S. J. Ott
University of Kiel
7 Papers
154 Citations
S. J. Ott is an academic researcher from University of Kiel. The author has contributed to research in topics: Genome-wide association study & Internal medicine. The author has an hindex of 5, co-authored 7 publications.
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Papers
Reduction in diversity of the colonic mucosa associated bacterial microflora in patients with active inflammatory bowel disease
S. J. Ott,Meike Musfeldt,D F Wenderoth,Jochen Hampe,O Brant,Ulrich R. Fölsch,Kenneth N. Timmis,Stefan Schreiber +7 more
TL;DR: Mucosal inflammation in inflammatory bowel disease is associated with loss of normal anaerobic bacteria, independent of NOD2/CARD15 status of patients.
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Bacterial and fungal microbiota in relation to probiotic therapy (VSL#3) in pouchitis
T Kühbacher,S. J. Ott,Ulf Helwig,Toshiki Mimura,Fernando Rizzello,Brigitta Kleessen,Paolo Gionchetti,Michael Blaut,Massimo Campieri,Ulrich R. Fölsch,Michael A. Kamm,Stefan Schreiber +11 more
TL;DR: Restoration of the integrity of a “protective” intestinal mucosa related microbiota could be a potential mechanism of probiotic bacteria in inflammatory barrier diseases of the lower gastrointestinal tract.
Influence of polymorphisms in the NOD1/CARD4 and NOD2/CARD15 genes on the clinical outcome of Helicobacter pylori infection.
Philip Rosenstiel,Stephan Hellmig,Jochen Hampe,S. J. Ott,Andreas Till,Wolfgang Fischbach,Hany Sahly,Ralph Lucius,Ulrich R. Fölsch,Dana J. Philpott,Stefan Schreiber +10 more
TL;DR: Host immune response influences the clinical outcome of Helicobacter pylori infection leading to ulcer disease, gastric carcinoma and mucosa‐associated lymphoid tissue (MALT) lymphoma.
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Genetic variants in matrix metalloproteinase genes are associated with development of gastric ulcer in H. Pylori infection.
TL;DR: Genetic variations in the MMP-7 and -9 gene may be part of a complex genetic risk profile to develop gastric ulcer in chronic H. pylori infection, and the level of association found is in agreement with the nature of acomplex genetic disease.
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A functional variant in the CARD4 gene and risk of premature coronary heart disease.
TL;DR: The results suggest that the analysed CARD4 mutations do not play a major role in the aetiology of CHD, and may be associated with inflammatory barrier diseases and asthma.
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