Relevant bibliographies by topics / Crohn's disease

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Crohn's disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Crohn's disease"

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Arnott, I. D. R. "Crohn's disease or Crohn's diseases?" Gut 52, no. 4 (April 1, 2003): 460–61. http://dx.doi.org/10.1136/gut.52.4.460.

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Haubich, William S. "Crohn of Crohn's disease." Gastroenterology 116, no. 5 (May 1999): 1034. http://dx.doi.org/10.1016/s0016-5085(99)70056-9.

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Catalin, Popescu Razvan, Leopa Nicoleta, Micu Luminita Gentiana, Costea Daniel Ovidiu, Olteanu Cornelia Minodora, Ciobanu Florin, and Dumitru Andrei. "Colon Cancer in Patients with Crohn’s Disease and Diabetes Mellitus." ARS Medica Tomitana 26, no. 3 (August 1, 2020): 150–53. http://dx.doi.org/10.2478/arsm-2020-0030.

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Abstract Introduction: Diabetes mellitus and colorectal cancer are diseases with an increasing impact on the population. Colorectal cancer is a well-recognized complication of inflammatory bowel diseases, such as ulcerative colitis and Crohn’s colitis. Here we describe an unusual case of diabetes mellitus, Crohn`s colitis-associated cancer. Case report: We report the case of a 49-year-old woman, known with Crohn's disease and diabetes, who developed a transverse colon adenocarcinoma associated with multiple outbreaks of high-grade or low-grade intraepithelial dysplasia/neoplasia, for which a subtotal proctocolectomy with ileorecto-anastomosis with “J” pouch it was made. Conclusions: The risk of colonic carcinoma in Crohn's disease is increasing. An association of colorectal cancer with diabet mellitus and inflammatory bowel disease has been established. From diagnosis to treatment the management of these cases can be difficult and challenging.
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Ainley, C. C., J. Cason, L. K. Carlsson, B. M. Slavin, and R. P. H. Thompson. "Zinc status in inflammatory bowel disease." Clinical Science 75, no. 3 (September 1, 1988): 277–83. http://dx.doi.org/10.1042/cs0750277.

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1. The zinc contents of plasma, erythrocytes, polymorphonuclear leucocytes and mononuclear leucocytes from 18 normal control subjects, 31 patients with Crohn's disease and 15 patients with ulcerative colitis were measured. 2. Plasma zinc levels were low in Crohn's disease, particularly in malnourished patients, and related to plasma albumin concentrations, but were normal in ulcerative colitis. 3. Erythrocyte zinc levels were normal in both Crohn's disease and ulcerative colitis. 4. Mean polymorphonuclear leucocyte zinc levels were normal in Crohn‘s disease and ulcerative colitis. Ten per cent of Crohn's disease patients had subnormal levels, which were associated with inactive disease, while 10% had elevated levels, which were associated with active disease. Seven per cent of ulcerative colitis patients had subnormal levels. Mononuclear leucocyte zinc levels were normal in Crohn's disease and in ulcerative colitis. 5. Tissue zinc depletion occurs in only a few patients with Crohn's disease and ulcerative colitis.
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Rożalski, Michał. "Extraintestinal Crohn's disease (metastatic Crohn's disease)." Dermatology Review 5 (2014): 418–22. http://dx.doi.org/10.5114/dr.2014.46074.

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Sachdev, Ritu, and David R. Cave. "When Is Crohn's Disease Crohn's Disease?" Inflammatory Bowel Diseases 10, no. 1 (January 2004): 63. http://dx.doi.org/10.1097/00054725-200401000-00012.

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Nurul Utami, Herdiana, Ira Munirah, Latifah Mukhlisatunnafsi, Marwa Zileikhadira Manzalina, Yusra Pintaningrum, and Jaini Rahma. "CROHN DISEASE: Patofisiologi, Diagnosis, dan Penatalaksanaan." Lombok Medical Journal 2, no. 1 (May 15, 2023): 5–13. http://dx.doi.org/10.29303/lmj.v2i1.2340.

