2015. Available from: http://hdl.handle.net/11343/58623

University of New South Wales

27. Timms, Verlaine. The mycobacteriology of inflammatory bowel disease.

Degree: Biotechnology & Biomolecular Sciences, 2014, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/53780 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12479/SOURCE02?view=true

► Inflammatory bowel diseases (IBD) are chronic idiopathic diseases of the gastrointestinal tract and often strike in the prime of life, remaining a lifelong burden. The… (more)

▼ Inflammatory bowel diseases (IBD) are chronic idiopathic diseases of the gastrointestinal tract and often strike in the prime of life, remaining a lifelong burden. The increasing prevalence of the two main types of IBD, Crohn’s disease (CD) and ulcerative colitis (UC) is indicative of an environmental cause. This thesis explores the mycobacteriology of IBD with emphasis on the gut pathogen, M. avium subspecies paratuberculosis. M. paratuberculosis normally infects livestock and is difficult to detect given its genetic homology with other subspecies of the M. avium complex. In addition, its fastidious growth requirements make isolation from cattle challenging and from sheep and humans extremely difficult, adding to significant controversy as to whether it infects humans. This study demonstrated a significant association between Crohn’s disease and M. paratuberculosis using three PCR assays. Further, the first human M. paratuberculosis ever reported from a patient with UC was isolated. This isolate, 43525, was characterized microbiologically and the genome sequenced on the fourth subculture. M. paratuberculosis 43525 displayed mycobactin dependency on only certain types of media, resistance to; ethambutol, rifampin, clofazamine and streptomycin and growth at 4 °C. Given 43525 was a human isolate of what is normally an animal pathogen, the genome sequence provided an opportunity to explore the subtle differences between subspecies of the MAC that infect animals and humans. One PPE along with one PE_PGRS protein was found to be present only in human MAC strains and two PPE/PE genes were unique to 43525 and a caprine M. paratuberculosis strain. The organisation and structure of the 43525 mycobactin cluster differed to other M. paratuberculosis strains providing an explanation for the in vitro phenotype. Finally, a unique mce operon was found to be flanked by two mycobactin genes in all M. paratuberculosis strains investigated. The culture method and validated PCR assays described in this work provide new methods to detect M. paratuberculosis in humans. In addition, the unique mce operon and the PPE/PE proteins highlighted, provide possible targets for diagnostic assays, vaccine candidates or treatment. Advisors/Committee Members: Neilan, Brett, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW, Mitchell, Hazel, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.

Subjects/Keywords: Mycobacerium paratuberculosis; Mycobacteria; Inflammatory bowel disease

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APA (6^th Edition):

Timms, V. (2014). The mycobacteriology of inflammatory bowel disease. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/53780 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12479/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Timms, Verlaine. “The mycobacteriology of inflammatory bowel disease.” 2014. Doctoral Dissertation, University of New South Wales. Accessed November 17, 2019. http://handle.unsw.edu.au/1959.4/53780 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12479/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Timms, Verlaine. “The mycobacteriology of inflammatory bowel disease.” 2014. Web. 17 Nov 2019.

Vancouver:

Timms V. The mycobacteriology of inflammatory bowel disease. [Internet] [Doctoral dissertation]. University of New South Wales; 2014. [cited 2019 Nov 17]. Available from: http://handle.unsw.edu.au/1959.4/53780 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12479/SOURCE02?view=true.

Council of Science Editors:

Timms V. The mycobacteriology of inflammatory bowel disease. [Doctoral Dissertation]. University of New South Wales; 2014. Available from: http://handle.unsw.edu.au/1959.4/53780 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:12479/SOURCE02?view=true

University of New South Wales

28. Ismail, Yazan. Campylobacter concisus and its possible role in inflammatory bowel disease.

Degree: Biotechnology & Biomolecular Sciences, 2012, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/52514 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11187/SOURCE01?view=true

► Inflammatory bowel disease (IBD) is an idiopathic gastrointestinal disease that covers a group of disorders with two major types, Crohn's disease (CD) and ulcerative Colitis… (more)

