Gotowe bibliografie tematyczne / Inflammatory bowel diseas

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Gotowa bibliografia na temat „Inflammatory bowel diseas”

Autor: Grafiati

Data publikacji: 1 lutego 2025

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Artykuły w czasopismach na temat "Inflammatory bowel diseas"

KASKI, M. CARPANI, i H. J. F. HODGSON. "Rolling review: inflammatory bowel diseas". Alimentary Pharmacology & Therapeutics 7, nr 5 (31.03.2007): 567–79. http://dx.doi.org/10.1111/j.1365-2036.1993.tb00134.x.

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O’Sullivan, Maria, i Colm O’Morain. "Nutritional therapy in inflammatory bowel diseas". Current Treatment Options in Gastroenterology 7, nr 3 (czerwiec 2004): 191–98. http://dx.doi.org/10.1007/s11938-004-0040-2.

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Mancho, Carolina, Ángel Sainz, Mercedes García-Sancho, Alejandra Villaescusa, Miguel A. Tesouro i Fernando Rodríguez-Franco. "Detection of Perinuclear Antineutrophil Cytoplasmic Antibodies and Antinuclear Antibodies in the Diagnosis of Canine Inflammatory Bowel Diseas". Journal of Veterinary Diagnostic Investigation 22, nr 4 (lipiec 2010): 553–58. http://dx.doi.org/10.1177/104063871002200409.

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Theocharidou, Eleni, Melachrini Mavroudi, Konstantinos Soufleris, Alexandros Mpoumponaris, Andreas Nakos, Theodora Griva, Nikolaos Grammatikos, Eleni Mavroudi, Geleris Paraschos i Nicolaos Evgenidis. "T1333 Increased Pulse Wave Velocity in Patients With Inflammatory Bowel Diseas. Preliminary Results of an Ongoing Study". Gastroenterology 138, nr 5 (maj 2010): S—539. http://dx.doi.org/10.1016/s0016-5085(10)62486-9.

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Alexander, Richard J., Asit Panja, Evonne Kaplan-Liss, Lloyd Mayer i Robert F. Raicht. "Expression of growth factor receptor-encoded mRNA by colonic epithelial cells is altered in inflammatory bowel diseas". Digestive Diseases and Sciences 40, nr 3 (marzec 1995): 485–94. http://dx.doi.org/10.1007/bf02064355.

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Eindor, A., L. Meleady i K. Jacobson. "P147 Progression to biologic treatment in very early onset inflammatory bowel disease patients- a long term follow up retrospective study". Journal of Crohn's and Colitis 15, Supplement_1 (1.05.2021): S229—S230. http://dx.doi.org/10.1093/ecco-jcc/jjab076.274.

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Abstract Background Very early onset inflammatory bowel disease (VEOIBD) prevalence has been increasing over the last decades. These young patients have been known to have special disease characteristics and disease location. Although it is known that only a low percentage of these patients require biologic treatment after diagnosis, there is only scarce evidence about their long- term outcome and biologic requirements. We aimed to assess the long term outcome of VEOIBD patients and the time of progression to biologic treatment. Methods We retrospectively reviewed IBD patients diagnosed under 6 years of age, between January 2005 and December 2019, from the British Columbia (BC) Pediatric IBD database. Demographic data, disease characteristics and symptoms at diagnosis were documented. The disease location and severity were documented according to the Paris classification. Data collected retrospectively until the last appointment recorded in the electronic medical records included whether the patient received biologic treatment at the time of follow up, the time to intiation of the treatment, the type of biologic treatment and response. Kaplan meier curves were used to asses the number of years to progression to biologic treatment and the parameters influencing it. Results 89 patients under the age of 6 were diagnosed with IBD during the study period. 3 patients failed to meet inclusion criteria and were excluded. Median age at diagnosis was 3.8 (IQR 2.6–5.1). 45.3% of patients had Crohn’s disease (CD) and 62.8% were males. Median time of follow up was 6.39 (IQR 3.71–10.55). 68.1% of the ulcerative colitis (UC) patients had pancolitis and 48.7% of CD patients had ileocolonic disease. 39.5% of patients were started on biologic treatment and 7.1% underwent surgery. Kaplan Meier curves demonstrated that patients diagnosed in the years 2012 -2019 had shorter duration of progression to biologics than those diagnosed 2005–2011 (p=0.0047). In patients with CD those with perianal or stricturing disease progressed faster to biologic treatment (p=0.024,p=0.038, respectively) and in UC patients those with high severity of disease (p=0.017). 63.6% of patients were reported to be on clinical remission on the biologic treatment. Conclusion Although VEOIBD patients have more extensive diseas, they require less biologic treatment than previously reported in older patients. Factors influencing shorter duration of progression to biologics were the severity of disease and behaviour and not disease location. Patients diagnosed more recently had shorter duration to biologic treatment which might reflect physicians perception on using biologic treatment in these young patients rather than disease severity.