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ABSTRAK Penyakit Crohn adalah kondisi radang usus idiopatik kronis, ditandai dengan lesi, yang dapat memengaruhi seluruh saluran cerna mulai dari mulut hingga anus. Insiden tahunan penyakit crohn mencapai 3 hingga 20 kasus per 100.000 dengan usia rata-rata 30 tahun. Patofisiologi penyakit crohn didasarkan pada peradangan jaringan oleh respons imun yang tidak dapat dikendalikan terhadap antigen bakteri. Penegakan diagnosis dengan Computed tomography (CT), magnetic resonance imaging (MRI), dan ultrasonografi menjadi standar diagnosis dari penyakit crohn. Prognosis dari penyakit crohn ini tergantung dari komplikasi yang muncul seperti fistula dan bowel obstruction usus serta kondisi remisi dari pasien, ataupun tingkat respon tiap pasien terhadap pengobatan sehingga dalam menangani penyakit crohn adalah mengobati kondisi peradangan aktif hingga cepat mengalami remisi dan mempertahankannya selama mungkin. Kata Kunci: crohn disease; patofisiologi; diagnosis; penatalaksanaan; prognosis ABSTRACT Crohn's disease is a chronic idiopathic inflammatory bowel condition, characterized by lesions, which can affect the entire gastrointestinal tract from the mouth to the anus. The annual incidence of Crohn's disease is 3 to 20 cases per 100,000 with a median age of 30 years. The pathophysiology of Crohn's disease is based on tissue inflammation by an uncontrollable immune response to bacterial antigens. Computed tomography (CT), magnetic resonance imaging (MRI), and ultrasonography have become the standard for the diagnosis of Crohn's disease. The prognosis of Crohn's disease depends on complications such as enteric fistula and intestinal neoplasia and the condition of remission of the patient, or the level of response of each patient to treatment so that in treating Crohn's disease is to treat the active inflammatory condition until it goes into remission quickly and maintain it as long as possible. Keyword: crohn disease; pathophysiology; diagnosis; treatment; prognosis
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Karateke, Faruk, Ebru Menekşe, Koray Das, Sefa Ozyazici, and Pelin Demirtürk. "Isolated Duodenal Crohn's Disease: A Case Report and a Review of the Surgical Management." Case Reports in Surgery 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/421961.

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Crohn's disease may affect any segment of the gastrointestinal tract; however, isolated duodenal involvement is rather rare. It still remains a complex clinical entity with a controversial management of the disease. Initially, patients with duodenal Crohn' s disease (DCD) are managed with a combination of antiacid and immunosuppressive therapy. However, medical treatment fails in the majority of DCD patients, and surgical intervention is required in case of complicated disease. Options for surgical management of complicated DCD include bypass, resection, or stricturoplasty procedures. In this paper, we reported a 33-year-old male patient, who was diagnosed with isolated duodenal Crohn’s diseases, and reviewed the surgical options in the literature.
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Pal, Anirban. "Crohn's disease." InnovAiT: Education and inspiration for general practice 7, no. 1 (November 20, 2013): 43–54. http://dx.doi.org/10.1177/1755738013512118.

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Brinberg, Don E., and Barbara E. Berkeley. "Crohn's disease." Postgraduate Medicine 86, no. 5 (October 1989): 257–65. http://dx.doi.org/10.1080/00325481.1989.11704450.

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Dissertations / Theses on the topic "Crohn's disease"

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Lomer, Miranda Clare Elizabeth. "Dietary microparticles and Crohn's disease." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401033.

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Biasci, Daniele. "Predicting prognosis in Crohn's disease." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/270034.

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Broadhurst, J. F. "Mesenteric fat in Crohn's disease." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1467053/.

