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Bernd Sido

Researcher at Heidelberg University

Publications -  28
Citations -  1117

Bernd Sido is an academic researcher from Heidelberg University. The author has contributed to research in topics: Intestinal mucosa & Lamina propria. The author has an hindex of 15, co-authored 28 publications receiving 1049 citations.

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Impairment of intestinal glutathione synthesis in patients with inflammatory bowel disease.

TL;DR: Investigation of constituent amino acid plasma levels and the GSH redox status in different compartments in IBD with emphasis on intestinal GSH synthesis in Crohn’s disease found reduced rGSH levels and increased GSSG levels were demonstrated in non-inflamed mucosa in patients with IBD.
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Carcinoid of the ampulla of Vater

TL;DR: Considering that the 5‐year survival rate in patients with neuro endocrine carcinomas of the ampulla of Vater is very low without radical resection, neuroendocrine tumors of theampullary carcinoids without definite histological differentiation should undergo extended surgery.
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Inflammatory response after abdominal surgery

TL;DR: Laroscopic surgery decreases the local and systemic production of cytokines and acute-phase reactants, and better preserves peritoneal immunity compared with open surgery, as concluded from animal studies, the gas used for the pneumoperitoneum may possess substantial immunomodulatory activity.
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Cytokine/chemokine messenger-RNA expression profiles in ulcerative colitis and Crohn's disease

TL;DR: In histologically noninflamed/inactive IBD samples mRNAs for several mediators were significantly enhanced, accompanied by elevated levels of migration-inhibition factor related protein (MRP) 14 transcripts, indicating a substantial overlap in cytokine/chemokine mRNA expression in UC and CD.
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Prolonged allograft survival but no tolerance induction by modulating CD28 antibody JJ319 after high-responder rat heart transplantation

TL;DR: CD28 antibody JJ319 induces profound immunosuppression after rat heart transplantation, however without development of transplant tolerance, and the underlying mechanism seems to be receptor modulation during primary alloantigen recognition.