subject:(Colitis)

University of Manitoba

1. Kapoor, Kunal. Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis.

Degree: Immunology, 2018, University of Manitoba

URL: http://hdl.handle.net/1993/33622

► Ulcerative colitis(UC) is characterized by a decreased level of chromofungin (CHR: Chormogranin-A 47-66) and a dysregulation of CD11c+ cells. We aimed to investigate the association… (more)

Subjects/Keywords: Ulcerative Colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kapoor, K. (2018). Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis. (Masters Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/33622

Chicago Manual of Style (16^th Edition):

Kapoor, Kunal. “Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis.” 2018. Masters Thesis, University of Manitoba. Accessed April 19, 2021. http://hdl.handle.net/1993/33622.

MLA Handbook (7^th Edition):

Kapoor, Kunal. “Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis.” 2018. Web. 19 Apr 2021.

Vancouver:

Kapoor K. Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis. [Internet] [Masters thesis]. University of Manitoba; 2018. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/1993/33622.

Council of Science Editors:

Kapoor K. Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis. [Masters Thesis]. University of Manitoba; 2018. Available from: http://hdl.handle.net/1993/33622

University of Tasmania

2. Perera, APP. Role of NLRP3 in colitis and colitis associated colorectal cancer.

Degree: 2019, University of Tasmania

URL: https://eprints.utas.edu.au/34330/1/Perera_whole_thesis.pdf ; Perera, APP ORCID: 0000-0002-3674-9940 <https://orcid.org/0000-0002-3674-9940> 2019 , 'Role of NLRP3 in colitis and colitis associated colorectal cancer', PhD thesis, University of Tasmania.

► Inflammatory bowel disease (IBD) is an idiopathic group of chronic disorders characterised by inflammation of the small intestine and colon. In Australia, more than 85,000… (more)

▼ Inflammatory bowel disease (IBD) is an idiopathic group of chronic disorders characterised by inflammation of the small intestine and colon. In Australia, more than 85,000 people live with IBD and by the year 2022 it is expected that this number will have surpassed 100,000. The two major types of IBD are Crohn’s disease (CD) and ulcerative colitis (UC). Both diseases are characterised by a series of relapses and remissions where the inflammation in the gastrointestinal tract becomes so severe that patients need hospitalisation or even surgery. A major complication of chronic inflammation (colitis), either by recurrent CD or UC is the development of colitis-associated colorectal cancer (CAC). Crohn and Rosenberg first reported the ulcerative colitis case associated with colorectal cancer development in 1925, thereafter many studies have been published linking gut inflammation as an important predisposing factor for the development of colorectal cancer. However, the understanding of specific underlying mechanism of how chronic inflammation is connected to the initiation and progression of colon cancer is yet to be established. Although the exact aetiology of IBD has yet to be elucidated, a defective innate immune system has been proposed as a primary mechanism in colitis. As an important arm of the innate immune system inflammasomes particularly the well characterised NLRP3, is involved in gut homeostasis and inflammatory pathologies. However, the role of NLRP3 in these processes is not well understood. Investigations on the role of NLRP3 in colitis is still controversial and inconclusive with some studies showing a protective role while other studies demonstrate a detrimental effect of NLRP3 activation. The reason for the discrepancies observed in the Nlrp3(^-/-) chemically induced colitis mouse model phenotype could be due to differences in length and concentration of chemical treatment or baseline differences in the composition of the intestinal microbiota in experimental mice. Thus, the overall aim of the PhD project was to address the above issues and define the role of NLRP3 in the development of colitis. This doctoral research thesis consists of seven chapters. Chapter 1 is an overall introduction to the rationale of the research, hypothesis and aims of the research project. Chapter 2 is a review article that critique the literature and summarises the role of NLRP3 in intestinal inflammation and CAC. Chapter 2a is a detailed description of the Winnie mouse model and methodology of generation and genetic confirmation of the novel mouse model Winnie x Nlrp3(^-/-). Chapter 3 is a review article on background of current experimental NLRP3 inhibitors that have been investigated in IBD experimental models and the potential mechanism of action of these inhibitors. Chapter 4 is a research article that describes the experiments and data generated that detail the effect of MCC950, a specific small molecule inhibitor of NLRP3 inflammasome on colonic inflammation in spontaneous colitis Winnie mice. Chapter 5…

Subjects/Keywords: NLRP3; colitis; colitis associated colon cancer; MCC950

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Perera, A. (2019). Role of NLRP3 in colitis and colitis associated colorectal cancer. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/34330/1/Perera_whole_thesis.pdf ; Perera, APP ORCID: 0000-0002-3674-9940 <https://orcid.org/0000-0002-3674-9940> 2019 , 'Role of NLRP3 in colitis and colitis associated colorectal cancer', 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):

Perera, APP. “Role of NLRP3 in colitis and colitis associated colorectal cancer.” 2019. Thesis, University of Tasmania. Accessed April 19, 2021. https://eprints.utas.edu.au/34330/1/Perera_whole_thesis.pdf ; Perera, APP ORCID: 0000-0002-3674-9940 <https://orcid.org/0000-0002-3674-9940> 2019 , 'Role of NLRP3 in colitis and colitis associated colorectal cancer', 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):

Perera, APP. “Role of NLRP3 in colitis and colitis associated colorectal cancer.” 2019. Web. 19 Apr 2021.

Vancouver:

Perera A. Role of NLRP3 in colitis and colitis associated colorectal cancer. [Internet] [Thesis]. University of Tasmania; 2019. [cited 2021 Apr 19]. Available from: https://eprints.utas.edu.au/34330/1/Perera_whole_thesis.pdf ; Perera, APP ORCID: 0000-0002-3674-9940 <https://orcid.org/0000-0002-3674-9940> 2019 , 'Role of NLRP3 in colitis and colitis associated colorectal cancer', 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:

Perera A. Role of NLRP3 in colitis and colitis associated colorectal cancer. [Thesis]. University of Tasmania; 2019. Available from: https://eprints.utas.edu.au/34330/1/Perera_whole_thesis.pdf ; Perera, APP ORCID: 0000-0002-3674-9940 <https://orcid.org/0000-0002-3674-9940> 2019 , 'Role of NLRP3 in colitis and colitis associated colorectal cancer', PhD thesis, University of Tasmania.

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

Universitat de Valencia

3. Pastor Juan, María del Rosario. Utilidad de la ecografía inicial para predecir la gravedad de la colitis isquémica .

Degree: 2015, Universitat de Valencia

URL: http://hdl.handle.net/10550/49743

► La colitis isquémica es la forma más frecuente de isquemia intestinal. Surge cuando el colon se ve privado del flujo vascular y en la mayoría… (more)

▼ La colitis isquémica es la forma más frecuente de isquemia intestinal. Surge cuando el colon se ve privado del flujo vascular y en la mayoría de los casos no se identifica ninguna causa específica. Desde el punto de vista anatomopatológico y de evolución se habla de una forma gangrenosa con necrosis transmural, con una alta mortalidad; y de una forma no gangrenosa caracterizada por lesiones limitadas a la mucosa o submucosa, y que se resuelve normalmente con solo tratamiento médico. En la literatura se han descrito ampliamente los hallazgos de la colitis isquémica en las exploraciones radiográficas con enema de bario y tomografía computarizada, sin embargo hay pocas publicaciones sobre los hallazgos ecográficos de esta entidad. La ecografía es una técnica muy usada ante una patología abdominal, por eso los radiólogos deberían conocer los hallazgos ecográficos de la colitis isquémica para evitar retrasos en el diagnóstico, errores de interpretación y fallos en el tratamiento. Por otra parte, muchos autores han intentado definir factores de riesgo que permitan diferenciar las formas gangrenosas de las no gangrenosas. Aunque varios estudios han detectado factores de riesgo clínico-biológicos, hay muy pocos que describan los hallazgos radiológicos constitutivos de factores de riesgo de la colitis isquémica. La hipótesis de este trabajo es que la valoración inicial ecográfica en los pacientes con colitis isquémica estratifica la gravedad en esta entidad al combinarla con los parámetros clínicos. El objetivo principal es evaluar y conocer la utilidad de la ecografía y sus hallazgos principales para predecir el pronóstico de la colitis isquémica y, con ello, inducir un cambio en la actitud terapéutica. El estudio consta de dos fases, en una primera fase se estudian de forma retrospectiva y consecutiva los casos diagnosticados de colitis isquémica en el Hospital Universitario Dr. Peset de Valencia, durante 11 años. En esta fase se realiza un estudio descriptivo de datos sociodemográficos, clínicos, analíticos y ecográficos, y después se valora la existencia de asociación de estos datos con la evolución del paciente (leve o grave) mediante un análisis univariante y multivariante. Si con el tratamiento conservador el cuadro se resolvía se trataba de una colitis isquémica leve y si el paciente requería cirugía o fallecía, una colitis isquémica grave. En la segunda fase se realiza la validación del modelo que se obtiene de la regresión logística del análisis multivariante usando una población con colitis isquémica independiente, recogida de forma prospectiva durante 2 años en el mismo hospital. Para describir las variables cuantitativas se utilizó media, desviación estándar, intervalo de confianza de la media al 95% y el rango de valores mínimo y máximo; cuando su distribución se apartaba de la normalidad se calculó mediana y rango intercuartil. Las variables cualitativas se describieron mediante frecuencia absoluta y porcentaje. En el análisis univariante, el test estadístico utilizado para analizar las relaciones entre la… Advisors/Committee Members: Martí Bonmatí, Luis (advisor).

Subjects/Keywords: colitis isquémica; ecografía

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Pastor Juan, M. d. R. (2015). Utilidad de la ecografía inicial para predecir la gravedad de la colitis isquémica . (Doctoral Dissertation). Universitat de Valencia. Retrieved from http://hdl.handle.net/10550/49743

Chicago Manual of Style (16^th Edition):

Pastor Juan, María del Rosario. “Utilidad de la ecografía inicial para predecir la gravedad de la colitis isquémica .” 2015. Doctoral Dissertation, Universitat de Valencia. Accessed April 19, 2021. http://hdl.handle.net/10550/49743.

MLA Handbook (7^th Edition):

Pastor Juan, María del Rosario. “Utilidad de la ecografía inicial para predecir la gravedad de la colitis isquémica .” 2015. Web. 19 Apr 2021.

Vancouver:

Pastor Juan MdR. Utilidad de la ecografía inicial para predecir la gravedad de la colitis isquémica . [Internet] [Doctoral dissertation]. Universitat de Valencia; 2015. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/10550/49743.

Council of Science Editors:

Pastor Juan MdR. Utilidad de la ecografía inicial para predecir la gravedad de la colitis isquémica . [Doctoral Dissertation]. Universitat de Valencia; 2015. Available from: http://hdl.handle.net/10550/49743

University of Cambridge

4. Ramona, Lauma. Integrating -Omics For Studying Functional Role Of Ulcerative Colitis Risk Associated Loci.

Degree: 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/317462

► Background: Ulcerative Colitis is chronic inflammatory condition of unknown etiology. Genome Wide Association Studies have successfully identified large number of UC risk associated loci, majority… (more)

▼ Background: Ulcerative Colitis is chronic inflammatory condition of unknown etiology. Genome Wide Association Studies have successfully identified large number of UC risk associated loci, majority of which are located in non-protein-coding DNA regions and been showed to be enriched within regulatory elements, such as enhancers. However, the function of these UC risk associated variants is still unknow. Aim: To delineate the functional role of GWAS risk associated loci in UC relevant cell types. Method: We assessed chromatin activity (ATAC seq) and transcriptional behavior (RNA seq) of primary cell types extracted from intestinal biopsies and blood from diseased and healthy participant. Next, to pinpoint the mechanistic of how UC associated loci contributes to disease risk, we intersected our disease and cell type specific differential expression and differential chromatin accessibility data with GWAS dataset. Results: Unfortunately, due to technical and financial reasons we failed to reach the target sequencing depth for both ATAC seq and RNA seq experiments. In addition, when combined with very low participant numbers, our data sets were not strong enough to reliably identify the functional role of GWAS variants. However, for practice, we proceeded with slightly simplistic proximity-based modeling and showed that intersecting the 3 -omics studies allowed us to identify 10 regions where the lowest p-value associated SNP was in proximity to differentially expressed gene and differentially accessible chromatin region. Conclusion: We were able to compare the first time the expression levels and chromatin conformation in purified immune cell populations from intestinal tissue and peripheral blood. Unfortunately, due to poor experimental design this study was markedly underpowered and any findings from RNA seq and ATAC seq experiments should be further validated before any biological conclusions are made or used for reliable prediction of functional role of UC associated risk variants.