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Falcón-Guerrero, Britto Ebert. "Coincidencia entre la periodontitis y la enfermedad inflamatoria del intestino". Kiru 20, nr 1 (31.03.2023): 28–33. http://dx.doi.org/10.24265/kiru.2023.v20n1.03.

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HUSNÍK, R., J. KLIMEŠ, K. TOMANOVÁ, J. SMOLA, R. HALOUZKA, F. TICHÝ i J. BRÁZDIL. "Lawsonia intracellularis in a dog with inflammatory bowel disease". Veterinární Medicína 48, No. 5 (30.03.2012): 141–45. http://dx.doi.org/10.17221/5761-vetmed.

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A two-year-old male German short-haired pointer was presented with a 1.5-year history of intermittent small-bowel diarrhoea. Inflammatory bowel disease (chronic lymphocytic-plasmacytic gastritis, enteritis and colitis) was diagnosed on the basis of histological examination of biopsies obtained on repeated endoscopy and by exclusion of other possible causes. Warthin-Starry silver staining of stomach mucosa revealed the presence of gastric spiral organisms. The evidence of L. intracellularis was provided by a positive nested polymerase chain reaction in one biopsy of duodenal mucosa and in one rectal smear. In 5 blood sera collected over a period of 8 months the IgG antibodies to L. intracellularis were found by an indirect fluorescent antibody test. Treatment with oral prednisone led only to a temporary improvement.

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Fernandes, Isabel, i Lúcia Gil. "Qualidade de vida da pessoa com doença inflamatória intestinal". Revista de Enfermagem Referência IV Série, nr 23 (23.12.2019): 89–98. http://dx.doi.org/10.12707/riv19048.

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Kumar Kasula Suresh, Bharath. "Emerging Therapies for Inflammatory Bowel Disease: A Systematic Overview". International Journal of Science and Research (IJSR) 13, nr 3 (5.03.2024): 1449–51. http://dx.doi.org/10.21275/mr24322201434.

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Rozprawy doktorskie na temat "Inflammatory bowel diseas"

Cotterill, Lynn. "Inflammatory bowel disease genetics". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/inflammatory-bowel-disease-genetics(daae1a60-2790-4280-b7d5-ac5ec7533c7c).html.

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Inflammatory bowel disease (IBD), which includes the subtypes Crohn's disease (CD) and ulcerative colitis (UC), is a common disease particularly in the Western world. IBD is characterised by inflammation of the small intestine and/or colon. The two subtypes affect different gut locations but both show an increased intestinal permeability or the 'leaky gut syndrome'. This led to the hypothesis that tight junction (TJ) proteins expressed in the epithelium may affect the intestinal permeability as a cause or effect of IBD.Initially, variants in the CARD15, IL23R and ATG16L1 genes, previously associated with an increased risk of IBD, were genotyped in a cohort of 500 IBD (295 CD and 205 UC) patients and 877 matched controls. These variants were significantly associated in our cohort. A random effects meta-analysis was undertaken on all previously reported CD associations with the variant rs2241880 from ATG16L1 (n=25, p=0.0017, OR: 1.36 95% CI 1.12-1.66) and with rs11209026 from IL23R (n=26, p=0.0006, OR: 0.37 95% CI 0.21-0.67), showing pooled odds ratios consistent with those reported in our cohort. Individuals carrying >1 CARD15 mutant variant were found to have a 2.5 fold increased risk of CD (p=0.0001). Candidate TJ proteins were chosen on the basis of previous reported associations and through the investigation of the claudin proteins which are abundant at TJs. Twenty one candidate genes were selected and 79 variants successfully genotyped in up to 1063 IBD (502 CD and 478 UC) and 870 control patients. Significant associations were detected with variants in the CLDN1, CLDN5 and CDH1 genes with CD; CLDN5, CLDN8 and CDH1 variants were associated to IBD; and the rs7791132 variant (between CLDN4 and ELN) and a CDH1 variant were associated to UC. The CLDN1 rs6809685 variant trended towards association in a Toronto ascertained IBD replication cohort (genotypic p=0.04, allelic p=0.06) suggesting this may be a novel IBD susceptibility variant. Small intestinal biopsies from CD patients with known rs6809685 genotypes showed a dose dependent reduced immunohistochemical staining of claudin 1 with carriage of the mutant G allele. Claudin 1 helps seal TJs and reduced levels may increase risk of CD.Peroxisome proliferator activator receptors (PPARs) can directly affect TJ proteins and could therefore affect intestinal permeability. Twelve PPARγ variants were genotyped in up to 1050 IBD (502 CD and 467 UC) and 725 control patients. Significant genotypic associations were found with the rs2067819 variant in CD (p=0.05) and IBD (p=0.02), and also the rs13099634 variant in UC (P=0.02). There was a strong gender difference particularly for rs2067819 and rs4135247, where allelic associations were highly significant and increased risk of IBD in men (p=0.01 and p=0.007 respectively). However no significant associations were found in the female cohort. Troglitazone a PPARα agonist increased Caco2 cell transepithelial electrical resistance (TEER), a marker of TJ integrity, and increased expression of claudins -3 and -4. In contrast, the PPARα antagonist GW6471 reduced the TEER without causing cell death and PPARγ ligands did not affect TEER measurements. In summary, using a robust cohort of cases and controls the data indicates that variants in genes encoding TJ proteins may affect susceptibility to IBD and that PPARs can regulate these proteins altering intestinal permeability.