▼ Inflammatory bowel disease (IBD) is an idiopathic gastrointestinal disease that covers a group of disorders with two major types, Crohn's disease (CD) and ulcerative Colitis (UC). The main characteristic of IBD is the uncontrolled inflammation of the intestines that can't be down-regulated, resulting in chronic activation of the mucosal immune system and chronic intestinal inflammation. Epidemiological studies reported in the past 50 years showed that there is dramatic increase in the incidence of IBD worldwide. Furthermore, it was found that IBD is a risk factor of colorectal cancer (CRC) which accounts for 15% of total deaths in IBD patients. The aetiology of IBD is unknown, but it is widely approved that the pathogenesis of IBD is an outcome of the interaction of multiple factors including environmental factors, immunological response dysregulation, genetic susceptibility and bacterial factors. Studies have shown that IBD arises as a result of the host immune defence response to the enteric commensal bacteria. However, what triggered the gut immune system to attack the enteric commensal bacteria, a cohort of organisms that the gut immune system has co-evolved and lived peacefully with, is still unknown. Recently, Campylobacter concisus has gained attention as an emerging human enteric pathogen and many recent studies have reported the association between C. concisus and IBD. Whereas, the role of C. concisus in the pathogenesis of IBD is still unknown, the major aim of this PhD thesis is to investigate the potential role that C. concisus plays in the pathogenesis of IBD.C. concisus is a Gram-negative curved rod; motile by means of a single polar flagellum. C. concisus was first isolated from human gingival plaque. Studies have shown that oral C. concisus is a source of intestinal colonizing C. concisus that is found in patients with IBD. In chapter 3, the prevalence of multiple (≥2) oral C. concisus strains in patients with IBD and in healthy controls was examined. A total of 288 oral C. concisus isolates were isolated from saliva samples of 15 patients with IBD (9 CD and 6 UC) and 17 healthy controls using a filtration method, C. concisus was identified by C. concisus specific PCR. Out of the 288 oral C. concisus isolates 52 different oral C. concisus strains were identified using whole protein profile. It was found that 60% (9/15) of patients with IBD were colonized with multiple oral C. concisus strains (≥ two strains), which was significantly (P < 0.05, Fisher's exact test) higher than that of the healthy controls (3/17, 18%). We then studied the adhesion and invasion properties of oral C. concisus strains to the human intestinal epithelial cell line Caco-2 using a modified gentamicin protection assay, 16 oral C. concisus strains isolated from the 9 patients with CD and 18 oral C. concisus strains isolated from 12 healthy controls were used in this study. It was found that the mean invasion index of oral C. concisus strains isolated from patients with CD (1.51±0.69) was significantly higher than… Advisors/Committee Members: Zhang, Li, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.

Subjects/Keywords: Innate Immunology; Inflammatory Bowel Disease; Campylobacter concisus

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

APA (6^th Edition):

Ismail, Y. (2012). Campylobacter concisus and its possible role in inflammatory bowel disease. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52514 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11187/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Ismail, Yazan. “Campylobacter concisus and its possible role in inflammatory bowel disease.” 2012. Doctoral Dissertation, University of New South Wales. Accessed November 17, 2019. http://handle.unsw.edu.au/1959.4/52514 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11187/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Ismail, Yazan. “Campylobacter concisus and its possible role in inflammatory bowel disease.” 2012. Web. 17 Nov 2019.

Vancouver:

Ismail Y. Campylobacter concisus and its possible role in inflammatory bowel disease. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2019 Nov 17]. Available from: http://handle.unsw.edu.au/1959.4/52514 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11187/SOURCE01?view=true.