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Crohn’s Disease is a chronic inflammatory disorder of the bowel affecting approximately 1 in 800 people in the UK. The terminal ileum is most commonly affected and the mesentery becomes thickened, a phenomenon known as ‘fat wrapping’. The cause is not understood. Elemental feeding can induce remission in Crohn’s disease and polyunsaturated fatty acid (PUFA) content may be the cause of a reduction in inflammation. Particular attention has focused on n-­‐3 and n-­‐6 PUFA content of elemental feeds. The aim of this study was to further characterize mesenteric fat in Crohn’s disease and to examine the effects of different PUFA on mesenteric inflammation in vitro. Samples of adipose tissue were collected from patients undergoing intestinal resection for Crohn’s disease and from controls. These were cultured in media and elemental (E028 and Emsogen) feeds containing different concentrations of n-­‐3 and n-­‐6 PUFA. Significant findings were that mesenteric (MF) and omental (OM) adipose tissue released more inflammatory cytokines IL-­‐6, leptin and MCP-­‐1 when cultured in media rich in n-­‐6 PUFA compared to media rich in n-­‐3 PUFAs. OM mean IL-­‐6 concentrations were 18.6(3.1-­‐21.8)ng/mL in n-­‐6 PUFA vs 3.07(0.62-­‐19.10)ng/mL in n-­‐3 PUFA (p=0.018), MF IL-­‐6 concentrations were 3.77(0.76-­‐9.52)ng/mL in n-­‐6 PUFA vs 1.5(0.42-­‐2.61)ng/mL in n-­‐3 PUFA (p=0.03). OM Leptin concentrations were 0.42(0.08-­‐0.90)ng/mL in n-­‐6 PUFA vs 0.08(0.07-­‐0.14)ng/mL in n-­‐3 PUFA (p=0.006), MF Leptin concentrations were 0.27(0.13-­‐2.62)ng/mL in n-­‐6 PUFA vs 0.12(0.07-­‐0.31)ng/mL in n-­‐3 PUFA (p=0.033). OM MCP-­‐1 concentrations were 18.80(4.39-­‐31.5)ng/mL in n-­‐6 PUFA vs 1.83(0.69-­‐4.82)ng/mL in n-­‐3 PUFA (p=0.002) and MF MCP-­‐1 concentration were 4.59(2.20-­‐13.72)ng/mL in n-­‐6 PUFA vs 1.20(0.82-­‐3.39)ng/mL in n-­‐3 PUFA (p=0.006). These findings show that n-­‐6 PUFAs stimulate a greater inflammatory response from omental and mesenteric fat in vitro and may assist in formulating a more effective elemental feed for inducing remission in patients with active flares of Crohn’s disease.
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Bernell, Olle. "Surgery and recurrence in Crohn's disease /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-628-5102-0/.

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Mohiuddin, Mohhamed Khalid. "Post-operative Crohn's disease : can non-invasive faecal markers predict post-operative course of Crohn's disease." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1147.

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Background: Identifying Crohn’s disease recurrence in symptomatic patients after ileocaecal resection is difficult as symptoms may reflect the effect of surgery rather than active disease. The aim of this study was to evaluate faecal concentrations of granulocyte degradation products (faecal calprotectin and faecal lactoferrin) in this post-operative setting. Methods: A post-operative cohort of 104 patients (median follow up of 24 months) provided a single stool sample. A second cohort of 13 patients was followed prospectively for 1 year with regular faecal calprotectin (FC) and faecal lactoferrin (FL) measurements. Faecal measurements were compared with symptom diaries, the Harvey Bradshaw Index (HBI), endoscopic examination, C-reactive protein (CRP) and platelet measurement. Results: Both faecal calprotectin and faecal lactoferrin correlated significantly with Harvey Bradshaw Index (r = 0.532, P< 0.001, r = 0.687, P< 0.001 respectively). Twenty eight patients with severely clinically active disease had high mean (s.e) levels of faecal calprotectin (661.1(119.1) μg/g) and faecal lactoferrin (116.6(32.2) μg/g); and forty three patients with clinically inactive disease had low levels of faecal calprotectin (70.2(27.1) μg/g) and faecal lactoferrin (5.9(2.4) μg/g). In patients with mild to moderately clinically active disease, faecal calprotectin and faecal lactoferrin identified individuals with and without recurrent inflammatory disease. In the uncomplicated course, both markers (faecal calprotectin and lactoferrin) normalized within 2 months. Faecal markers were more accurate at predicting clinical disease activity than C-reactive protein, platelet count or endoscopic appearance. Conclusion: Faecal calprotectin and faecal lactoferrin are non-invasive tests that can help to identify disease recurrence in symptomatic post-operative patients [1].
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Baker, John Summers. "The function of innate immune genes in Crohn's disease." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.560924.