Subjects/Keywords: Ulcerative Colitis; GWAS

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ramona, L. (2019). Integrating -Omics For Studying Functional Role Of Ulcerative Colitis Risk Associated Loci. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/317462

Chicago Manual of Style (16^th Edition):

Ramona, Lauma. “Integrating -Omics For Studying Functional Role Of Ulcerative Colitis Risk Associated Loci.” 2019. Doctoral Dissertation, University of Cambridge. Accessed April 19, 2021. https://www.repository.cam.ac.uk/handle/1810/317462.

MLA Handbook (7^th Edition):

Ramona, Lauma. “Integrating -Omics For Studying Functional Role Of Ulcerative Colitis Risk Associated Loci.” 2019. Web. 19 Apr 2021.

Vancouver:

Ramona L. Integrating -Omics For Studying Functional Role Of Ulcerative Colitis Risk Associated Loci. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Apr 19]. Available from: https://www.repository.cam.ac.uk/handle/1810/317462.

Council of Science Editors:

Ramona L. Integrating -Omics For Studying Functional Role Of Ulcerative Colitis Risk Associated Loci. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/317462

Universidad de Chile

5. Bitrán Ambler, Mirit Luisa. Estudio de la regulación de la vía esteroidogénica intestinal y su caracterización en pacientes con colitis ulcerosa.

Degree: 2019, Universidad de Chile

URL: http://repositorio.uchile.cl/handle/2250/172803

► Las enfermedades inflamatorias del intestino (EII) son condiciones de inflamación crónica del tracto gastrointestinal y abarca dos manifestaciones clínicas principales: Enfermedad de Crohn (EC) y… (more)

▼ Las enfermedades inflamatorias del intestino (EII) son condiciones de inflamación crónica del tracto gastrointestinal y abarca dos manifestaciones clínicas principales: Enfermedad de Crohn (EC) y Colitis Ulcerosa (CU). En Chile no se cuenta con información epidemiológica exacta de cifras de prevalencia o incidencia, sin embargo, estudios uni- y multicéntricos han demostrado el constante aumento de la incidencia de EII, atribuible principalmente a la CU. La CU es una enfermedad inflamatoria crónica idiopática, para la que aún no existe un tratamiento curativo definitivo, caracterizada por etapas de actividad (comúnmente con sangrado en las deposiciones y diarreas recurrentes) e inactividad/remisión. Los glucocorticoides (GC), son el tratamiento base y de primera línea en CU puesto que, debido a su acción anti-inflamatoria e inmunomoduladora, son altamente efectivos en la inducción de la remisión clínica y endoscópica. Sin embargo, a pesar que más de la mitad de los pacientes con EII responden al tratamiento con GC, el 19% son refractarios o resistentes al tratamiento y el 20% de los pacientes sometidos a terapia prolongada con GC, se hacen dependientes del fármaco. Numerosas vías han sido propuestas para explicar los efectos anti-inflamatorios e inmunomodulatorios de los GCs exógenos una vez que se unen al receptor de glucocorticoides (GR). Adicionalmente, estudios más recientes han identificado al epitelio intestinal como una importante fuente de GCs endógenos extra-adrenales, los que no son regulados por la actividad del eje HPA (ni afectarían la producción sistémica de GCs), sin embargo, con capacidad de ejercer sus efectos localmente. Esta esteroidogénesis intestinal representaría un mecanismo fundamental para la mantención de la homeostasis y estaría, por lo tanto, adaptado y sujeto a las necesidades locales, presentándose como un importante mecanismo inmuno-regulatorio tejido-específico. Además, la producción de GCs es inducida por estimulación de las células inmunes y el microambiente inflamatorio característico de la CU. En particular, la vía enzimática de síntesis de cortisol (a partir de colesterol) parece ser idéntica a la operante en la glándula adrenal, pero regulada por moléculas y eventos de señalización diferentes. Así, la actividad del factor transcripcional Liver receptor homologue 1 (LRH-1) ha cobrado especial relevancia para comprender en profundidad el mecanismo de regulación de las enzimas esteroidogénicas (CYP11A1 y CYP11B1), corroborando una elevada expresión a nivel del epitelio intestinal. xv En base a los antecedentes expuestos, la hipótesis propuesta en esta tesis es: Los glucocorticoides inducen la expresión de LRH-1 y la activación de la vía esteroidogénica intestinal. Así, el desarrollo de esta investigación pretendió determinar el efecto de los GCs sobre la expresión de LRH-1 y la activación de la vía esteroidogénica intestinal, y, en este contexto, caracterizar sus componentes en la mucosa intestinal de pacientes con CU y la posible relación con la respuesta a la terapia…

Subjects/Keywords: Colitis ulcerosa; Glucocorticoides

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Bitrán Ambler, M. L. (2019). Estudio de la regulación de la vía esteroidogénica intestinal y su caracterización en pacientes con colitis ulcerosa. (Thesis). Universidad de Chile. Retrieved from http://repositorio.uchile.cl/handle/2250/172803

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):

Bitrán Ambler, Mirit Luisa. “Estudio de la regulación de la vía esteroidogénica intestinal y su caracterización en pacientes con colitis ulcerosa.” 2019. Thesis, Universidad de Chile. Accessed April 19, 2021. http://repositorio.uchile.cl/handle/2250/172803.

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

MLA Handbook (7^th Edition):

Bitrán Ambler, Mirit Luisa. “Estudio de la regulación de la vía esteroidogénica intestinal y su caracterización en pacientes con colitis ulcerosa.” 2019. Web. 19 Apr 2021.

Vancouver:

Bitrán Ambler ML. Estudio de la regulación de la vía esteroidogénica intestinal y su caracterización en pacientes con colitis ulcerosa. [Internet] [Thesis]. Universidad de Chile; 2019. [cited 2021 Apr 19]. Available from: http://repositorio.uchile.cl/handle/2250/172803.

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

Council of Science Editors:

Bitrán Ambler ML. Estudio de la regulación de la vía esteroidogénica intestinal y su caracterización en pacientes con colitis ulcerosa. [Thesis]. Universidad de Chile; 2019. Available from: http://repositorio.uchile.cl/handle/2250/172803

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

University of Alberta

6. Tabor, Junetta P. Effect of bypass on epithelial morphometrics and kinetics in experimental colonic inflammation.

Degree: PhD, Department of Anatomy, 1985, University of Alberta

URL: https://era.library.ualberta.ca/files/37720f72h

Subjects/Keywords: Colitis – Surgery.

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Tabor, J. P. (1985). Effect of bypass on epithelial morphometrics and kinetics in experimental colonic inflammation. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/37720f72h

Chicago Manual of Style (16^th Edition):

Tabor, Junetta P. “Effect of bypass on epithelial morphometrics and kinetics in experimental colonic inflammation.” 1985. Doctoral Dissertation, University of Alberta. Accessed April 19, 2021. https://era.library.ualberta.ca/files/37720f72h.

MLA Handbook (7^th Edition):

Tabor, Junetta P. “Effect of bypass on epithelial morphometrics and kinetics in experimental colonic inflammation.” 1985. Web. 19 Apr 2021.

Vancouver:

Tabor JP. Effect of bypass on epithelial morphometrics and kinetics in experimental colonic inflammation. [Internet] [Doctoral dissertation]. University of Alberta; 1985. [cited 2021 Apr 19]. Available from: https://era.library.ualberta.ca/files/37720f72h.

Council of Science Editors:

Tabor JP. Effect of bypass on epithelial morphometrics and kinetics in experimental colonic inflammation. [Doctoral Dissertation]. University of Alberta; 1985. Available from: https://era.library.ualberta.ca/files/37720f72h

Universiteit Utrecht

7. Zheng, B. Microbiome manupulation in the management of acute and chronic colitis : A preclinical research approach.

Degree: 2015, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/322960

► Inflammatory bowel disease (IBD) is a chronic inflammatory disease that can affect all parts of the intestinal tract. This disease has a large impact on… (more)

▼ Inflammatory bowel disease (IBD) is a chronic inflammatory disease that can affect all parts of the intestinal tract. This disease has a large impact on both the social and personal life, since it dramatically reduces the quality of life and work capability of the patients. The last fifty years, both the incidence and prevalence of IBD have risen sharply and this increase is more than 10 fold in Western countries within this time frame. In addition, studies examining the epidemiology of childhood-onset IBD indicate that the incidence in young kids is also rising internationally. Despites the increased demand for an improved IBD therapy, a curative therapy for this disease remains absence. The existing treatment methods are all symptom-fighting therapies and often have undesirable side effects. More studies on new and more effective treatment method or means are therefore desirable and necessary. Although the etiology of development of IBD remains unclear, increasing data indicate that the composition of the microbiota and related immune balance between the microbiota and the immune system of the host play an important role in the pathogenesis of IBD . A changed composition of the microbiota is often observed in the intestine of IBD patients. There is speculation that restoring the original composition will microbiota may lead to recover from IBD patients. Probiotics, defined as “live microorganisms which when administrated in adequate amounts confer a healthy benefit for the host” have the capability to remodel the microbiota balance, which makes it a potential candidate to prevent or treat IBD. Data from different remodeling IBD animal models do indeed show that probiotics can have beneficial effects for preventing or treating against IBD. The purpose of this thesis is to provide a better understanding of the disturbed immune responses during IBD development by using dextran sulfate sodium induced mouse colitis model. In addition, selected probiotic strains that can modulate the intestinal microbiome were applied to investigate the possible effects on inflammation and tissue damage in acute and chronic colitis. Advisors/Committee Members: Folkerts, Gert, Garssen, Johan, Kraneveld, Aletta, Morgan, Liz.

Subjects/Keywords: IBD; probiotic; colitis; PRRs; TLRs

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Zheng, B. (2015). Microbiome manupulation in the management of acute and chronic colitis : A preclinical research approach. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/322960

Chicago Manual of Style (16^th Edition):

Zheng, B. “Microbiome manupulation in the management of acute and chronic colitis : A preclinical research approach.” 2015. Doctoral Dissertation, Universiteit Utrecht. Accessed April 19, 2021. http://dspace.library.uu.nl:8080/handle/1874/322960.

MLA Handbook (7^th Edition):

Zheng, B. “Microbiome manupulation in the management of acute and chronic colitis : A preclinical research approach.” 2015. Web. 19 Apr 2021.

Vancouver:

Zheng B. Microbiome manupulation in the management of acute and chronic colitis : A preclinical research approach. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2015. [cited 2021 Apr 19]. Available from: http://dspace.library.uu.nl:8080/handle/1874/322960.