Council of Science Editors:

Ismail Y. Campylobacter concisus and its possible role in inflammatory bowel disease. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52514 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11187/SOURCE01?view=true

University of Newcastle

29. Mateer, Sean W. Mechanism of lung inflammation associated with inflammatory bowel disease.

Degree: PhD, 2017, University of Newcastle

URL: http://hdl.handle.net/1959.13/1342488

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Research Doctorate - Doctor of Philosophy (PhD)

Inflammatory bowel disease (IBD) is associated with a number of immune-mediated pathologies in peripheral tissues, termed extra-intestinal manifestations… (more)

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Research Doctorate - Doctor of Philosophy (PhD)

Inflammatory bowel disease (IBD) is associated with a number of immune-mediated pathologies in peripheral tissues, termed extra-intestinal manifestations (EIM). The organs affected by EIM include the lung, liver, skin and eyes. IBD-induced respiratory pathologies are amongst the most prevalent comorbidities associated with IBD. Approximately 54% of IBD patients have some form of respiratory pathology. The respiratory pathologies associated with IBD range from subclinical respiratory inflammation to active respiratory disease. Bronchiectasis and chronic bronchitis are the most common respiratory diseases associated with IBD. The mechanism by which IBD can induce respiratory pathologies is unknown, this knowledge gap is partially due to a lack of basic science research in this field. Thus, the aim of this study was to utilize murine models of colitis to investigate the immunological mechanisms by which IBD can induce respiratory inflammation. In this study it was found that the DSS, TNBS and <i>Winnie</i> models of colitis develop pulmonary inflammation that is associated with leucocyte infiltration surrounding the pulmonary vasculature. Pulmonary inflammation in DSS colitis is characterised by neutrophil and monocyte recruitment to the lung. Systemic IL-6 levels were elevated in the DSS colitis model and IL-6 was identified to be a factor that contributes to neutrophil recruitment. It was found that systemic IL-6 mediates neutrophil development in the bone marrow thereby providing the cells required to perpetuate inflammation in the lung. Platelet activating factor receptor (PAFR), IL-1β and CCL2 expression were increased in the lungs of DSS colitis mice. PAFR signalling in the lung induces the expression of IL-1β and the recruitment of neutrophils, PAFR signalling did not induce CCL2 expression. It was found that immunomodulatory factors in the serum of DSS colitis induce IL-1β production and CCL2 gene expression in alveolar macrophage through PAFR signalling. The results from this study identify a number of potential pathogenic factors that may be involved in the development of IBD-induced respiratory pathologies.

Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine, School of Biomedical Sciences and Pharmacy.

Subjects/Keywords: inflammatory bowel disease; immunology; systemic inflammation; PAFR

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

APA (6^th Edition):

Mateer, S. W. (2017). Mechanism of lung inflammation associated with inflammatory bowel disease. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1342488

Chicago Manual of Style (16^th Edition):

Mateer, Sean W. “Mechanism of lung inflammation associated with inflammatory bowel disease.” 2017. Doctoral Dissertation, University of Newcastle. Accessed November 17, 2019. http://hdl.handle.net/1959.13/1342488.

MLA Handbook (7^th Edition):

Mateer, Sean W. “Mechanism of lung inflammation associated with inflammatory bowel disease.” 2017. Web. 17 Nov 2019.

Vancouver:

Mateer SW. Mechanism of lung inflammation associated with inflammatory bowel disease. [Internet] [Doctoral dissertation]. University of Newcastle; 2017. [cited 2019 Nov 17]. Available from: http://hdl.handle.net/1959.13/1342488.

Council of Science Editors:

Mateer SW. Mechanism of lung inflammation associated with inflammatory bowel disease. [Doctoral Dissertation]. University of Newcastle; 2017. Available from: http://hdl.handle.net/1959.13/1342488

University of New South Wales

30. Wang, Yiming. Investigation of GS1 and GS2 C. concisus adaptation in the human gastrointestinal tract and their effects on PD-L1 expression in human intestinal epithelial cells.