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Crohn's Disease (CD) is a debilitating condition characterised by chronic intermittent intestinal inflammation. More than 90 genetic polymorphisms are associated with CD susceptibility, including several in genes of the innate immune system. Here I present a series of experiments designed to enhance our knowledge of the roles of CD-associated polymorphisms in pathogenesis. Many therapeutic regimens are employed in CD treatment, but patients' responses to treatment and disease progression vary widely. There is great interest in studying whether analysis of patients' genotype at CD-associated polymorphisms can be used to predict their disease course, and guide clinical decision-making. To answer these questions, it is essential to be able routinely and cost- effectively to genotype patients at the full range of known CD-associated polymorphisms. The first project presented here describes the design and initial successful testing of a CD-specific genotyping microarray for use in genotype-phenotype studies. The polymorphism most strongly associated with CD susceptibility is in the pattern recognition receptor NOD2; the remaining experiments presented here study the function of NOD2 in primary human monocyte-derived Dendritic Cells (DCs). First, a microarray study is presented which characterises global transcriptional responses to NOD2 stimulation in DCs. NOD2 stimulation is shown to enhance transcriptional changes induced by Toll-Like Receptor 2 stimulation, and NOD2-mediated transcriptional regulation is shown to be lost in DCs expressing CD-associated NOD2 variants. Second, experiments are presented which describe development of a new protocol for proteomic analysis of post-translational protein modifications, and which identify a number of novel candidate targets of NOD2 signalling in DCs. Finally, a project is presented which demonstrates for the first time that NOD2 stimulation induces autophagy in DCs, in an NF-kB and RIPK2-dependent pathway. CD-associated polymorphisms in NOD2 and ATG 16Ll abolish NOD2-mediated autophagy induction, resulting in impaired bacterial handling and antigen presentation.
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Fernandez-Hernandez, Heriberto. "The Role of LRRK2 in Crohn's Disease." Thesis, Icahn School of Medicine at Mount Sinai, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10793069.

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Crohn’s Disease (CD) is a type of Inflammatory Bowel Disease (IBD) with increasing incidence worldwide. In the US alone, prevalence of CD is shown to be 214 per 100,000. CD is not fatal, but deeply impacts the quality of life of an individual. While existing therapies alleviate the symptoms of the disease, there is no cure yet. Even with proper treatment, as many as two-thirds to three-quarters of people with CD will require surgery, which involves high risk of compromised bowel function and malnutrition. Therefore, there is a great need for the development of novel therapies for treatment and prevention of the disease. A better understanding of how CD-associated genetic mutations impact biological pathways involved in disease pathogenesis could offer insights into the development of new therapeutic strategies.

An autophagy gene associated with CD is Leucine-rich repeat kinase 2 (LRRK2). LRRK2 is a multidomain protein with numerous suggested biological functions including vesicular traffic, immune response regulation and autophagy. While LRRK2’s involvement in Parkinson’s disease (PD) development has been investigated for over a decade, only recently have studies detected associations between LRRK2 mutations and susceptibility to CD. Recently, our group identified novel association signals at LRRK2 conferring CD risk, N2081D; or protection, N551K, tagging the R1398H-associated haplotype. Interestingly, the LRRK2 N2081D CD risk allele is located in the same kinase domain as G2019S, a mutation that is the major genetic cause of familial and sporadic PD.

The main goal of my thesis was to elucidate the functional consequences of these novel CD-associated LRRK2 mutations, N2081D and N551K+R1398H, on the autophagy process. To study autophagy and its role in regulating inflammation, the major component of CD, we utilized macrophages, white blood cells, important in the process of phagocytosis that highly express LRRK2. Through our study of human-derived macrophages, we found that carriers of the LRRK2 N2081D mutation exhibited impaired autophagy when compared to N551K+R1398H carriers and non-carriers. We also found that impaired autophagy in N2081D carriers was associated with increased total LRRK2 protein levels and defective lysosomal pH and tubulin acetylation regulation. Additionally, we studied autophagy in macrophages from wildtype (WT) and Lrrk2 knockout (KO) mice and found that the regulation of lysosomal pH in KO macrophages was significantly affected, further suggesting that LRRK2 may play a role in autophagy through regulation of lysosomal pH. Another experimental goal was to determine if knocking out Lrrk2 would result in changes to the microbiota in a mouse model with induced colitis and without. Specifically, we explored Lrrk2’s role in association with the microbiota and found that Lrrk2 participates in regulating microbial taxa under inflammatory circumstances.

In summary, our findings suggest that CD–associated mutations in the LRRK2 gene conferring risk (N2081D) or protection (N551K+R1398H) affect gene expression, lysosomal acidity and tubulin acetylation in monocyte-derived macrophages (MDM) implicating them in the process of autophagy. We also propose Lrrk2 as a modulator of microbiota changes under inflammation. These results should warrant future studies to explore LRRK2 as a potential target for new therapies to treat CD.