Council of Science Editors:

Zheng B. Microbiome manupulation in the management of acute and chronic colitis : A preclinical research approach. [Doctoral Dissertation]. Universiteit Utrecht; 2015. Available from: http://dspace.library.uu.nl:8080/handle/1874/322960

Loyola University Chicago

8. Kuprys, Paulius. Alcohol Induced Bacterial Changes in the Setting of Colitis.

Degree: PhD, Cell Biology, Neurobiology and Anatomy, 2019, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_diss/3345

► Inflammatory bowel diseases (IBD) affect a large number of individuals around the world. This group of diseases is largely composed of two types: Crohn's disease… (more)

▼ Inflammatory bowel diseases (IBD) affect a large number of individuals around the world. This group of diseases is largely composed of two types: Crohn's disease (CD) and ulcerative colitis (UC). Upon development of IBD, patients experience cyclical episodes of inflammation, known as flares. Flare induction appears to arise from multiple factors, which can also vary on a person-to-person basis. Alcohol has been shown to trigger IBD flares and onset, though the underlying mechanism has not been established.Defining factors of the IBD intestinal environment include an altered microbiome, bacterial infiltration of the intestinal epithelium, and increased leakage of proinflammatory bacterial byproducts. In particular there are noted increases in the pro-inflammatory Enterobacteriaceae bacteria and decreases in bacteria that promote intestinal health. Many of these bacterial changes in IBD parallel those seen in alcohol consumption, therefore we hypothesized that alcohol enhances the symptoms associated with colitis by altering intestinal bacterial populations.Using a patient database, we identified that individuals admitted for IBD with a concurrent documented history of alcohol use and admission for IBD had increased intestinal infections, increased diagnostic procedures, and increased antibiotic usage. Using a mouse model of colitis and ethanol administration developed in our lab, we identified that the combination of alcohol in the setting of colitis exacerbates overgrowth of the pro-inflammatory Enterobacteriaceae and limiting growth of healthy bacteria like Lactobacillus. This was found to be related to increased expression of intestinal nitric oxide synthase 2 (Nos2), which can facilitate growth of Enterobacteriaceae. Inhibition of nitrate production and nitrate utilization limited Enterobacteriaceae growth in colitis, but when alcohol was administered after colitis, the rise in Enterobacteriaceae was only slightly depressed. The combination of ethanol and colitis also led to alterations in the liver inflammatory response. In summary, the results of these studies have implications for limiting the exacerbation of colitis flares and possibly the induction of colitis flare through the promotion of a healthy intestinal microbiome and limitation of alcohol consumption.

Subjects/Keywords: Alcohol; Colitis; Microbiome; Biology

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kuprys, P. (2019). Alcohol Induced Bacterial Changes in the Setting of Colitis. (Doctoral Dissertation). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_diss/3345

Chicago Manual of Style (16^th Edition):

Kuprys, Paulius. “Alcohol Induced Bacterial Changes in the Setting of Colitis.” 2019. Doctoral Dissertation, Loyola University Chicago. Accessed April 19, 2021. https://ecommons.luc.edu/luc_diss/3345.

MLA Handbook (7^th Edition):

Kuprys, Paulius. “Alcohol Induced Bacterial Changes in the Setting of Colitis.” 2019. Web. 19 Apr 2021.

Vancouver:

Kuprys P. Alcohol Induced Bacterial Changes in the Setting of Colitis. [Internet] [Doctoral dissertation]. Loyola University Chicago; 2019. [cited 2021 Apr 19]. Available from: https://ecommons.luc.edu/luc_diss/3345.

Council of Science Editors:

Kuprys P. Alcohol Induced Bacterial Changes in the Setting of Colitis. [Doctoral Dissertation]. Loyola University Chicago; 2019. Available from: https://ecommons.luc.edu/luc_diss/3345

Texas A&M University

9. Kim, Hye Mee. Polyphenolics from Mango (Mangifera indica L.) and Pomegranate (Punica granatum L.) Suppress Inflammation in in vivo and in vitro Models for Colitis.

Degree: PhD, Nutrition, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151871

► Ulcerative colitis is a chronic inflammation of the large intestine, and it may increase risk of human colorectal cancer. Polyphenolics from mango and pomegranate have… (more)

▼ Ulcerative colitis is a chronic inflammation of the large intestine, and it may increase risk of human colorectal cancer. Polyphenolics from mango and pomegranate have been shown to have potent anti-inflammatory properties, thus they could be the potential therapeutic agents for colitis. However, the mechanism underlying these effects of polyphenolics has not yet been elucidated. To determine the anti-inflammatory effects and possible mechanisms of polyphenolics from mango (gallic acid and gallotannins), and pomegranate (ellagic acid and ellagitannins) in dextran sodium sulfate (DSS)-induced colitis in rats, Sprague Dawley rats were administered control, mango, or pomegranate juice, and were exposed to three cycles of 3% DSS followed by 2-week recovery period. Colon inflammation and injury scores were assessed, and cell proliferation was evaluated by immunohistochemical detection of Ki-67. The mRNA and protein expressions involved in the inflammatory response and the mTOR pathway were analyzed by qRT-PCR, low density arrays, western blot analysis and multiplex bead assay. The involvement of miRNAs was additionally investigated with the antagomiR-126 and antagomiR-145 in lipopolysaccharide (LPS)-treated CCD-18Co, non-cancer colon fibroblasts cell lines. Both mango and pomegranate showed anti-inflammatory properties in vitro and in vivo. Mango and pomegranate juice reduced DSS-induced colon inflammation score (41% and 50%) and cell proliferative index (38% and 36%) during chronic colitis in rats compared to control juice. Mango and pomegranate juice significantly attenuated the pro-inflammatory cytokines, CRP, TNF-alpha, IL-1beta, GM-CSF, and IL-6 levels in colonic tissues. In addition, mango and pomegranate juice suppressed COX-2 and iNOS mRNA and protein expressions. Mango juice suppressed HIF-1alpha by decreasing the PI3K(p85beta)/AKT-mTOR signaling axis via up-regulation of miR-126, while pomegranate decreased p70S6K and HIF-1alpha by up-regulating miR-145. The interactions of mango with miR-126/PI3K(p85beta) and pomegranate with miR-145/p70S6K1 were additionally identified in CCD-18Co cells, where mango and pomegranate extract reversed the effect of the antagomiR. In addition, the modulation of microbiota composition (Blautia, Fusobacterium, and Ruminococcaceae) by pomegranate and short-chain fatty acids (SCFA; Isovalerate and valerate) production by mango may be involved in at least in part the anti-inflammatory effects of polyphenolics. These results suggest that both mango and pomegranate polyphenolics seem to have potential in the prevention and mitigation of colon inflammation. Advisors/Committee Members: Talcott, Susanne M (advisor), Lupton, Joanne R (committee member), Allred, Clinton (committee member), Ivanov, Ivan (committee member), Suchodolski, Jan S (committee member).

Subjects/Keywords: Mango; Pomegranate; Colitis; Rat; mTOR

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kim, H. M. (2013). Polyphenolics from Mango (Mangifera indica L.) and Pomegranate (Punica granatum L.) Suppress Inflammation in in vivo and in vitro Models for Colitis. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151871

Chicago Manual of Style (16^th Edition):

Kim, Hye Mee. “Polyphenolics from Mango (Mangifera indica L.) and Pomegranate (Punica granatum L.) Suppress Inflammation in in vivo and in vitro Models for Colitis.” 2013. Doctoral Dissertation, Texas A&M University. Accessed April 19, 2021. http://hdl.handle.net/1969.1/151871.

MLA Handbook (7^th Edition):

Kim, Hye Mee. “Polyphenolics from Mango (Mangifera indica L.) and Pomegranate (Punica granatum L.) Suppress Inflammation in in vivo and in vitro Models for Colitis.” 2013. Web. 19 Apr 2021.

Vancouver:

Kim HM. Polyphenolics from Mango (Mangifera indica L.) and Pomegranate (Punica granatum L.) Suppress Inflammation in in vivo and in vitro Models for Colitis. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/1969.1/151871.

Council of Science Editors:

Kim HM. Polyphenolics from Mango (Mangifera indica L.) and Pomegranate (Punica granatum L.) Suppress Inflammation in in vivo and in vitro Models for Colitis. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151871

Texas A&M University

10. Piefer, Leigh. Quercetin and Chlorogenic Acid Mitigate DSS-Induced Changes in Expression of Select Pro-Inflammatory Cytokines and Short Chain Fatty Acid Transporter Genes.

Degree: MS, Nutrition, 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11654

► Quercetin (Q) and chlorogenic acid (CA), two bioactive compounds found in stonefruits, may protect against inflammation and cancer because of anti-cancer, anti-oxidant, and anti-inflammatory properties.… (more)

▼ Quercetin (Q) and chlorogenic acid (CA), two bioactive compounds found in stonefruits, may protect against inflammation and cancer because of anti-cancer, anti-oxidant, and anti-inflammatory properties. Since these compounds reach the colon undigested, they affect the luminal environment before they are metabolized by the microbiota and transported into epithelial cells. We hypothesized that Q and CA may suppress expression of pro-inflammatory molecules, alter the luminal environment, and alter the cell cycle, thereby protecting against injury/colitis. To test this hypothesis, 63 male weanling rats were given one of three diets (basal, 0.45% Q, 0.05% CA). After 3 wk of acclimation, colitis was induced in 11 rats/diet [3% dextran sodium sulfate (DSS), 48 h, 3 treatments, 2 wk separation] and 10 rats/diet served as control (0% DSS). All rats were terminated at wk 9. Measurements included: fecal moisture content, fecal short chain fatty acid (SCFA) concentrations (gas chromatography), epithelial injury and inflammation in the distal colon, proliferation (PCNA), and NF-kappaB activity (ELISA method) and gene expression (real time RT-PCR) in mucosal scrapings. Fecal moisture content was significantly increased by DSS exposure (p<0.05), and never returned to control levels. Fecal SCFA concentrations also increased with DSS (acetate, p<0.05; butyrate, p<0.05). Increased SCFA concentrations could indicate decreased SCFA uptake. Experimental diets were able to mitigate DSS-induced decreases in SLC5A8 (SCFA transporter) expression. DSS significantly increased injury (p<0.0001) and inflammation (p<0.01) scores. Compared to the basal diet, CA decreased NF-kappaB activity in DSS-treated rats (p<0.05). Q and CA may maintain healthy regulation of NF-kappaB through maintaining expression levels of IkappaBalpha and Tollip, molecules that inhibit NF-kappaB activation. Q and CA mitigated DSS-induced increases in pro-inflammatory cytokine expression, specifically IL-1. Q enhanced expression of injury-repair molecule FGF-2 (p<0.01), but neither diet nor DSS treatment altered proliferation. Although Q and CA did not protect against DSS-induced increases in injury and inflammation scores or fecal SCFA concentrations, their influence on expression of injury repair molecules, pro-inflammatory cytokines, SCFA transport proteins, and NF-kappaB inhibitory molecules suggests beneficial influences on major pathways involved in DSS-induced injury/inflammation. The combined benefit of these compounds could have additive/synergistic effects and, therefore, deserve further examination. Advisors/Committee Members: Turner, Nancy D. (advisor), Allred, Clinton (committee member), Byrne, David (committee member).

Subjects/Keywords: Quercetin; Chlorogenic Acid; colitis; DSS

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Piefer, L. (2012). Quercetin and Chlorogenic Acid Mitigate DSS-Induced Changes in Expression of Select Pro-Inflammatory Cytokines and Short Chain Fatty Acid Transporter Genes. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11654

Chicago Manual of Style (16^th Edition):

Piefer, Leigh. “Quercetin and Chlorogenic Acid Mitigate DSS-Induced Changes in Expression of Select Pro-Inflammatory Cytokines and Short Chain Fatty Acid Transporter Genes.” 2012. Masters Thesis, Texas A&M University. Accessed April 19, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11654.

MLA Handbook (7^th Edition):

Piefer, Leigh. “Quercetin and Chlorogenic Acid Mitigate DSS-Induced Changes in Expression of Select Pro-Inflammatory Cytokines and Short Chain Fatty Acid Transporter Genes.” 2012. Web. 19 Apr 2021.

Vancouver:

Piefer L. Quercetin and Chlorogenic Acid Mitigate DSS-Induced Changes in Expression of Select Pro-Inflammatory Cytokines and Short Chain Fatty Acid Transporter Genes. [Internet] [Masters thesis]. Texas A&M University; 2012. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11654.

Council of Science Editors:

Piefer L. Quercetin and Chlorogenic Acid Mitigate DSS-Induced Changes in Expression of Select Pro-Inflammatory Cytokines and Short Chain Fatty Acid Transporter Genes. [Masters Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11654

University of Guelph

11. Mehdizadeh Gohari, Iman. Clostridium perfringens and its potential role in equine colitis.

Degree: MS, Department of Pathobiology, 2012, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3582

► Although progress has been made in the last decade in understanding the causes of colitis in horses, perhaps 60% of cases of fatal colitis in… (more)

Subjects/Keywords: Clostridium perfringens-equine colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Mehdizadeh Gohari, I. (2012). Clostridium perfringens and its potential role in equine colitis. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3582

Chicago Manual of Style (16^th Edition):

Mehdizadeh Gohari, Iman. “Clostridium perfringens and its potential role in equine colitis.” 2012. Masters Thesis, University of Guelph. Accessed April 19, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3582.