Degree: Biotechnology & Biomolecular Sciences, 2018, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/60214

► Campylobacter concisusis a Gram-negative bacterium with a singular polar flagellum and curved morphology that enables it to traverse the mucus layer and directly contact the… (more)

▼ Campylobacter concisusis a Gram-negative bacterium with a singular polar flagellum and curved morphology that enables it to traverse the mucus layer and directly contact the intestinal epithelium, providing the opportunity to trigger intestinal inflammation and facilitate the progression of inflammatory diseases to cancer. This thesis reports novel findings regarding the adaptation of different genomospecies of C. concisus to the human gastrointestinal tract and the potential for C. concisus to affect the PD-1 and PD-L1 pathway and thus the development of inflammatory-driven cancer.C. concisus was previously reported to be associated with inflammatory bowel disease (IBD). It has two genomospecies (GS) that carry distinct and specific genes, suggesting they may have different pathogenic potentials. Previous studies have found that GS2 C. concisus strains are invasive to intestinal epithelial cells, suggesting that they may contribute to the initiation of IBD. However, no clinical studies to date have demonstrated GS2 strains to be more associated with IBD. In Chapter 2, the colonization of the human gastrointestinal tract by GS1 and GS2 C. concisus is systematically examined in patients with IBD and in healthy controls. This chapter provides novel information regarding the adaptation of different genomospecies of C. concisus to the human gastrointestinal tract. Two new PCR methods were developed and validated for detecting and quantifying C. concisus strains, based on polymorphisms of the 23S rRNA gene. These PCR methods were used to evaluate GS1 and GS2 C. concisus prevalence in 56 oral and enteric samples. Quantitative PCR showed significantly higher level of GS2 C. concisus than GS1 C. concisus in samples collected from the upper and lower gastrointestinal tracts of both patients with IBD and healthy controls, indicating that GS2 C. concisus is better adapted to the human gastrointestinal tract. A meta-analysis of the compositions of GS1 and GS2 C. concisus strains isolated in previous studies was also conducted, and showed similar findings except that a significantly lower number of GS2 strains were isolated from faecal samples of healthy individuals; this suggests a potential difference between healthy controls and patients with gastrointestinal diseases in either colonizing strains or the enteric environment. Overall, the human gastrointestinal tract harbours a complex community of bacteria, some of which are pathogens capable of establishing chronic infections. These microbes may be involved in the development of inflammation-driven cancer. The immune system uses various effector cells and molecules to control and eradicate infectious agents and cancer cells. In particular, cytotoxic T cells (CTL) are major effector cells in anti-tumour immune responses. However, the functions of these effector cells can be inhibited by immune checkpoint proteins and molecules in tumour environments; this inhibition contributes to cancer cell immune evasion. Accordingly, the blockade of immune checkpoint proteins and molecules,… Advisors/Committee Members: Zhang, Li, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.

Subjects/Keywords: PD-L1; Campylobacter concisus; Inflammatory bowel disease

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

APA (6^th Edition):

Wang, Y. (2018). Investigation of GS1 and GS2 C. concisus adaptation in the human gastrointestinal tract and their effects on PD-L1 expression in human intestinal epithelial cells. (Masters Thesis). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/60214

Chicago Manual of Style (16^th Edition):

Wang, Yiming. “Investigation of GS1 and GS2 C. concisus adaptation in the human gastrointestinal tract and their effects on PD-L1 expression in human intestinal epithelial cells.” 2018. Masters Thesis, University of New South Wales. Accessed November 17, 2019. http://handle.unsw.edu.au/1959.4/60214.

MLA Handbook (7^th Edition):

Wang, Yiming. “Investigation of GS1 and GS2 C. concisus adaptation in the human gastrointestinal tract and their effects on PD-L1 expression in human intestinal epithelial cells.” 2018. Web. 17 Nov 2019.

Vancouver:

Wang Y. Investigation of GS1 and GS2 C. concisus adaptation in the human gastrointestinal tract and their effects on PD-L1 expression in human intestinal epithelial cells. [Internet] [Masters thesis]. University of New South Wales; 2018. [cited 2019 Nov 17]. Available from: http://handle.unsw.edu.au/1959.4/60214.

Council of Science Editors:

Wang Y. Investigation of GS1 and GS2 C. concisus adaptation in the human gastrointestinal tract and their effects on PD-L1 expression in human intestinal epithelial cells. [Masters Thesis]. University of New South Wales; 2018. Available from: http://handle.unsw.edu.au/1959.4/60214

Open Access Theses and Dissertations