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Soroosh, Artin. "The Role of KIAA1199 in Crohn's Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1396386453.

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Simmons, Jonathan David. "Candidate genes in inflammatory bowel disease - defining susceptibility, disease phenotype and long term outcome." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249575.

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Lapidus, Annika. "Crohn's disease in Stockholm county : epidemiological panorama and associated gallstone disease /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2908-4.

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Books on the topic "Crohn's disease"

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Rajesh, Arumugam, and Rakesh Sinha, eds. Crohn's Disease. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-01913-0.

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B, Morris Jon, ed. Crohn's disease. Philadelphia: Saunders, 2001.

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B, Morris Jon, ed. Crohn's disease. Philadelphia: W.B. Saunders, 2001.

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National Institutes of Health (U.S.) and National Institute of Diabetes and Digestive and Kidney Diseases (U.S.), eds. Crohn's disease. [Bethesda, MD] (2 Information Way, Bethesda 20892-3570): National Digestive Diseases Information Clearnighouse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 1992.

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National Institutes of Health (U.S.) and National Institute of Diabetes and Digestive and Kidney Diseases (U.S.), eds. Crohn's disease. [Bethesda, MD] (2 Information Way, Bethesda 20892-3570): National Digestive Diseases Information Clearnighouse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 1992.

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Lichtenstein, Gary R. Crohn's Disease. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003523468.

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1939-, Prantera Cosimo, and Korelitz Burton I. 1926-, eds. Crohn's disease. New York: M. Dekker, 1996.

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J, Mulder C. J., and Tytgat G. N. J, eds. Is Crohn's disease a mycobacterial disease? Dordrecht: Kluwer Academic Publishers, 1992.

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Greig, Emma R. Management of Crohn's disease. London: Martin Dunitz, 2003.

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Saibil, Fredric G. Crohn's disease & ulcerative colitis. Toronto: Key Porter Books, 1996.

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Book chapters on the topic "Crohn's disease"

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Oviedo, Jaime A., and Francis A. Farraye. "Disease Modifiers in Inflammatory Bowel Disease." In Crohn's Disease, 77–90. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003523468-9.

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Alexander, A., C. Davies, and J. du Plessis. "Crohn's Disease." In ABC of Pediatric Surgical Imaging, 28–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-89385-1_14.

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Vermeire, Séverine, Gert Van Assche, and Paul Rutgeerts. "Crohn's Disease." In Textbook of Clinical Gastroenterology and Hepatology, 372–93. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781118321386.ch50.

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De Felice, Kara M., and Sunanda V. Kane. "Crohn's Disease." In Practical Gastroenterology and Hepatology Board Review Toolkit, 273–78. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119127437.ch45.

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Proctor, Briley E., and John H. Kranzler. "Crohn's disease." In Health-related disorders in children and adolescents: A guidebook for understanding and educating., 197–203. Washington: American Psychological Association, 1998. http://dx.doi.org/10.1037/10300-028.

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Torres, Joana, and Jean-Frédéric Colombel. "Crohn's Disease." In Mount Sinai Expert Guides, 366–78. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118932759.ch35.

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Weinstock, Joel V. "Crohn's Disease." In Granulomatous Infections and Inflammations, 293–320. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817879.ch11.

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Marcellier, Gabriel, and Xavier Treton. "Crohn's Disease." In Hematopoietic Stem Cell Transplantation and Cellular Therapies for Autoimmune Diseases, 489–97. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781315151366-52.

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Theisler, Charles. "Crohn's Disease." In Adjuvant Medical Care, 81–84. New York: CRC Press, 2022. http://dx.doi.org/10.1201/b22898-94.

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Dubinsky, Maria. "Crohn's Disease." In Gut Instincts, 117–22. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003524489-19.

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Conference papers on the topic "Crohn's disease"

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Niehaus, Katherine E., Holm H. Uhlig, and David A. Clifton. "Phenotypic characterisation of Crohn's disease severity." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7320009.