MLA Handbook (7^th Edition):

Mehdizadeh Gohari, Iman. “Clostridium perfringens and its potential role in equine colitis.” 2012. Web. 19 Apr 2021.

Vancouver:

Mehdizadeh Gohari I. Clostridium perfringens and its potential role in equine colitis. [Internet] [Masters thesis]. University of Guelph; 2012. [cited 2021 Apr 19]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3582.

Council of Science Editors:

Mehdizadeh Gohari I. Clostridium perfringens and its potential role in equine colitis. [Masters Thesis]. University of Guelph; 2012. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/3582

Boston University

12. Twyble, Ellsworth. The etiology of chronic ulcerative colitis.

Degree: Doctor of Medicine, Medicine, 1945, Boston University

URL: http://hdl.handle.net/2144/26076

Subjects/Keywords: Ulcerative colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Twyble, E. (1945). The etiology of chronic ulcerative colitis. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/26076

Chicago Manual of Style (16^th Edition):

Twyble, Ellsworth. “The etiology of chronic ulcerative colitis.” 1945. Doctoral Dissertation, Boston University. Accessed April 19, 2021. http://hdl.handle.net/2144/26076.

MLA Handbook (7^th Edition):

Twyble, Ellsworth. “The etiology of chronic ulcerative colitis.” 1945. Web. 19 Apr 2021.

Vancouver:

Twyble E. The etiology of chronic ulcerative colitis. [Internet] [Doctoral dissertation]. Boston University; 1945. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/2144/26076.

Council of Science Editors:

Twyble E. The etiology of chronic ulcerative colitis. [Doctoral Dissertation]. Boston University; 1945. Available from: http://hdl.handle.net/2144/26076

Universitat de Valencia

13. Marín Vàzquez, Marta. Efecte protector dels compostos fenòlics àcid el·làgic, apocinina i rutina en el tractament de la colitis ulcerosa induïda per dextranosulfat sòdic .

Degree: 2014, Universitat de Valencia

URL: http://hdl.handle.net/10550/35209

► L’ús de productes naturals entre aquells pacients que pateixen malalties cròniques s’inclou dins de les opcions més emprades dels tractaments complementaris i/o alternatius a la… (more)

▼ L’ús de productes naturals entre aquells pacients que pateixen malalties cròniques s’inclou dins de les opcions més emprades dels tractaments complementaris i/o alternatius a la medicina convencional. Entre els constituents naturals d'origen vegetal amb interès terapèutic destaquen els compostos fenòlics, alguns dels quals han demostrat ser efectius en el tractament de la colitis ulcerosa (CU). Aquesta malaltia, d’etiologia desconeguda, es caracteritza per una inflamació del còlon que afecta la mucosa des del recte fins a la seua totalitat. El present treball ha abordat l’avaluació de les propietats protectores de tres compostos amb estructura fenòlica -àcid el·làgic, apocinina i rutina-, incorporats en la dieta normal dels ratolins, en la colitis experimental induïda per l’agent químic dextranosulfat sòdic (DSS) administrat en l’aigua de beguda, amb l’objectiu d’establir el seu potencial com agents terapèutics o coadjuvants en el tractament de la CU en humans. En les experiències de colitis aguda i crònica, la suplementació de les dietes amb els principis actius assajats (4 i 1,25 g/kg/d, respectivament) va protegir de la inflamació intestinal induïda per DSS, amb la reducció del dany intestinal macroscòpic i histològic, així com la millora dels signes clínics característics de la malaltia. Aquesta millora va estar justificada per una afectació de l’activació dels principals factors de transcripció implicats en el desenvolupament de la malaltia, el factor de transcripció nuclear κB (NF-κB) i el transductor del senyal i activador de la transcripció (STAT) 3. A més, l’estudi bioquímic revelava una menor producció de les citocines factor de necrosi tumoral (TNF)-α, interleucina (IL)-6 i interferó (IFN)-γ en la mucosa del còlon, així com una inhibició de l’expressió proteica dels enzims ciclooxigenasa (COX)-2 i l’òxid nítric sintasa induïble (iNOS), possiblement degut al seu efecte sobre el factor de transcripció NF-kB, i la producció dels seus principals metabòlits, la prostaglandina (PG)E2 i l’òxid nítric (NO), sent en aquest últim cas la inhibició més acusada a la zona distal del còlon, coincidint aquesta zona amb la més afectada per la CU. En l’estudi agut, la dosi d’àcid el·làgic incorporada en la dieta dels ratolins durant 7 dies no va ser suficient per tal de prevenir la inflamació aguda intestinal induïda per DSS, si sols es tenen en compte els paràmetres clínics i l’anàlisi histològica. El seu efecte beneficiós adquiria una major rellevància en el cas del seu tractament en la dieta perllongat en el temps en l’estudi d’inflamació crònica. Per contra, l’addició en la dieta d’apocinina i rutina va mostrar un efecte antiinflamatori en les fases primerenques, després d’un atac agut, i tardanes de la malaltia. Per tant, el present estudi posa de manifest que els tres compostos seleccionats per la seua naturalesa fenòlica, àcid el·làgic, apocinina i rutina, administrats per via oral suplementats en la dieta, són efectius i segurs en el tractament de la CU, modulant les principals vies implicades en el… Advisors/Committee Members: Giner Pons, Rosa María (advisor).

Subjects/Keywords: medicamentos naturales; colitis ulcerosa

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Marín Vàzquez, M. (2014). Efecte protector dels compostos fenòlics àcid el·làgic, apocinina i rutina en el tractament de la colitis ulcerosa induïda per dextranosulfat sòdic . (Doctoral Dissertation). Universitat de Valencia. Retrieved from http://hdl.handle.net/10550/35209

Chicago Manual of Style (16^th Edition):

Marín Vàzquez, Marta. “Efecte protector dels compostos fenòlics àcid el·làgic, apocinina i rutina en el tractament de la colitis ulcerosa induïda per dextranosulfat sòdic .” 2014. Doctoral Dissertation, Universitat de Valencia. Accessed April 19, 2021. http://hdl.handle.net/10550/35209.

MLA Handbook (7^th Edition):

Marín Vàzquez, Marta. “Efecte protector dels compostos fenòlics àcid el·làgic, apocinina i rutina en el tractament de la colitis ulcerosa induïda per dextranosulfat sòdic .” 2014. Web. 19 Apr 2021.

Vancouver:

Marín Vàzquez M. Efecte protector dels compostos fenòlics àcid el·làgic, apocinina i rutina en el tractament de la colitis ulcerosa induïda per dextranosulfat sòdic . [Internet] [Doctoral dissertation]. Universitat de Valencia; 2014. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/10550/35209.

Council of Science Editors:

Marín Vàzquez M. Efecte protector dels compostos fenòlics àcid el·làgic, apocinina i rutina en el tractament de la colitis ulcerosa induïda per dextranosulfat sòdic . [Doctoral Dissertation]. Universitat de Valencia; 2014. Available from: http://hdl.handle.net/10550/35209

Queens University

14. Turki, Razan. Increased calcium intake regulates colonic CaSR expression and inhibits induced colitis and Wnt/β-catenin signaling .

Degree: Physiology, 2012, Queens University

URL: http://hdl.handle.net/1974/7699

► One of the major complications in patients with long standing inflammatory bowel disease (IBD) is colitis-associated colon cancer. The signaling pathways that promote the transformation… (more)

▼ One of the major complications in patients with long standing inflammatory bowel disease (IBD) is colitis-associated colon cancer. The signaling pathways that promote the transformation of colitis to colorectal cancer (CRC) are unknown but one candidate is the prolonged interaction between tumor necrosis factor alpha (TNF-α) and its receptor, TNFR1. This interaction may stimulate a defective Wnt signaling pathway to evoke epithelial cells to hyperproliferate. This crypt hyperproliferation can lead to the development CRC. Activation of Extracellular Calcium-sensing receptor (CaSR) a G-protein coupled receptor, on sub-epithelial myfibroblasts has been found to stimulate the expression of Wnt5a, a member of Wnt family, while CaSR activation on the epithelial cells stimulates Wnt5a receptor, Ror2, a member of receptor tyrosine kinase family. Wnt5a/Ror2 (non canonical signaling) interaction has been suggested to decrease TNFR1 expression and inhibit Wnt/β-catenin signaling to regulate cellular growth. The aims of this thesis were to determine whether increased dietary calcium will increase colonic CaSR expression, characterize the colons of “rescued” CaSR/PTH double homozygous knockout and their response to an acute model of colitis, and assess whether CaSR activation influenced the status of Low-density lipoprotein receptor-related protein 6 (pLRP6), co-receptor for Wnt, in cell culture models. Our results demonstrated that CaSR expression is higher in the colon of the NIH-Swiss Webster mice after feeding them 2% calcium alone or in conjunction with vitamin D for four weeks compared to two weeks, suggesting that dietary calcium alone or together with vitamin D can regulate colonic CaSR expression. We found the CaSR-/PTH- colons had a significant reduction in the non canonical signaling and enhanced Wnt/β-catenin signaling and the amount of inflammation was increased, suggesting that CaSR can inhibit Wnt/β-catenin signaling in the colonic crypt and acts as an anti-inflammatory signal. Our results demonstrated that CaSR activation alone in CaSR-HEK and RKO cells reduced Wnt-stimulated LRP6 phosphorylation suggesting a crucial role of CaSR in the inhibition of LRP6 phosphorylation. The observations seen in this study strongly suggest a role for CaSR in inhibiting the defective Wnt/β-catenin signaling pathway, induced colitis, and LRP6 phosphorylation to regulate cellular growth.

Subjects/Keywords: Bowel disease ; Colon cancer ; Colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Turki, R. (2012). Increased calcium intake regulates colonic CaSR expression and inhibits induced colitis and Wnt/β-catenin signaling . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7699

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):

Turki, Razan. “Increased calcium intake regulates colonic CaSR expression and inhibits induced colitis and Wnt/β-catenin signaling .” 2012. Thesis, Queens University. Accessed April 19, 2021. http://hdl.handle.net/1974/7699.

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

MLA Handbook (7^th Edition):

Turki, Razan. “Increased calcium intake regulates colonic CaSR expression and inhibits induced colitis and Wnt/β-catenin signaling .” 2012. Web. 19 Apr 2021.

Vancouver:

Turki R. Increased calcium intake regulates colonic CaSR expression and inhibits induced colitis and Wnt/β-catenin signaling . [Internet] [Thesis]. Queens University; 2012. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/1974/7699.

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

Council of Science Editors:

Turki R. Increased calcium intake regulates colonic CaSR expression and inhibits induced colitis and Wnt/β-catenin signaling . [Thesis]. Queens University; 2012. Available from: http://hdl.handle.net/1974/7699

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

University of New South Wales

15. Ng, Wa Sang Watson. Appendicitis protects against colitis: an exploration of underlying immune mechanisms.

Degree: Medical Sciences, 2008, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/41442 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:2129/SOURCE02?view=true

► Inflammatory bowel disease-(IBD) is a chronic relapsing and remitting disorder of the gastrointestinal tract characterised byinflammation. The underlying immunopathogenesis is unknown but excessive effector and… (more)

▼ Inflammatory bowel disease-(IBD) is a chronic relapsing and remitting disorder of the gastrointestinal tract characterised byinflammation. The underlying immunopathogenesis is unknown but excessive effector and defective regulatory immuneresponses play a significant role. The aetiology of IBD is not yet fully resolved, but interactions between genetic andenvironmental factors, including the gut flora, contribute significantly to the development of IBD.Appendicectomy for intra-abdominal inflammatory conditions before the age of 20 protects against colitis. The mechanismunderlying this protective effect is unclear. This thesis examined the hypothesis that appendiceal regulatory T lymphocytes(Treg) mediate the protection.Despite human and murine data showing that the appendix is involved in the prevention of colitis, few studies of human ormurine appendices have been reported. A novel murine model of appendicitis was created using an operative technique ofband-ligation of an induced-tubular-appendix. Histological assessment showed that this model recapitulated all of thehistological features of human acute appendicitis, namely mucosal ulceration, transmural neutrophilic and lymphocyticinfiltration and serositis. This local pathology was associated with a systemic host response, evidenced by raised serum Creactive-protein.The impact of inflammation on the appendiceal lymphocyte constituents was assessed by flow cytometry. The inflammationcaused a shift from B-lymphocyte to T-lymphocyte predominance. In particular there was a 75% increment in Treg numbers,which was restricted to juvenile mice only (< 10 weeks old). Furthermore, appendiceal Treg expressed the gut-homingchemokine-receptor, CCR9, and the intestine-specific integrin, α4β7. These cells were shown to preferentially migrate to thecolonic lamina propria.Lastly, appendicitis and appendicectomy protected against TNBS-colitis which was also restricted to juvenile mice. Evidencefor antigen dependence was suggested by the effect being heightened when mice were pre-sensitised against TNBS.Exploration of the colonic lamina propria (cLP) lymphocyte population showed an increase in Treg, especially CD8+Foxp3+-Treg, in “protected” mice only, which may have originated in the appendix.Intracytoplasmic cytokine detection showed that these cLP-Treg were potent producers of the regulatory cytokine, IL-10.These findings strongly suggest that appendicitis triggers an expansion of Treg which then emigrate to the colon and mediatelong-lasting protection against colitis.