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Pozuelo, del Río Marta. "Metagenomics in inflammatory bowel disease". Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/669437.

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La microbiota intestinal desempeña un papel crucial en el manteniendo la homeostasis intesitnal. Alteraciones en la composición microbiana, también conocidas como disbisosis, pueden poner en peligro el estado de salud e incrementar el riesgo a padecer una enfermedad. Aunque muchas enfermedades se han asociado a cambios en la microbiota intestinal, todavía se desconoce si dichas alteraciones son la causa o la consecuencia de las patologías. La enfermedad inflamatoria intestinal (EII) es una enfermedad inflamatoria crónica que se caracteriza por periodos de inflamación y constituye un problema de salud dado. La EII presenta dos subtipos: enfermedad de Crohn y colitis ulcerosa, con síntomas similares pero diferentes manifestaciones clínicas. La EII se ha relacionado ampliamente con cambios en la microbiota intestinal. A pesar de los múltiples estudios que existen, no hay un claro consenso en el perfil microbiano asociado a la enfermedad. Las principales discordancias se dan entre las diferencias asociadas a enfermedad de Crohn y la colitis ulcerosa. Algunos investigadores han demostrado que la composición microbiana en colitis ulcerosa es muy similar a la de individuos sanos y ambas difieren de la composición de enfermos de Crohn. En cambio, otros investigadores han visto que las diferencias de colitis ulcerosa y Crohn respecto a sanos son muy similares por lo que consideran ambos subtipos como una única enfermedad (EII). El principal objetivo de esta tesis es determinar la disbiosis en una cohorte de EII española para evaluar hasta qué punto las funciones y composición microbiana difieren entre Crohn y colitis y si los datos de microbioma podrían emplearse como herramientas de diagnóstico. Para ello, analizamos muestras fecales de sanos, enfermos de Crohn y enfermos de colitis usando dos metodologías: secuenciación del gen 16SARNr (o 16S ADNr) y secuenciación por fragmentación del genoma. Como se preveía, observamos la presencia de disbiosis en EII. Además, vimos que las alteraciones en composición microbiana y funciones eran diferentes para Crohn que para colitis, mostrando una mayor disbiosis en Crohn que en enfermos de colitis ulcerosa y con colitis mostrando un patrón muy similar a la microbiota de individuos sanos. Los resultados funcionales encontrados en esta tesis confirman la mayor disbiosis descrita en pacientes de Crohn en comparación con pacientes de colitis ulcerosa en composición microbiana. Estos individuos presentan una mayor cantidad de genes principalmente asociados a metabolismo y enfermedades inmunes que los enfermos de colitis ulcerosa y sanos. A pesar de que los datos de 16S ADNr y secuenciación por fragmentación no detectaron las mismas diferencias entre Crohn y colitis, ambas metodologías permitieron la clasificación de los distintos subtipos de EII con una proporción similar. Más estudios son necesarios para validar los resultados de esta tesis en otras cohortes de pacientes que incluyan Crohn localizado en colon o pacientes recién diagnosticados que no hayan sido sometidos a tratamiento antes de la aplicación de estas metodologías como herramientas diagnósticas en clínica.
The gut commensal microbiota is known to play a crucial role in maintaining intestinal homeostasis. Alterations in the microbial community composition, also known as dysbiosis, may put health status in risk and increase susceptibility to diseases. Although several diseases have been related to shifts in the gut microbiome composition, it is still uncertain whether those alterations are the cause or consequence of the disease. Inflammatory bowel disease (IBD) is a chronic inflammatory disease with periods of active and inactive inflammation that constitutes to an important health problem. It is divided in two subtypes: Crohn’s disease (CD) and ulcerative colitis (UC) that present similar symptoms but different clinical manifestations. IBD has been widely associated with an alteration of the gut microbiome composition. Nevertheless, there is no clear consensus on the microbial pattern characteristic of the disorders. Main discordances between studies are related to differences between UC and CD. Some previous publications indicate that UC microbial composition is very similar to healthy and differs from CD whereas others consider both subtypes as a unique entity and find high alterations in UC and CD microbial composition in comparison with the microbiome of healthy individuals. The aim of this thesis was to characterize the dysbiosis in a Spanish IBD cohort to evaluate to which extend the gut microbiome composition and function could be differentiated between CD and UC and whether microbiome data could be used as diagnostic and prognostic tools. For this purpose, we analyzed fecal samples of healthy individuals, CD (affected in the ileum) and UC patients using two different methodologies: 16S rRNA gene (or 16S rDNA) and shotgun (short genomic fragments) sequencing. As expected, we observed the presence of dysbiosis in IBD. Furthermore, we showed that microbial composition and function alterations were different for CD and UC, with greater dysbiosis in CD than in UC and with UC resembling more to a healthy state. Functional findings also confirmed this higher dysbiosis in CD than in UC and revealed genes implicated in metabolism pathways and in immune diseases in higher abundance in CD compared with healthy individuals and UC. Although 16S rDNA and shotgun data did not detect differences in the dysbiosis in CD and UC in a consistent manner, both methodologies allowed the classification of IBD subtypes in a similar proportion. Future studies should validate these results using other patient cohorts such as colonic CD or recently diagnosed patients before the application of these techniques as diagnostic tools in clinical practice.