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Silva, Cleison Sanches, Natália C. Talim, Ana C. Cotta Queiroz, Beatriz Silva Lombardi, Clara Pinhati, Denison Pedrosa, Emerson C. Oliveira, et al. "Bilateral Optic Neuritis in Crohn's Disease." In PROCEEDINGS OF THE BCTRIMS 24TH ANNUAL MEETING. Galoa, 2023. http://dx.doi.org/10.17648/bctrims-2023-167492.

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Hauser, G., V. Licul, B. Candrlic, G. Palcevski, and D. Stimac. "ACCURACY OF IMAGING SCORING INDEXES IN PEDIATRIC CROHN'S DISEASE PATIENTSACCURACY OF IMAGING SCORING INDEXES IN PEDIATRIC CROHN'S DISEASE PATIENTS." In ESGE Days 2018 accepted abstracts. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1637087.

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Im, J., K. C. Jensen, and W. G. Kuschner. "Necrobiotic Mass in Crohn's Disease: A Case Report." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1395.

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Manerowska, Anna, Maciej Dadalski, Piotr Socha, and Jan Mulawka. "On exploration of medical database of Crohn's disease." In Photonics Applications in Astronomy, Communications, Industry, and High-Energy Physics Experiments 2010, edited by Ryszard S. Romaniuk. SPIE, 2010. http://dx.doi.org/10.1117/12.872240.

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Silva, M., A. Peixoto, S. Gomes, AL Santos, P. Moreira, A. Corte Real Nunes, S. Lopes, and G. Macedo. "PATENCY CAPSULE IN CROHN'S DISEASE – IS IT SAFE?" In ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681705.

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Oda, Masahiro, Takayuki Kitasaka, Kazuhiro Furukawa, Osamu Watanabe, Takafumi Ando, Hidemi Goto, and Kensaku Mori. "Development of CAD prototype system for Crohn's disease." In SPIE Medical Imaging, edited by Nico Karssemeijer and Ronald M. Summers. SPIE, 2010. http://dx.doi.org/10.1117/12.844590.

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Benhamdane, A., B. Aourarh, K. Boualiten, S. Berrag, T. Adioui, M. Tamzaouret, and A. Aourarh. "PREDICTORS OF CROHN'S DISEASE ACTIVITY IN BIOTHERAPY PATIENTS." In ESGE Days 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1744862.

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Novacek, G., W. Reinisch, S. Reinisch, C. Primas, W. Eigner, H. Vogelsang, C. Dejaco, et al. "Risk factors for first intestinal surgery in Crohn's disease." In 52. Jahrestagung & 30. Fortbildungskurs der Österreichischen Gesellschaft für Gastroenterologie & Hepatologie (ÖGGH). Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1691864.

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Mao, Weidong, and Jeonghwa Lee. "A Combinatorial Analysis of Genetic Data for Crohn's Disease." In 2007 1st International Conference on Bioinformatics and Biomedical Engineering. IEEE, 2007. http://dx.doi.org/10.1109/icbbe.2007.267.

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Reports on the topic "Crohn's disease"

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Qiu, Yunfeng, Changfeng Li, and Shihou Sheng. Stem cell based therapy for Crohn's disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2023. http://dx.doi.org/10.37766/inplasy2023.10.0047.

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Kostoff, Ronald N. Literature-Related Discovery: Common Factors for Parkinson's Disease and Crohn's Disease. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada525269.

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Hasstedt, Nicole. The Role of the Gut Brain Axis and Microbiome in Colorectal Cancer, Alzheimer's Disease, and Crohn's Disease. Ames (Iowa): Iowa State University, January 2019. http://dx.doi.org/10.31274/cc-20240624-1488.

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Lewis, James D., Robert Sandler, Carol Brotherton, Colleen Brensinger, Hongzhe Li, Michael D. Kappelman, Scott G. Daniel, et al. Comparing Two Diets to Decrease Symptoms from Crohn's Disease -- The DINE-CD Study. Patient-Centered Outcomes Research Institute (PCORI), October 2021. http://dx.doi.org/10.25302/10.2021.pprnd.150731465.

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Peng, Liangxin, Qiang Wu, Lichao Yang, Yawei Zhang, and Lianwen Yuan. The Impact of Preoperative Anti-TNF Therapy on Postoperative Complications in Crohn's Disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2024. http://dx.doi.org/10.37766/inplasy2024.6.0029.