Subjects/Keywords: Appendicitis; Colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ng, W. S. W. (2008). Appendicitis protects against colitis: an exploration of underlying immune mechanisms. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/41442 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:2129/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Ng, Wa Sang Watson. “Appendicitis protects against colitis: an exploration of underlying immune mechanisms.” 2008. Doctoral Dissertation, University of New South Wales. Accessed April 19, 2021. http://handle.unsw.edu.au/1959.4/41442 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:2129/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Ng, Wa Sang Watson. “Appendicitis protects against colitis: an exploration of underlying immune mechanisms.” 2008. Web. 19 Apr 2021.

Vancouver:

Ng WSW. Appendicitis protects against colitis: an exploration of underlying immune mechanisms. [Internet] [Doctoral dissertation]. University of New South Wales; 2008. [cited 2021 Apr 19]. Available from: http://handle.unsw.edu.au/1959.4/41442 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:2129/SOURCE02?view=true.

Council of Science Editors:

Ng WSW. Appendicitis protects against colitis: an exploration of underlying immune mechanisms. [Doctoral Dissertation]. University of New South Wales; 2008. Available from: http://handle.unsw.edu.au/1959.4/41442 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:2129/SOURCE02?view=true

16. Francisco JosÃ Batista de Lima JÃnior. AÃÃo AntiespasmÃdica e Anti-inflamatÃria do Cinamato de Metila em Trato Gastrintestinal de Ratos Submetidos a Modelo de Colite por Ãcido AcÃtico.

Degree: 2013, Universidade Federal do CearÃ; Programa de PÃs-GraduaÃÃo em Farmacologia; UFC; BR

URL: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11592

►

nÃo hÃ

Previamente demonstrou-se que o Ãleo essencial de Ocimum micranthum (OEOM) e seu constituinte majoritÃrio, cinamato de metila (CM), tÃm aÃÃes miorrelaxante e antinflamatÃria… (more)

▼

nÃo hÃ

Previamente demonstrou-se que o Ãleo essencial de Ocimum micranthum (OEOM) e seu constituinte majoritÃrio, cinamato de metila (CM), tÃm aÃÃes miorrelaxante e antinflamatÃria em tecidos traqueais de ratos, e efeito antinociceptivo em camundongos. O objetivo deste estudo foi avaliar o potencial antiespasmÃdico e anti-inflamatÃrio do CM no trato gastrintestinal de ratos submetidos a modelo de colite induzida por Ãcido acÃtico. OEOM inibiu contraÃÃes induzidas por carbamilcolina (CCh; 1 M) e KCl (60 mM) em tiras de fundo de estÃmago com CI50 de 91,9 g/mL e 46,8 g/mL, respectivamente, e reduziu significativamente o tÃnus basal e amplitudes de contraÃÃes espontÃneas de duodeno. CM, em conformaÃÃes isomÃricas (Z)- ou (E)-, tambÃm inibiu essas respostas induzidas por CCh e KCl em fundo, antro, duodeno e cÃlon, sem diferenÃas nos efeitos dos isÃmeros em cada segmento. CM comeÃa a inibir as contraÃÃes induzidas por CCh em concentraÃÃo mais baixa que KCl, contudo com potÃncia menor se comparado aos efeitos da atropina. (E)-CM inibe contraÃÃes dependentes dos estoques intracelulares de cÃlcio, e seu efeito inibitÃrio parece nÃo depender da aÃÃo da Ãxido nÃtrico sintase ou da abertura de canais de potÃssio. Analisadas em microscÃpio confocal, cÃlulas de cÃlon dissociadas a fresco tiveram nÃvel citossÃlico de cÃlcio reduzido para 60% do basal apÃs exposiÃÃo a (E)-CM (600M). Avaliando a pressÃo intragÃstrica in vivo, uma dose de (E)-CM 50 mg/kg nÃo afeta amplitude das contraÃÃes gÃstricas, mas se repetida apÃs 30 minutos, as diminui por atÃ 10 minutos. A induÃÃo de colite foi atravÃs de instilaÃÃo de Ãcido acÃtico a 5% via retal. O grupo sham recebeu instilaÃÃo apenas de salina, e os grupos tratados, alÃm da instilaÃÃo de Ãcido receberam (E)-CM 50 mg/kg/dia ou prednisolona 1 mg/kg/dia durante trÃs dias. A instilaÃÃo com Ãcido acÃtico induziu colite confirmada por alteraÃÃo macroscÃpica, leucocitose, aumento de interleucina-1 tecidual e dÃficit funcional de resposta dependente de canais para cÃlcio operados por voltagem. Esses parÃmetros foram revertidos pelos tratamentos com (E)-CM e prednisolona. Portanto, OEOM e CM apresentam aÃÃo antiespasmÃdica em trato gastrintestinal de ratos in vitro. O efeito do CM passa pela reduÃÃo dos nÃveis intracelulares basais de cÃlcio e independe da participaÃÃo da enzima Ãxido nÃtrico sintase e de canais de potÃssio. CM possui aÃÃo anti-inflamatÃria de magnitude comparÃvel Ã prednisolona.

It was previously shown that the essential oil of Ocimum micranthum (EOOM), and its major constituent, methyl cinnamate (MC), have myorelaxant action on tracheal smooth muscle, airway anti-inflammatory and anti-nociceptive on rodents. The present work aimed to evaluate the antispasmodic and anti-inflammatory potential of MC on gastrointestinal tissues from rats subjected to acetic acid-induced colitis model. EOOM inhibited carbamylcholine- (CCh; 1 M) and KCl-induced (60 mM) contractions in stomach fundus strips with IC50 of 91.9 g/mL and 46.8…

Advisors/Committee Members: Pedro Jorge Caldas MagalhÃes, ArmÃnio Aguiar dos Santos, Marcellus Henrique Loiola Ponte de Souza.

Subjects/Keywords: Gastrointestinal tract; Colitis; FARMACOLOGIA

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

JÃnior, F. J. B. d. L. (2013). AÃÃo AntiespasmÃdica e Anti-inflamatÃria do Cinamato de Metila em Trato Gastrintestinal de Ratos Submetidos a Modelo de Colite por Ãcido AcÃtico. (Masters Thesis). Universidade Federal do CearÃ; Programa de PÃs-GraduaÃÃo em Farmacologia; UFC; BR. Retrieved from http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11592

Chicago Manual of Style (16^th Edition):

JÃnior, Francisco JosÃ Batista de Lima. “AÃÃo AntiespasmÃdica e Anti-inflamatÃria do Cinamato de Metila em Trato Gastrintestinal de Ratos Submetidos a Modelo de Colite por Ãcido AcÃtico.” 2013. Masters Thesis, Universidade Federal do CearÃ; Programa de PÃs-GraduaÃÃo em Farmacologia; UFC; BR. Accessed April 19, 2021. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11592.

MLA Handbook (7^th Edition):

JÃnior, Francisco JosÃ Batista de Lima. “AÃÃo AntiespasmÃdica e Anti-inflamatÃria do Cinamato de Metila em Trato Gastrintestinal de Ratos Submetidos a Modelo de Colite por Ãcido AcÃtico.” 2013. Web. 19 Apr 2021.

Vancouver:

JÃnior FJBdL. AÃÃo AntiespasmÃdica e Anti-inflamatÃria do Cinamato de Metila em Trato Gastrintestinal de Ratos Submetidos a Modelo de Colite por Ãcido AcÃtico. [Internet] [Masters thesis]. Universidade Federal do CearÃ; Programa de PÃs-GraduaÃÃo em Farmacologia; UFC; BR; 2013. [cited 2021 Apr 19]. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11592.

Council of Science Editors:

JÃnior FJBdL. AÃÃo AntiespasmÃdica e Anti-inflamatÃria do Cinamato de Metila em Trato Gastrintestinal de Ratos Submetidos a Modelo de Colite por Ãcido AcÃtico. [Masters Thesis]. Universidade Federal do CearÃ; Programa de PÃs-GraduaÃÃo em Farmacologia; UFC; BR; 2013. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11592

Virginia Tech

17. Lee, Christina K. Modulation of Neutrophil Functions and Anti-Tumor Immune Responses by Innate Suppressors.

Degree: PhD, Translational Biology, Medicine and Health, 2018, Virginia Tech

URL: http://hdl.handle.net/10919/98571

► Neutrophils are known to be key innate defenders through performing vital and diverse functions such as degranulation, oxidative burst, and generation of extracellular trap (NET).… (more)

Subjects/Keywords: Neutrophil; Polarization; Tollip; Colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lee, C. K. (2018). Modulation of Neutrophil Functions and Anti-Tumor Immune Responses by Innate Suppressors. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/98571

Chicago Manual of Style (16^th Edition):

Lee, Christina K. “Modulation of Neutrophil Functions and Anti-Tumor Immune Responses by Innate Suppressors.” 2018. Doctoral Dissertation, Virginia Tech. Accessed April 19, 2021. http://hdl.handle.net/10919/98571.

MLA Handbook (7^th Edition):

Lee, Christina K. “Modulation of Neutrophil Functions and Anti-Tumor Immune Responses by Innate Suppressors.” 2018. Web. 19 Apr 2021.

Vancouver:

Lee CK. Modulation of Neutrophil Functions and Anti-Tumor Immune Responses by Innate Suppressors. [Internet] [Doctoral dissertation]. Virginia Tech; 2018. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/10919/98571.

Council of Science Editors:

Lee CK. Modulation of Neutrophil Functions and Anti-Tumor Immune Responses by Innate Suppressors. [Doctoral Dissertation]. Virginia Tech; 2018. Available from: http://hdl.handle.net/10919/98571

18. Kondo, Satoru. Down-regulation of trefoil factor-3 expression in the rectum is associated with the development of ulcerative colitis-associated cancer.

Degree: 博士(医学), 2017, Mie University / 三重大学

URL: http://hdl.handle.net/10076/00017111

►

Diagnostic markers can facilitate more selective screening and treatment strategies for ulcerative colitis (UC)-associated cancer (UCAC). We analyzed trefoil factor-3 (TFF3), which has an important… (more)

Subjects/Keywords: trefoil factor-3; ulcerative colitis; colitis-associated cancer; field effect; surveillance

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kondo, S. (2017). Down-regulation of trefoil factor-3 expression in the rectum is associated with the development of ulcerative colitis-associated cancer. (Thesis). Mie University / 三重大学. Retrieved from http://hdl.handle.net/10076/00017111

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):

Kondo, Satoru. “Down-regulation of trefoil factor-3 expression in the rectum is associated with the development of ulcerative colitis-associated cancer.” 2017. Thesis, Mie University / 三重大学. Accessed April 19, 2021. http://hdl.handle.net/10076/00017111.

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

MLA Handbook (7^th Edition):

Kondo, Satoru. “Down-regulation of trefoil factor-3 expression in the rectum is associated with the development of ulcerative colitis-associated cancer.” 2017. Web. 19 Apr 2021.

Vancouver:

Kondo S. Down-regulation of trefoil factor-3 expression in the rectum is associated with the development of ulcerative colitis-associated cancer. [Internet] [Thesis]. Mie University / 三重大学; 2017. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/10076/00017111.