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Geerling, B. J. "Inflammatory bowel disease and nutrition". Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=7216.

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Smith, Graeme Drummond. "Counselling in inflammatory bowel disease". Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/12244.

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Introduction; The inflammatory bowel diseases (IBD), Crohn's disease (CD) and ulcerative colitis (UC), affect well over 100,000 people in the United Kingdom Health related quality of life (HRQOL) is influenced by many factors in IBD including; the nature and severity of the disease, socio-economic factors, age, psychological well-being as well as· the efficacy and complications of treatment. Pilot Studies; Quality of life was assessed in 140 IBD patients (70 CD/70 UC). Diarrhoea was, not surprisingly, the most commonly reported physical symptom in both CD and UC and impaired faecal continence caused great social disability, with 72% CD patients and 68% UC patients reporting urgency or incontinence. Over a third of all patients reported occupational problems associated with their disease. Anxiety, but not depression, was common in the CD group and a major source of anxiety in many cases was lack of information. Three-quarters of patients felt additional information would have enabled them to cope with their chronic illness. It is a common perception that the provision of psychological support, such as the use of counselling skills, may alleviate many of the psychosocial problems associated with IBD, but this has not yet been proven. Hypothesis: That a nurse led counselling service improves HRQOL in IB D patients. Study Group/Design: Fifty patients with CD (aged 16-64, 33 females), 50 UC patients (aged 17-60, 26 females), 50 healthy volunteers (HV, aged 17- 61, 27 females) and a disease control group comprising 28 psoriatic arthritis (PS) patients (aged 22-66, 16 females) undeiwent structured interviews and completed a range of questionnaires measuring several facets of quality of life and psychological well-being (Hospital Anxiety and Depression Score (HAD), Attitudes and Preferences (AP), Styles and Strategies (SS) and Short-form 36 (SF36)). Patients with IBD were then randomised to receive either a counselling package or routine clinical follow-up. The counselling package consisted of disease specific information and teaching of stress management techniques, based on the "Challenge to change" programme devised by Dr. Derek Roger at the University of York. HRQOL scores were compared on entry at 6 and 12 months. Results; At baseline the scores for all questionnaires were within the nonnal range in the UC, PS, and HV groups. However CD patients recorded significantly higher anxiety scores (p

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Gustavsson, Anders. "Therapy in inflammatory bowel disease". Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-25599.