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Xie, Yingxia, Letian Qiao, and Yuan Liu. Meta-analysis of efficacy and safety of ulinuzumab in the treatment of moderate to severe active Crohn's disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2023. http://dx.doi.org/10.37766/inplasy2023.11.0096.

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Shpigel, Nahum, Raul Barletta, Ilan Rosenshine, and Marcelo Chaffer. Identification and characterization of Mycobacterium paratuberculosis virulence genes expressed in vivo by negative selection. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7696510.bard.

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Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of a severe inflammatory bowel disease (IBD) in ruminants, known as Johne’s disease or paratuberculosis. Johne’s disease is considered to be one of the most serious diseases affecting dairy cattle both in Israel and worldwide. Heavy economic losses are incurred by dairy farmers due to the severe effect of subclinical infection on milk production, fertility, lower disease resistance and early culling. Its influence in the United States alone is staggering, causing an estimated loss of $1.5 billion to the agriculture industry every year. Isolation of MAP from intestinal tissue and blood of Crohn's patients has lead to concern that it plays a potential pathogenic role in promoting human IDB including Crohn’s disease. There is great concern following the identification of the organism in animal products and shedding of the organism to the environment by subclinically infected animals. Little is known about the molecular basis for MAP virulence. The goal of the original proposed research was to identify MAP genes that are required for the critical stage of initial infection and colonization of ruminants’ intestine by MAP. We proposed to develop and use signature tag mutagenesis (STM) screen to find MAP genes that are specifically required for survival in ruminants upon experimental infection. This research projected was approved as one-year feasibility study to prove the ability of the research team to establish the animal model for mutant screening and alternative in-vitro cell systems. In Israel, neonatal goat kids were repeatedly inoculated with either one of the following organisms; MAP K-10 strain and three transposon mutants of K-10 which were produced and screened by the US PI. Six months after the commencement of inoculation we have necropsied the goats and taken multiple tissue samples from the jejunum, ileum and mesenteric lymph nodes. Both PCR and histopathology analysis indicated on efficient MAP colonization of all the inoculated animals. We have established several systems in the Israeli PI’s laboratory; these include using IS900 PCR for the identification of MAP and using HSP65-based PCR for the differentiation between MAV and MAP. We used Southern blot analysis for the differentiation among transposon mutants of K-10. In addition the Israeli PI has set up a panel of in-vitro screening systems for MAP mutants. These include assays to test adhesion, phagocytosis and survival of MAP to/within macrophages, assays that determine the rate of MAPinduced apoptosis of macrophages and MAP-induced NO production by macrophages, and assays testing the interference with T cell ã Interferon production and T cell proliferation by MAP infected macrophages (macrophage studies were done in BoMac and RAW cell lines, mouse peritoneal macrophages and bovine peripheral blood monocytes derived macrophages, respectively). All partners involved in this project feel that we are currently on track with this novel, highly challenging and ambitious research project. We have managed to establish the above described research systems that will clearly enable us to achieve the original proposed scientific objectives. We have proven ourselves as excellent collaborative groups with very high levels of complementary expertise. The Israeli groups were very fortunate to work with the US group and in a very short time period to master numerous techniques in the field of Mycobacterium research. The Israeli group has proven its ability to run this complicated animal model. This research, if continued, may elucidate new and basic aspects related to the pathogenesis MAP. In addition the work may identify new targets for vaccine and drug development. Considering the possibility that MAP might be a cause of human Crohn’s disease, better understanding of virulence mechanisms of this organism might also be of public health interest as well.
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Jiang, Tianxiang, Chunjuan Liu, and Bo Zhang. Treatment of Postoperative Recurrence of Crohn’s Disease: A Systematic Review and Network Meta-analysis Protocol. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2023. http://dx.doi.org/10.37766/inplasy2023.11.0021.

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Grueso-Navarro, Elena, Leticia Rodríguez-Alcolado, Ángel Arias, Emilio J. Laserna-Mendieta, and 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, February 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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Kappelman, Michael, Jeremy Adler, Rana Ammoury, Dorsey Bass, Julie Bass, Keith Benkov, Margie Boccieri, et al. Comparing the Safety and Effectiveness of Medicines to Treat Crohn’s Disease in Children and Adolescents – The COMBINE Trial. Patient-Centered Outcomes Research Institute (PCORI), November 2023. http://dx.doi.org/10.25302/11.2023.pcs.140618643.

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