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

Council of Science Editors:

Kondo S. Down-regulation of trefoil factor-3 expression in the rectum is associated with the development of ulcerative colitis-associated cancer. [Thesis]. Mie University / 三重大学; 2017. Available from: http://hdl.handle.net/10076/00017111

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

University of Sydney

19. Chen, Jo-Hua. Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements .

Degree: 2017, University of Sydney

URL: http://hdl.handle.net/2123/17592

► Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements Abstract Inroduction: Acute severe ulcerative colitis (ASUC) is a potentially life-threatening complication of ulcerative colitis. Intravenous corticosteroid… (more)

▼ Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements Abstract Inroduction: Acute severe ulcerative colitis (ASUC) is a potentially life-threatening complication of ulcerative colitis. Intravenous corticosteroid use has significantly improved the mortality rate. However, colectomy rates have remained stable due to limited adoption of rescue medical therapies. Given this and the uncommon but serious nature of the condition, consensus statements based on a systematic review of the literature may assist in the improved outcome of patients with ASUC. Method: The Delphi method was used in the development of the consensus statements. A steering committee generated the statements of interest. Five levels of agreement were used: A: agree completely; B: agree with minor reservation; C: agree with major reservation; D: reject with some reservation, E: reject completely. ≥80% agreement of level A and B determined acceptance of statements. Three rounds of anonymous voting were carried out to achieve the final results. Level of evidence and grade of recommendation were endorsed following further discussion. Results: A total of 33 statements were developed. From 22 multi-disciplinary clinicians, there was 100% agreement for 24 out of 33 statements; 80-99% for 6 statements; and 3 statements were rejected. Key recommendations include that patients with ASUC should be: hospitalised, undergo unprepared flexible sigmoidoscopy to assess severity and to exclude cytomegalovirus colitis, and be provided with venous thromboembolism prophylaxis and intravenous hydrocortisone 100mg 3 or 4 times daily with close monitoring by a multidisciplinary team. Rescue therapy such as infliximab or cyclosporin should be started if insufficient response by day 3, and colectomy considered if no response to 7 days of rescue therapy or earlier if deterioration. With such an approach it is expected that colectomy rate during admission will be below 30% and mortality less than 1% in specialist centres. Conclusion: These evidenced-based consensus statements on ASUC developed by a multidisciplinary group provide up-to-date best practice recommendations that improve and harmonise management as well as provide auditable quality assessments.

Subjects/Keywords: Inflammatory bowel disease; acute severe ulcerative colitis; ulcerative colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chen, J. (2017). Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17592

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):

Chen, Jo-Hua. “Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements .” 2017. Thesis, University of Sydney. Accessed April 19, 2021. http://hdl.handle.net/2123/17592.

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

MLA Handbook (7^th Edition):

Chen, Jo-Hua. “Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements .” 2017. Web. 19 Apr 2021.

Vancouver:

Chen J. Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements . [Internet] [Thesis]. University of Sydney; 2017. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/2123/17592.

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

Council of Science Editors:

Chen J. Acute Severe Ulcerative Colitis: Evidence Based Consensus Statements . [Thesis]. University of Sydney; 2017. Available from: http://hdl.handle.net/2123/17592

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

Universitat Autònoma de Barcelona

20. Robles Alonso, Virginia. Microbiota intestinal y colitis ulcerosa, abordaje metagenómico.

Degree: Departament de Medicina, 2017, Universitat Autònoma de Barcelona

URL: http://hdl.handle.net/10803/458621

► There have been described changes in fecal microbiota composition in patients with UC with inflammatory activity versus healthy individual, but it is not clear whether… (more)

Subjects/Keywords: Microbiota; Microbiome; Colitis ulcerosa; Colitis ulcerosa; Ulcerative colitis; Metagenòmica; Metagenómica; Metagenomics; Ciències de la Salut; 616.3

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Robles Alonso, V. (2017). Microbiota intestinal y colitis ulcerosa, abordaje metagenómico. (Thesis). Universitat Autònoma de Barcelona. Retrieved from http://hdl.handle.net/10803/458621

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):

Robles Alonso, Virginia. “Microbiota intestinal y colitis ulcerosa, abordaje metagenómico.” 2017. Thesis, Universitat Autònoma de Barcelona. Accessed April 19, 2021. http://hdl.handle.net/10803/458621.

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

MLA Handbook (7^th Edition):

Robles Alonso, Virginia. “Microbiota intestinal y colitis ulcerosa, abordaje metagenómico.” 2017. Web. 19 Apr 2021.

Vancouver:

Robles Alonso V. Microbiota intestinal y colitis ulcerosa, abordaje metagenómico. [Internet] [Thesis]. Universitat Autònoma de Barcelona; 2017. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/10803/458621.

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

Council of Science Editors:

Robles Alonso V. Microbiota intestinal y colitis ulcerosa, abordaje metagenómico. [Thesis]. Universitat Autònoma de Barcelona; 2017. Available from: http://hdl.handle.net/10803/458621

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

University of Florida

21. Shenoy, Anitha Kota. Role of Wnt Signaling Pathway in Colitis-to-Cancer Transition.

Degree: PhD, Medical Sciences - Molecular Cell Biology (IDP), 2012, University of Florida

URL: https://ufdc.ufl.edu/UFE0044003

► One of the severe complications of ulcerative colitis (UC) is colorectal cancer (CRC). However, very little is known about the transition from colitis-to-cancer. The transition… (more)

▼ One of the severe complications of ulcerative colitis (UC) is colorectal cancer (CRC). However, very little is known about the transition from colitis-to-cancer. The transition involves a poorly understood inflammation-dysplasia-carcinoma sequence, while sporadic CRC is associated with well-characterized adenoma-carcinoma sequence. One of the early events in this sequence of sporadic CRC is the activating mutation in genes involved in Wnt/Beta-catenin signaling. Similar to sporadic CRC, in the current study we have demonstrated an early activation of Wnt/Beta-catenin signaling in the colitis-to-cancer transition. We observed intermediate level of Wnt activity in the cells of UC when compared to normal colon and CRC by performing Beta-catenin immunostaining on patient derived colon tissues. These Wnt-pathway-active cells constitute a major subpopulation (52%+7.21) of ALDH+ cells that in UC are referred to as precursor-colon cancer stem cells (pCCSC). By in vitro clonogenicity assays and serial xenograft transplantations we established the ability of Wnthigh pCCSCs to exhibit cancer stem cell (CSC) properties like self-renewal and tumor initiation. Moreover, a single Wnthigh pCCSC was sufficient to initiate the tumor, suggesting the association of Wnt/Beta-catenin signaling with the transformation of pCCSCs to CCSCs and thus the colitis-to-cancer transition. This was confirmed by shRNA-mediated down-regulation of Beta-catenin in Wnthigh pCCSCs in vivo. Furthermore, pharmacological inhibition of Wnt/Beta-catenin signaling was achieved by using FDA approved drug, indomethacin that resulted in reduced tumor growth rate. Thus, high levels of Wnt/Beta-catenin signaling not only further demarcate (with ALDH positivity) the tumor-initiating cell compartment of the non-dysplastic epithelium of UC patients, but also represent a plausible diagnostic marker and a therapeutic target for early intervention in the colitis-to-cancer transition. ( en ) Advisors/Committee Members: Scott, Edward W (committee chair), Huang, Emina (committee member), Chan, Edward K (committee member), Swanson, Maurice S (committee member).

Subjects/Keywords: Cancer; Catenins; Cells; Colitis; Colon; Colorectal cancer; Crypts; Stem cells; Tumors; Ulcerative colitis; ccsc – colitis – colon

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Shenoy, A. K. (2012). Role of Wnt Signaling Pathway in Colitis-to-Cancer Transition. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0044003

Chicago Manual of Style (16^th Edition):

Shenoy, Anitha Kota. “Role of Wnt Signaling Pathway in Colitis-to-Cancer Transition.” 2012. Doctoral Dissertation, University of Florida. Accessed April 19, 2021. https://ufdc.ufl.edu/UFE0044003.

MLA Handbook (7^th Edition):

Shenoy, Anitha Kota. “Role of Wnt Signaling Pathway in Colitis-to-Cancer Transition.” 2012. Web. 19 Apr 2021.

Vancouver:

Shenoy AK. Role of Wnt Signaling Pathway in Colitis-to-Cancer Transition. [Internet] [Doctoral dissertation]. University of Florida; 2012. [cited 2021 Apr 19]. Available from: https://ufdc.ufl.edu/UFE0044003.

Council of Science Editors:

Shenoy AK. Role of Wnt Signaling Pathway in Colitis-to-Cancer Transition. [Doctoral Dissertation]. University of Florida; 2012. Available from: https://ufdc.ufl.edu/UFE0044003

Ruhr Universität Bochum

22. Rottmann, Sabrina. Orale Applikation von Taurolidin in der chronischen DSS-Colitis der Maus : Abschwächung der Krankheitsaktivität und Mortalität.

Degree: 2012, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-35219

► Problem: Die Zielsetzung dieser Studie bestand darin, die Toxizität von oral appliziertem Taurolidin darzustellen und die Auswirkungen dieser Applikationsform auf den Krankheitsprozess der experimentellen Colitis… (more)

Subjects/Keywords: Taurolidin; Chronische Darmerkrankung; Maus; Colitis ulcerosa; Dickdarmentzündung

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Rottmann, S. (2012). Orale Applikation von Taurolidin in der chronischen DSS-Colitis der Maus : Abschwächung der Krankheitsaktivität und Mortalität. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-35219

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):

Rottmann, Sabrina. “Orale Applikation von Taurolidin in der chronischen DSS-Colitis der Maus : Abschwächung der Krankheitsaktivität und Mortalität.” 2012. Thesis, Ruhr Universität Bochum. Accessed April 19, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-35219.

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

MLA Handbook (7^th Edition):

Rottmann, Sabrina. “Orale Applikation von Taurolidin in der chronischen DSS-Colitis der Maus : Abschwächung der Krankheitsaktivität und Mortalität.” 2012. Web. 19 Apr 2021.

Vancouver:

Rottmann S. Orale Applikation von Taurolidin in der chronischen DSS-Colitis der Maus : Abschwächung der Krankheitsaktivität und Mortalität. [Internet] [Thesis]. Ruhr Universität Bochum; 2012. [cited 2021 Apr 19]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-35219.

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

Council of Science Editors:

Rottmann S. Orale Applikation von Taurolidin in der chronischen DSS-Colitis der Maus : Abschwächung der Krankheitsaktivität und Mortalität. [Thesis]. Ruhr Universität Bochum; 2012. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-35219

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

University of Manchester

23. Glymenaki, Maria. The role of gut flora in epithelial barrier function and immunity.

Degree: 2016, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:305972

► Inflammatory bowel disease (IBD) is associated with an inappropriate immune response to the gut microbiota and disruption of intestinal homeostasis. IBD patients and experimental animal… (more)

▼ Inflammatory bowel disease (IBD) is associated with an inappropriate immune response to the gut microbiota and disruption of intestinal homeostasis. IBD patients and experimental animal models have consistently shown alterations in the gut microbiota composition. However, these studies have mainly focused on faecal microbiota samples taken after the onset of inflammation and IBD establishment. The colonic microbiota inhabits both the gut lumen and the mucus layer covering the intestinal epithelium. Thus, information about mucus-resident microbiota is not necessarily conveyed in the routine microbiota analyses of faecal samples. To address potential changes in microbial composition and function before the onset of IBD, we compared both mucus and faecal microbiota in the mdr1a-/- spontaneous model of colitis over times that we histologically defined as before onset of colitis, during and after colitis onset. We showed that alterations in microbiota composition preceded the onset of intestinal inflammation and that these changes were evident in the mucus, but not in faeces. This altered microbiota composition was coupled with a reduced inner mucus layer, indicating a compromised mucus barrier prior to colitis development. Upon emergence of inflammation, compositional differences were found in both mucus and faecal microbial communities. Spatial segregation of microbiota with intestinal mucosa was also disrupted on disease onset which we hypothesise contributes to a more severe intestinal pathology. Therefore, our data indicate that microbial changes start locally in the mucus and then proceed to the faecal matter concomitantly with colitis development.Next, we examined whether microbial gene functional potential and endogenous metabolite profiles followed alterations in gut microbiota taxonomic composition. Our findings showed that the microbial gene content was similar between mdr1a-/- mice and wild-type littermate controls, demonstrating stability of the gut microbiome at the face of ensuing gut inflammation. In further support of these findings, urinary metabolite analysis revealed that metabolite profiles were unaffected by intestinal inflammation. Metabolites previously reported to change in IBD were similar between mdr1a-/- and wild-type mice at stages preceding and during inflammation. We also found that changes in metabolite profiles did not correlate with colitis scores. However, metabolite changes could discriminate mdr1a-/- mice from wild-type controls, suggesting they could have value in predicting risk of IBD with a potential clinical use in at least a subset of individuals with MDR1A polymorphisms.To assess whether changes in antimicrobial proteins (AMPs) accounted for observed differences in mucus microbiota composition, we also investigated the expression of regenerating islet-derived protein 3 γ (Reg3γ), angiogenin 4 (Ang4), β-defensin 1 and resistin-like molecule beta (Relm-β) in the colon. We found similar levels of these AMPs as well as IgA-producing plasma cells between mdr1a-/- and wild-type mice,… Advisors/Committee Members: ELSE, KATHRYN KJ, MCBAIN, ANDREW AJ, WARHURST, GEOFFREY G, Else, Kathryn, Mcbain, Andrew, Warhurst, Geoffrey, Cruickshank, Sheena.