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The aim of this thesis is to study treatment of inflammatory bowel disease with respect to an acute severe attack of ulcerative colitis and endoscopic balloon dilation in stricturing Crohn’s disease. A retrospective follow-up was made in 158 patients who were given intensive intravenous corticosteroid treatment due a severe, moderate, or mild attack of ulcerative colitis between 1975 and 1982. After 10 years, the colectomy frequency in the severe disease group was 64%, and 49% and28% in the moderate and mild groups, respectively. Severity of the original attack did not influence the subsequent clinical course with respect to colectomy. In 2005, a controlled Swedish–Danish trial of infliximab as rescue therapy in an acute severe attack of steroid refractory ulcerative colitis showed that colectomy frequencies after 3 months were lower in infliximab-treated patients (29%) compared to placebo-treated patients (67%). After 3 years, a statistically significantly lower colectomy frequency remained in patients treated with infliximab (50%) compared to placebo (76%). Between 1989 and 2009, 178 patients underwent endoscopic balloon dilation due to intestinal strictures in Crohn’s disease. Seventy-five patients,with a follow-up of 5 years or longer, underwent dilations due to symptomatic strictures only. After 5 years of follow-up, 39/75 (52%) of the patients had undergone no further intervention or one additional dilation only, and 36% had had surgery. The complication frequency was 5.3%, of which 10 patients (1.3%) required surgery. In 83 patients, we studied whether smoking at diagnosis affected the outcome after index dilation. In the group of active smokers, 31/32 (97%) underwent another intervention compared to 18/33 (55%) in never smokers (HR 2.18, 95% CI: 1.22-3.93,p = 0.01). Clinical parameters such as sex, age at diagnosis, age at first dilation, balloon size, localisation of stricture, treatment with azathioprine and treatment period did not influence outcome.

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Matini, Lawrence. "Adaptation to Inflammatory Bowel Disease". Thesis, University of Surrey, 2017. http://epubs.surrey.ac.uk/841456/.

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Inflammatory bowel disease (IBD) is a term used to describe two chronic diseases of the gastrointestinal tract: Ulcerative Colitis (UC) and Crohn's Disease (CD). Although the efficacy of treatment is continuously improving, Quality of Life (QoL) in this illness population remains low with many patients suffering from psychological and psychiatric comorbidities. Psychological interventions aimed at improving outcomes in these patients have largely demonstrated little improvement. This thesis argues that this may be the result of poor understanding of the experience of living with this condition with too little focus on the adaptation of the patient to their illness. This thesis aimed to address this gap in the literature through four empirical studies. Firstly, Study 1 used a qualitative design to (n = 22) to explore the lived experiences of patients with IBD and to conceptualise adaptation to IBD. The results highlighted the importance of making sense of the illness and the impact and feelings associated with the illness. This was transcended by a notion of uncertainty which was resolved by employing coping mechanisms to restore equilibrium between their identity before and after diagnosis, resulting in a 'new normal'. Study 2 then employed a cross-sectional design (n = 307) to develop a new measure of adaptation to IBD (the A-IBD) which after psychometric analysis revealed four subscales including person identity, patient identity, acceptance and expectations. This study also explored the degree of association of the A-IBD with existing measures of sense making (BIPQ) and QoL (IBDQ), to assess the ability of the A-IBD in predicting QoL and ascertain whether it could predict QoL over and above sense making. The results suggested the A-IBD was not synonymous with these constructs and had utility as a predictor of QoL even when accounting for the predictive ability of the BIPQ. Finally, Study 3 used a combination of qualitative and quantitative design (n = 16). Patients scoring in the top and bottom 25% of the A-IBD from Study 2 completed the measure again to assess the dynamic nature of adaptation and were interviewed about the factors that either encouraged or inhibited their degree of adaptation. This analysis revealed that adaptation is indeed dynamic, and that antecedents of adaptation include 'engagement', 'resilience' and certain 'contingencies' including disease and social factors. Overall, the findings from this thesis indicate that the treatment of IBD must be approached in a biopsychosocial manner, that adaptation can be measured effectively with the new tool and that adaptation, with an emphasis on the notion of person, not patient, predicts quality of life.

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Gerasimidis, Konstantinos. "Nutritional aspects and gut microbiota in paediatric inflammatory bowel disease". Thesis, Thesis restricted. Connect to e-thesis to view abstract, 2009. http://theses.gla.ac.uk/826/.

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Thesis (Ph.D.) - University of Glasgow, 2009.
Ph.D. thesis submitted to the Division of Developmental Medicine, Faculty of Medicine, University of Glasgow, 2009. Includes bibliographical references. Print version also available.