Subjects/Keywords: gut microbiota IBD colitis mucus metabolites

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Glymenaki, M. (2016). The role of gut flora in epithelial barrier function and immunity. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:305972

Chicago Manual of Style (16^th Edition):

Glymenaki, Maria. “The role of gut flora in epithelial barrier function and immunity.” 2016. Doctoral Dissertation, University of Manchester. Accessed April 19, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:305972.

MLA Handbook (7^th Edition):

Glymenaki, Maria. “The role of gut flora in epithelial barrier function and immunity.” 2016. Web. 19 Apr 2021.

Vancouver:

Glymenaki M. The role of gut flora in epithelial barrier function and immunity. [Internet] [Doctoral dissertation]. University of Manchester; 2016. [cited 2021 Apr 19]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:305972.

Council of Science Editors:

Glymenaki M. The role of gut flora in epithelial barrier function and immunity. [Doctoral Dissertation]. University of Manchester; 2016. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:305972

Vanderbilt University

24. Pope, Jillian Lashea. The Role of Claudin-1 in Inflammation and Colon Cancer.

Degree: PhD, Cancer Biology, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/11127

► Perturbation of physiological processes stimulate a cascade of events resulting in adverse pathogical conditions, the most predominant being cancer. Colorectal cancer (CRC) is the third… (more)

▼ Perturbation of physiological processes stimulate a cascade of events resulting in adverse pathogical conditions, the most predominant being cancer. Colorectal cancer (CRC) is the third most common cancer in the United States and the third leading cause of cancer deaths among men and women. CRC is most commonly initiated by mutation of Adenomatous polyposis coli (APC), a tumor suppressor gene of the Wingless/Wnt pathway, which leads to constitutive activation of Wnt signaling responsible for the majority of CRC cases. Although significant progress has been made in understanding the sequential genetic events leading to cancer development, the precise genes and associated molecular events underlying tumor progression are still poorly understood. Our lab has previously reported a correlation between increased expression of claudin-1, a tight junction protein, in primary and metastatic tumor samples of CRC patients. Additionally, in adenomas of the APCMin mouse, an experimental model for CRC, and human cell lines harboring mutations in APC, claudin-1 expression is highly increased and mislocalized. Taken together, these studies suggest existence of a potential interplay between dysregulated claudin-1 expression and APC, thus supporting an essential role in the regulation of sporadic colonic neoplasia. In addition to genetic stimuli, CRC can be initiated by an inflammatory stimulus. Patients with inflammatory bowel disease, a chronic disorder of the gastrointestinal tract, are at high risk for developing CRC. This may be attributed, in part, to repeated injury and repair, which induces transformation of the colonic epithelium. As such, increased Claudin-1 expression is also reported to be associated with active IBD and colitis-associated cancer, yet its distinct role in inflammation has yet to be elucidated. This study investigates the specific contribution of increased claudin-1 expression to inflammation and CRC. These results identify a role for Claudin-1 in epithelial differentiation through a novel interaction with Notch signaling. Additionally, claudin-1 enhances tumorigenesis through upregulation of inflammation, IL-23/IL17 signaling, when combined with mutant APC. Once understood how overexpression claudin-1 contributes to tumor progression, we can better investigate its potential as a target for therapy. Advisors/Committee Members: Punita Dhawan (committee member), R. Daniel Beauchamp (committee member), Anna L. Means (committee member), Albert B. Reynolds (Committee Chair).

Subjects/Keywords: differentiation; colitis; tight junction; Notch; Mucin-2

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Pope, J. L. (2014). The Role of Claudin-1 in Inflammation and Colon Cancer. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11127

Chicago Manual of Style (16^th Edition):

Pope, Jillian Lashea. “The Role of Claudin-1 in Inflammation and Colon Cancer.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed April 19, 2021. http://hdl.handle.net/1803/11127.

MLA Handbook (7^th Edition):

Pope, Jillian Lashea. “The Role of Claudin-1 in Inflammation and Colon Cancer.” 2014. Web. 19 Apr 2021.

Vancouver:

Pope JL. The Role of Claudin-1 in Inflammation and Colon Cancer. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/1803/11127.

Council of Science Editors:

Pope JL. The Role of Claudin-1 in Inflammation and Colon Cancer. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/11127

Texas A&M University

25. Ritchie, Lauren E. Diet, Disease State, and the Space Environment Modify the Intestinal Microbiota and Mucosal Environment via Microbiota-directed Alterations in Colonocyte Signalling.

Degree: PhD, Genetics, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/151706

► Microbial dysbiosis and toll-like receptor (TLR) signaling play a role in colonic injury and inflammation. Ulcerative colitis and radiation are known to alter microbiota, and… (more)

▼ Microbial dysbiosis and toll-like receptor (TLR) signaling play a role in colonic injury and inflammation. Ulcerative colitis and radiation are known to alter microbiota, and diets containing polyphenols impact bacterial populations. We hypothesized that diet can mitigate dextran sodium sulfate (DSS) colitis (sorghum bran diets containing polyphenols) and space environment-induced alterations (normal iron content) in colonic microbiota and TLR signaling. To test this we utilized two experimental paradigms; DSS-induced colitis (3% DSS, 48-hr, 3 exposures, 2 wk separation), and three models to emulate the space environment: 1) fractionated low linear energy transfer (LET) γ radiation (RAD) (3 Gy) and high Fe diet (IRON) (650 mg/kg), 2) high LET Si particle exposure (50 cGy) and 1/6 G hind limb unloading (HLU), and 3) 13 d spaceflight. Bran diets upregulated proliferation, and repair protein (TFF3 and TGFβ) and short chain fatty acid (SCFA) transporter (Slc16a1 and Slc5a8) expression post-DSS. Diet significantly affected 24-hr fecal butyrate production, with Cellulose and Black bran having numerically higher concentrations. Two predominant phyla were identified, Firmicutes and Bacteroidetes, and this ratio was higher in Cellulose DSS. Post DSS#3 the proportion of Bacteroidales, Clostridiales, and Lactobacillales was reduced compared to post DSS#2 for all diets. Black bran non-DSS rats had the highest richness and diversity. Colonic injury negatively correlated with the proportion of Firmicutes, Actinobacteria, and Lactobacillales, and positively correlated with Unknown and Unclassified groups. Bran diets reduced the severity of epithelial injury, maintained fecal butyrate, and prevented microbial dysbiosis and depletion during DSS-induced colitis. IRON+RAD decreased SCFA concentrations. Low and high LET radiation, HLU, IRON and spaceflight increased Bacteroidetes and decreased Firmicutes. HLU and spaceflight increased Clostridiales and decreased Lactobacillales. RAD and IRON+RAD animals had increased Lactobacillales and significantly lower Clostridiales compared to CON and IRON. TLR9 and IL-6 were downregulated by RAD. TLR4, TFF3 and TGFβ differentially changed with IRON and spaceflight. Microgravity independently affected the microbiota, regardless of radiation energy or dose. Each environmental insult differentially altered the microbiota and mucosal gene expression, with distinct diet, microgravity, and radiation effects observed. Bran diets mitigated deleterious effects of colitis, maintained barrier integrity, and prevented microbiota dysbiosis. Advisors/Committee Members: Turner, Nancy D (advisor), Lupton, Joanne R (committee member), Chapkin, Robert S (committee member), Riggs, Penny K (committee member), Sturino, Joseph M (committee member).

Subjects/Keywords: polyphenols; microbiota; radiation; microgravity; ulcerative colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ritchie, L. E. (2013). Diet, Disease State, and the Space Environment Modify the Intestinal Microbiota and Mucosal Environment via Microbiota-directed Alterations in Colonocyte Signalling. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/151706

Chicago Manual of Style (16^th Edition):

Ritchie, Lauren E. “Diet, Disease State, and the Space Environment Modify the Intestinal Microbiota and Mucosal Environment via Microbiota-directed Alterations in Colonocyte Signalling.” 2013. Doctoral Dissertation, Texas A&M University. Accessed April 19, 2021. http://hdl.handle.net/1969.1/151706.

MLA Handbook (7^th Edition):

Ritchie, Lauren E. “Diet, Disease State, and the Space Environment Modify the Intestinal Microbiota and Mucosal Environment via Microbiota-directed Alterations in Colonocyte Signalling.” 2013. Web. 19 Apr 2021.

Vancouver:

Ritchie LE. Diet, Disease State, and the Space Environment Modify the Intestinal Microbiota and Mucosal Environment via Microbiota-directed Alterations in Colonocyte Signalling. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/1969.1/151706.

Council of Science Editors:

Ritchie LE. Diet, Disease State, and the Space Environment Modify the Intestinal Microbiota and Mucosal Environment via Microbiota-directed Alterations in Colonocyte Signalling. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/151706

University of California – Irvine

26. Klaus, Suzanne Michelle. CXCR2-mediated immune cell recruitment to the intestinal mucosa confers protection against infection with Salmonella Typhimurium.

Degree: Biomedical Sciences, 2018, University of California – Irvine

URL: http://www.escholarship.org/uc/item/9kz3f3hg

► Salmonella enterica serovar Typhimurium (S. Typhimurium) is a food-borne pathogen that causes severe diarrhea but can also cause fatal bacteremia if it reaches the bloodstream.… (more)

▼ Salmonella enterica serovar Typhimurium (S. Typhimurium) is a food-borne pathogen that causes severe diarrhea but can also cause fatal bacteremia if it reaches the bloodstream. During S. Typhimurium infection, a massive number of neutrophils migrate to the intestine; this response is important to prevent dissemination of S. Typhimurium into the bloodstream. Although some of the mechanisms by which neutrophils are protective during S. Typhimurium infection are known, the specific signals regulating their recruitment to the intestinal mucosa are not well elucidated. Most neutrophils express the chemokine receptor CXCR2, through which neutrophils sense CXC chemokines from inflamed or infected tissues. To better understand the role of CXCR2 during S. Typhimurium infection, we depleted CXCR2+ neutrophils in mice using antibody treatment, and we employed mice with a deletion of the Cxcr2 gene. During S. Typhimurium infection, mice lacking CXCR2+ neutrophils showed significantly fewer neutrophils in intestinal tissue, indicating that CXCR2 is a major receptor for intestinal neutrophil recruitment during S. Typhimurium colitis. Consistent with a protective role for neutrophils, S. Typhimurium numbers in peripheral organs were higher in mice lacking CXCR2+ neutrophils. Notably, and reported here for the first time, Cxcr2-/- mice exhibit fewer B cells in Peyer’s patches, which correlated to a nearly 100-fold higher S. Typhimurium burden in this tissue. Furthermore, we demonstrated that Peyer’s patch B cells migrate in response to CXCR2 chemokines, and that the role of Peyer’s patch B cells in protection against S. Typhimurium is independent of intestinal IgA levels. To better understand the specific contribution of neutrophil recruitment in protection against Salmonella, we generated mice selectively lacking Cxcr2 in granulocytes, which exhibited similar defects in neutrophil migration and S. Typhimurium dissemination as Cxcr2-/- mice. In contrast to Cxcr2-/- mice, granulocyte-specific deletion of Cxcr2 was not associated with higher S. Typhimurium colonization in Peyer’s patches, and Peyer’s patch B cells were not reduced. Altogether, this work expanded our understanding of CXCR2-mediated neutrophil recruitment in influencing outcomes of Salmonella infection and uncovered an important, IgA-independent role for CXCR2 on B cells in Peyer’s patches and in host defense against Salmonella intestinal infection.