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Campbell, Simon Scott. "Azathioprine use in inflammatory bowel disease". Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/24109.

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Ljung, Tryggve. "Nitric oxide in inflammatory bowel disease /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-602-2/.

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Parkes, Miles. "The genetics of inflammatory bowel disease". Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326030.

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Książki na temat "Inflammatory bowel diseas"

Cohen, Russell D. Inflammatory Bowel Disease. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593119.

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Rajapakse, Ramona, red. Inflammatory Bowel Disease. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81780-0.

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Sobrado, Carlos Walter, i Wilton Schmidt Cardozo. Inflammatory Bowel Disease. Wyd. 2. New York: River Publishers, 2022. http://dx.doi.org/10.1201/9781003338550.

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Stein, Daniel J., i Reza Shaker, red. Inflammatory Bowel Disease. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14072-8.

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Cohen, Russell D., red. Inflammatory Bowel Disease. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53763-4.

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Cohen, Russell D., red. Inflammatory Bowel Disease. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-60327-433-3.

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Sutherland, L. R., S. M. Collins, F. Martin, R. S. McLeod, S. R. Targan, J. L. Wallace i C. N. Williams, red. Inflammatory Bowel Disease. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5.

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1909-, Kirsner Joseph B., i Shorter Roy G. 1925-, red. Inflammatory bowel disease. Wyd. 4. Baltimore: Williams & Wilkins, 1995.

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A, Anagnostides A., Hodgson H. J. F i Kirsner Joseph B. 1909-, red. Inflammatory bowel disease. London: Chapman and Hall Medical, 1991.

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G, Farmer Richard, red. Inflammatory bowel disease. Philadelphia: Saunders, 1990.

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Części książek na temat "Inflammatory bowel diseas"

Kirsner, Joseph B. "Inflammatory Bowel Disease (Ulcerative Colitis, Crohn’s Disease)". W Inflammatory Bowel Disease, 1–16. Totowa, NJ: Humana Press, 2003. https://doi.org/10.1007/978-1-59259-311-8_1.

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Yang, H., i J. I. Rotter. "Subclinical markers of human IBD". W Inflammatory Bowel Disease, 5–14. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_1.

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Braun, J., Y. Valles-Ayoub, L. Berberian, M. Eggena, L. K. Gordon i S. Targan. "On the pathogenesis trail: what marker B cell clones tell us about IBD". W Inflammatory Bowel Disease, 96–103. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_10.

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Wright, N. A. "Growth factors in IBD". W Inflammatory Bowel Disease, 107–20. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_11.

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Grisham, M. B., S. Aiko i T. E. Zimmerman. "Nitric oxide and chronic colitis". W Inflammatory Bowel Disease, 121–26. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_12.

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Barrett, K. E. "Cytokine interactions with epithelium". W Inflammatory Bowel Disease, 129–38. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_13.

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Perdue, M. H. "Immunomodulation of epithelium". W Inflammatory Bowel Disease, 139–48. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_14.

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Sharkey, K. A., i E. J. Parr. "The enteric nervous system in intestinal inflammation". W Inflammatory Bowel Disease, 149–61. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_15.

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Collins, S. M., I. Khan, B. Vallance i C. Hogaboam. "The role of smooth muscle in intestinal inflammation". W Inflammatory Bowel Disease, 162–69. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_16.

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Weingarten, H. P. "Brain—gut interactions in IBD: mechanisms of anorexia in animal models of experimental colitis". W Inflammatory Bowel Disease, 170–79. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-009-0371-5_17.

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Streszczenia konferencji na temat "Inflammatory bowel diseas"

Sitaraman, Surendar Rama, Myasar Mundher Adnan, K. Maharajan, R. Krishna Prakash i R. Dhilipkumar. "A Classification of Inflammatory Bowel Disease using Ensemble Learning Model". W 2024 First International Conference on Software, Systems and Information Technology (SSITCON), 1–5. IEEE, 2024. https://doi.org/10.1109/ssitcon62437.2024.10796250.

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Vallelunga, Rosarina, Marianna Milano, Rocco Spagnuolo, Lidia Giubilei, Evelina Suraci, Mario Cannataro i Francesco Luzza. "Visualization of Comorbidities in Inflammatory Bowel Diseases through Networks". W 2024 IEEE International Conference on Bioinformatics and Biomedicine (BIBM), 4392–98. IEEE, 2024. https://doi.org/10.1109/bibm62325.2024.10821713.

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Rojas-Velazquez, David, Sarah Kidwai, Luciënne de Vries, Péter Tözsér, Luis Oswaldo Valencia-Rosado, Johan Garssen, Alberto Tonda i Alejandro Lopez-Rincon. "Machine-Learning Analysis of mRNA: An Application to Inflammatory Bowel Disease". W 2024 16th International Conference on Human System Interaction (HSI), 1–7. IEEE, 2024. http://dx.doi.org/10.1109/hsi61632.2024.10613568.

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Kolawole, Bisi Bode, Ujwala Chaudhari, Giovanni Santacroce, Irene Zammarchi, Rocio Del Amor, Pablo Meseguer, Andrea Buda i in. "Inflammation Detection Using Ensemble Endoscopic Multimodal Assessment in Inflammatory Bowel Disease". W 2024 IEEE International Symposium on Biomedical Imaging (ISBI), 1–4. IEEE, 2024. http://dx.doi.org/10.1109/isbi56570.2024.10635162.

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Cai, Lingrui, Ryan W. Stidham, Emily Wittrup i Kayvan Najarian. "Adapting Segment Anything Model for Ulcer Segmentation in Inflammatory Bowel Disease". W 2024 46th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC), 1–4. IEEE, 2024. https://doi.org/10.1109/embc53108.2024.10781516.

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Gao, Ziyang, Kai-Yuan Chen, Olaf Mueller, Han Zhang, Nikolai Rakhilin, Jiande Chen i Xiling Shen. "Microbiota of Inflammatory Bowel Disease Models". W 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8512848.

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Stark, Christopher M., Gregory Gorman i Cade Nylund. "Pediatric Inflammatory Bowel Disease and Urolithiasis". W Selection of Abstracts From NCE 2016. American Academy of Pediatrics, 2018. http://dx.doi.org/10.1542/peds.141.1_meetingabstract.756.

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Irandost, M., i R. Alalawi. "Pulmonary Manifestations of Inflammatory Bowel Disease". W American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a2654.

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Kean, Siobhan, Jennifer Massey, Martin Jude i Matthew Silsby. "3133 Ocrelizumab and inflammatory bowel disease". W ANZAN Annual Scientific Meeting 2024 Abstracts, A42.2—A42. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/bmjno-2024-anzan.118.

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King, Dominic, Joht Chandan, Tom Thomas, Nij Bhala, Krish Narantharan, Nicola Adderley, Raoul Reulen i Nigel Trudgill. "P120 Risk of inflammatory bowel disease in subjects with dermatological disorders associated with inflammatory bowel disease". W Abstracts of the BSG Campus, 21–29 January 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2020-bsgcampus.195.

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Raporty organizacyjne na temat "Inflammatory bowel diseas"

Grueso-Navarro, Elena, Leticia Rodríguez-Alcolado, Ángel Arias, Emilio J. Laserna-Mendieta i Alfredo J. Lucendo. Influence of HLA-DQA1*05 allele in the response to anti-TNFα drugs in inflammatory bowel diseases. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, luty 2023. http://dx.doi.org/10.37766/inplasy2023.2.0076.

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Review question / Objective: Do patients with inflammatory bowel disease and treated with any anti-TNFα drug who had the HLA-DQA1*05 allele (in heterozygosis or homozygosis) have lower response or persistence to those drugs than patients without HLA-DQA1*05 allele? Condition being studied: Inflammatory bowel diseases (IBD), which includes Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory condition that may affect any part of the digestive tract (CD) or be limited to the colon (UC). While the specific aetiology of IBD remains unknown, it is believed to involve a complex impairment in the immunity of the gut mucosa due to a combination of several genetic and environmental factors, being the microbiota one of the latest that more attraction has received in recent years. Symptoms of IBD (such as abdominal pain, diarrhoea, fever, tiredness or rectal bleeding) may be either constant or alternate between periods of limited disease activity and flares with remarkable presence of symptoms. As IBD is associated with significant morbidity and disability, pharmacological treatment is required in most cases, especially in CD, aimed at reducing the inflammatory response and attenuating the activity of the immune system. In the moderate and severe forms of the disease, therapy is usually based on immunosuppressant and/or biological drugs. Among the latest, anti-TNFα drugs (infliximab or adalimumab) are normally chosen as the initial biological therapy.

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Olsen, A. S., i C. T. Wake. Inflammatory Bowel Disease Gene Discovery Final Report CRADA No. TC-1335-96. Office of Scientific and Technical Information (OSTI), marzec 2018. http://dx.doi.org/10.2172/1430922.

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Sun, Lina, Yanan Han, Hua Wang, Huanyu Liu, Shan Liu, Hongbin Yang, Xiaoxia Ren i Ying Fang. MicroRNAs as Potential Biomarkers for the Diagnosis of Inflammatory Bowel Disease: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, luty 2022. http://dx.doi.org/10.37766/inplasy2022.2.0027.

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Review question / Objective: The purpose of this systematic review was to systematically review the clinical studies regarding miRNAs as diagnostic biomarkers for inflammatory bowel disease and assess the overall diagnostic accuracy of miRNAs. Condition being studied: The symptoms of inflammatory bowel disease (IBD) are highly variable. The diagnosis of IBD must be made through medical history, physical, laboratory, radiologic, endoscopic, and histological examinations. However, these diagnostic techniques are not specific and sometimes even equivocal. Therefore, reliable biomarkers are urgently needed in the diagnosis of IBD. Several clinical and preclinical researches have shown that dysregulated microRNAs (miRNAs) play a crucial role in IBD development. miRNAs, as single-stranded noncoding RNAs that contain 22-24 nucleotides, can post-transcriptionally regulate gene expression by blocking mRNA translation or degrading target mRNAs. miRNAs are widely involved in physiological and pathological cellular processes, such as differentiation, proliferation and apoptosis. Besides, they are stable, noninvasive, and resistant to degradation by ribonucleases, making them valuable targets in the diagnosis, monitoring, prognosis, and treatment of diseases. To date, inconsistent results have been found about miRNA expression profiling in the patients with IBD. Moreover, the diagnostic accuracy of miRNAs for IBD has not been reported in any meta-analysis.

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Güngör, Darcy, Perrine Nadaud, Carol Dreibelbis, Concetta LaPergola, Nancy Terry, Yat Ping Wong, Steve Abrams i in. Never Versus Ever Feeding Human Milk and Inflammatory Bowel Disease: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, kwiecień 2019. http://dx.doi.org/10.52570/nesr.pb242018.sr0222.

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Cai, Lun, Jie Liu, Rongrong Yang, Liping Wei, Huazheng Luo i Xiongbin Gui. Meta-analysis of the Risk of Allergic Rhinitis in Patients with Inflammatory Bowel Disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2023. http://dx.doi.org/10.37766/inplasy2023.5.0077.

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ZHENG, Jiansheng, i Tang ZHU. Polymorphism of fucosyltransferase 3 (FUT3) gene is associated with inflammatory bowel disease (IBD) — a systematic review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2022. http://dx.doi.org/10.37766/inplasy2022.3.0001.

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Review question / Objective: Polymorphism of fucosyltransferase 3 (FUT3) gene is associated with inflammatory bowel disease (IBD) — a systematic review and Meta-analysis. Condition being studied: This study collected relevant literatures and analyzed the relationship between the polymorphism of the FUT3 genes at rs3745635, rs3894326, and rs28362459 to the IBD with Meta-analysis, in order to further explore the possible mechanism of the polymorphism of the FUT3 gene and IBD.

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Lewis, James, Meenakshi Bewtra, Frank Scott, Colleen Brensinger, Shelby Reed, Jason Roy, Mark Osterman i in. Patient Valued Comparative Effectiveness of Corticosteroids versus Anti-TNF Alpha Therapy for Inflammatory Bowel Disease. Patient-Centered Outcomes Research Institute (PCORI), listopad 2018. http://dx.doi.org/10.25302/11.2018.ce.12114143.

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Shi, Shanzhen, Jiaxing Feng, Yu Li i Huaxiu Shi. Risk factors for vitamin D deficiency in inflammatory bowel disease: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2020. http://dx.doi.org/10.37766/inplasy2020.6.0028.

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Kokkotou, Efi. Investigation of the Role of Stress in Inflammatory Bowel Disease Using Zebrafish as an Experimental Model. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2012. http://dx.doi.org/10.21236/ada566781.

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Güngör, Darcy, Perrine Nadaud, Carol Dreibelbis, Concetta LaPergola, Nancy Terry, Yat Ping Wong, Steve Abrams i in. Shorter Versus Longer Durations of Exclusive Human Milk Feeding and Inflammatory Bowel Disease: A Systematic Review. U.S. Department of Agriculture, Food and Nutrition Service, Center for Nutrition Policy and Promotion, Nutrition Evidence Systematic Review, kwiecień 2019. http://dx.doi.org/10.52570/nesr.pb242018.sr0224.

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