Subjects/Keywords: Immunology; Microbiology; colitis; CXCR2; neutrophil; Salmonella

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Klaus, S. M. (2018). CXCR2-mediated immune cell recruitment to the intestinal mucosa confers protection against infection with Salmonella Typhimurium. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/9kz3f3hg

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):

Klaus, Suzanne Michelle. “CXCR2-mediated immune cell recruitment to the intestinal mucosa confers protection against infection with Salmonella Typhimurium.” 2018. Thesis, University of California – Irvine. Accessed April 19, 2021. http://www.escholarship.org/uc/item/9kz3f3hg.

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

MLA Handbook (7^th Edition):

Klaus, Suzanne Michelle. “CXCR2-mediated immune cell recruitment to the intestinal mucosa confers protection against infection with Salmonella Typhimurium.” 2018. Web. 19 Apr 2021.

Vancouver:

Klaus SM. CXCR2-mediated immune cell recruitment to the intestinal mucosa confers protection against infection with Salmonella Typhimurium. [Internet] [Thesis]. University of California – Irvine; 2018. [cited 2021 Apr 19]. Available from: http://www.escholarship.org/uc/item/9kz3f3hg.

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

Council of Science Editors:

Klaus SM. CXCR2-mediated immune cell recruitment to the intestinal mucosa confers protection against infection with Salmonella Typhimurium. [Thesis]. University of California – Irvine; 2018. Available from: http://www.escholarship.org/uc/item/9kz3f3hg

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

27. Ma, Xiaojun. Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth. : 大腸癌微小環境下に於けるプロスタグランジンE2-EP2シグナルは炎症と腫瘍増殖を促進する.

Degree: 博士(医科学), 2016, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/215461 ; http://dx.doi.org/10.14989/doctor.k19635

Final publication is available at http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=26018088

新制・課程博士

甲第19635号

医科博第73号

Subjects/Keywords: Prostaglandin; Colon cancer; Neutrophil; Colitis; EP2

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ma, X. (2016). Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth. : 大腸癌微小環境下に於けるプロスタグランジンE2-EP2シグナルは炎症と腫瘍増殖を促進する. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/215461 ; http://dx.doi.org/10.14989/doctor.k19635

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):

Ma, Xiaojun. “Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth. : 大腸癌微小環境下に於けるプロスタグランジンE2-EP2シグナルは炎症と腫瘍増殖を促進する.” 2016. Thesis, Kyoto University / 京都大学. Accessed April 19, 2021. http://hdl.handle.net/2433/215461 ; http://dx.doi.org/10.14989/doctor.k19635.

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

MLA Handbook (7^th Edition):

Ma, Xiaojun. “Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth. : 大腸癌微小環境下に於けるプロスタグランジンE2-EP2シグナルは炎症と腫瘍増殖を促進する.” 2016. Web. 19 Apr 2021.

Vancouver:

Ma X. Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth. : 大腸癌微小環境下に於けるプロスタグランジンE2-EP2シグナルは炎症と腫瘍増殖を促進する. [Internet] [Thesis]. Kyoto University / 京都大学; 2016. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/2433/215461 ; http://dx.doi.org/10.14989/doctor.k19635.

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

Council of Science Editors:

Ma X. Definition of prostaglandin E2-EP2 signals in the colon tumor microenvironment that amplify inflammation and tumor growth. : 大腸癌微小環境下に於けるプロスタグランジンE2-EP2シグナルは炎症と腫瘍増殖を促進する. [Thesis]. Kyoto University / 京都大学; 2016. Available from: http://hdl.handle.net/2433/215461 ; http://dx.doi.org/10.14989/doctor.k19635

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

University of Ottawa

28. 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

Record Details Similar Records Cite « Share

❌

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

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 April 19, 2021. 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. 19 Apr 2021.

Vancouver:

Deeke S. Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease . [Internet] [Thesis]. University of Ottawa; 2019. [cited 2021 Apr 19]. 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 Guelph

29. Costa, Marcio. Characterization of the Equine Intestinal Microbiota by High Throughput Sequencing.

Degree: PhD, Department of Pathobiology, 2014, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8188

► This study was performed to characterize the intestinal microbiota of horses by the use of new sequencing technologies, which allow for a broader coverage of… (more)

▼ This study was performed to characterize the intestinal microbiota of horses by the use of new sequencing technologies, which allow for a broader coverage of the organisms inhabiting complex ecosystems. The first study of this thesis characterized the fecal microbiota of healthy horses and horses with undifferentiated colitis. Actinobacteria, Spirochaetes and Clostridia were significantly more abundant in healthy horses, while Fusobacteria were more abundant in horses with colitis. Members of the Lachnospiraceae were the most frequently shared organisms among healthy individuals. The second study of this thesis found that newborn foals have a rich and diverse bacterial community during the first day of life, comprised by several low abundant genera that were unique at this age. The microbiota present during the first month of life was less diverse compared to older animals, with the majority of organisms classified as Akkermansia spp.. After 60 days of life, bacterial structure tended to remain stable, but differences in community membership were still present between nine month old animals and adult mares. The third study investigated changes in the fecal microbiota associated with antimicrobial administration. Significant changes of population structure and community membership were observed after the use of penicillin, ceftiofur and trimethoprim sulfadiazine, with the last drug causing the most marked changes and significant decrease of richness and diversity. Changes induced by antimicrobial administration were specific for each drug. Recover of the intestinal microbiota was observed, but differences were still evident 30 days after the beginning of the trial. In the last study, we characterized the microbiota present in different intestinal compartments of healthy horses. As expected, marked differences were present among compartments. Lactobacillus spp. and Sarcina spp. predominated in the stomach, Streptococcus spp. in the duodenum, Actinobacillus and Clostridium sensu stricto, in the ileum and “5 genus incertae sedis” from the large colon through feces. There was a significant increase in diversity towards the distal gut with a stable profile observed from the cecum through feces. Our results demonstrated the complexity of the intestinal microbiota in horses and the consequences that factors like age and antimicrobial usage have on this ecosystem. Advisors/Committee Members: Weese, J Scott (advisor).

Subjects/Keywords: Intestinal microbiota; microbiome; horses; bacteria; colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Costa, M. (2014). Characterization of the Equine Intestinal Microbiota by High Throughput Sequencing. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8188

Chicago Manual of Style (16^th Edition):

Costa, Marcio. “Characterization of the Equine Intestinal Microbiota by High Throughput Sequencing.” 2014. Doctoral Dissertation, University of Guelph. Accessed April 19, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8188.

MLA Handbook (7^th Edition):

Costa, Marcio. “Characterization of the Equine Intestinal Microbiota by High Throughput Sequencing.” 2014. Web. 19 Apr 2021.

Vancouver:

Costa M. Characterization of the Equine Intestinal Microbiota by High Throughput Sequencing. [Internet] [Doctoral dissertation]. University of Guelph; 2014. [cited 2021 Apr 19]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8188.

Council of Science Editors:

Costa M. Characterization of the Equine Intestinal Microbiota by High Throughput Sequencing. [Doctoral Dissertation]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8188

University of Adelaide

30. Costello, Samuel Paul. Faecal Microbiota Transplantation for the Treatment of Active Ulcerative Colitis.

Degree: 2019, University of Adelaide

URL: http://hdl.handle.net/2440/120499

► Introduction Ulcerative colitis (UC) is an inflammatory bowel disease that has high rates of persistent or relapsing symptoms despite available therapies. Many of these therapies… (more)

▼ Introduction Ulcerative colitis (UC) is an inflammatory bowel disease that has high rates of persistent or relapsing symptoms despite available therapies. Many of these therapies also have the potential for unacceptable side effects including allergy, intolerance, serious infection and malignancy due to long-term immunosuppression. It is for these reasons that new therapies for UC are required; particularly therapies that target novel pathways and do not suppress the immune system. Faecal microbiota transplantation (FMT) has demonstrated efficacy in the treatment of recurrent and refractory Clostridium difficile infection (CDI) and has been proposed as a novel therapy for UC. Aims The aims of this thesis were to: 1. establish a stool bank of screened donor stool containing viable organisms 2. assess the efficacy and safety of FMT for the induction of remission of UC 3. explore the mechanisms by which FMT may alter the disease process of UC. Methods Methods of stool donor recruitment and screening as well as anaerobic stool processing were developed and optimised. The viability of culturable organisms was validated after 6 months of frozen storage. A double-blind randomised controlled trial of a short duration of FMT using anaerobically prepared stool for the induction of remission of mild to moderate UC was undertaken with clinical and endoscopic remission assessed at 8 weeks and 12 months. Exploratory immunological, microbiological and metabolomic analyses were undertaken. A systematic review and meta-analysis was undertaken to assess the broader evidence for FMT as therapy for the induction of remission of UC. Results A stool bank of anaerobically prepared donor stool was established; 14 (31%) of 44 respondents to donor recruitment questionnaires were eligible. Bacterial viability was similar to baseline at both 2 and 6 months in specimens stored with saline and 10% glycerol and at 2 months in stool stored only in saline, but was reduced by >1 log at 6 months for aerobes, coliforms and lactobacilli in saline alone. In patients undergoing FMT with stool frozen for 2–10 months in 10% glycerol, the cure rate for rCDI was 88% after a single FMT. In mild to moderate active UC, clinical and endoscopic remission was achieved in 12 of the 38 participants (32%) who received pooled donor FMT, compared with 3 of the 35 (9%) who received autologous FMT (odds ratio [OR] 5.0 [95% CI 1.2–20.1]; P = 0.03). A number of bacterial species were associated with the observed donor FMT treatment effect. Neither lamina propria mononuclear cell populations nor short-chain fatty acid levels were associated with the donor FMT treatment effect. Meta-analysis of randomised controlled trials of FMT for UC demonstrated that clinical remission was achieved in 39 of 140 (28%) patients in the donor FMT groups, compared with 13 of 137 (9%) patients in the placebo groups (OR 3.67 [95% CI 1.82– 7.39]; P < 0.01]. Conclusions Establishing a bank of anaerobically prepared frozen donor stool facilitates the delivery of FMT for clinical and clinical trial… Advisors/Committee Members: Andrews, Jane (advisor), Roberts-Thomson, Ian (advisor), Hughes, Patrick (advisor), Conlon, Michael (advisor), Adelaide Medical School (school).

Subjects/Keywords: FMT; faecal; microbiome; stool; ulcerative colitis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Costello, S. P. (2019). Faecal Microbiota Transplantation for the Treatment of Active Ulcerative Colitis. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/120499

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):

Costello, Samuel Paul. “Faecal Microbiota Transplantation for the Treatment of Active Ulcerative Colitis.” 2019. Thesis, University of Adelaide. Accessed April 19, 2021. http://hdl.handle.net/2440/120499.

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

MLA Handbook (7^th Edition):

Costello, Samuel Paul. “Faecal Microbiota Transplantation for the Treatment of Active Ulcerative Colitis.” 2019. Web. 19 Apr 2021.

Vancouver:

Costello SP. Faecal Microbiota Transplantation for the Treatment of Active Ulcerative Colitis. [Internet] [Thesis]. University of Adelaide; 2019. [cited 2021 Apr 19]. Available from: http://hdl.handle.net/2440/120499.

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

Council of Science Editors:

Costello SP. Faecal Microbiota Transplantation for the Treatment of Active Ulcerative Colitis. [Thesis]. University of Adelaide; 2019. Available from: http://hdl.handle.net/2440/120499

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

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations