ileitis/tyrosine

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Innate dysfunction promotes linear growth failure in pediatric Crohn's disease and growth hormone resistance in murine ileitis.

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BACKGROUND Growth failure remains a common complication of pediatric Crohn's disease (CD) and has been associated with small bowel involvement and need for surgery. We have reported that patients with elevated (≥ 1.6 μg/mL) granulocyte macrophage colony stimulating factor autoantibodies (GM-CSF Ab)

The influence of ileitis on the neurochemistry of the caudal mesenteric ganglion in the pig.

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BACKGROUND Some literature data suggest that there is a regulatory neuronal circuit between the small and the large bowel. To verify this hypothesis the present study investigated: (i) the distribution, chemical coding and routing of caudal mesenteric ganglion (CaMG) neurons participating in an

Role of inducible nitric oxide synthase expression and peroxynitrite formation in guinea pig ileitis.

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OBJECTIVE Inflammatory bowel disease is characterized by increased synthesis of nitric oxide. The aim of this study was to determine if inducible NO synthase (iNOS) was responsible for tissue injury, potentially via peroxynitrite formation, in the guinea pig model of gut

[Urinary excretion of phenol in Crohn disease during total parenteral nutrition].

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Urinary phenol is a product of dietary tyrosine metabolism generated in the gut by bacteria. In our previous study we found in 42 patients with Crohn's disease a significantly higher level of urinary phenol in terminal ileitis and ileal resection when compared with Crohn's segmental colitis. Urinary

Hypothalamic digoxin, hemispheric chemical dominance, and inflammatory bowel disease.

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The isoprenoid pathway produces three key metabolites--endogenous digoxin, dolichol, and ubiquinone. It was considered pertinent to assess the pathway in inflammatory bowel disease (ulcerative colitis and regional ileitis). Since endogenous digoxin can regulate neurotransmitter transport, the

Neurochemical coding in the small intestine of patients with Crohn's disease.

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BACKGROUND There have been conflicting results regarding the effect of Crohn's disease on the neurochemical composition of the enteric nervous system. OBJECTIVE To examine the effect of Crohn's disease on the neurochemical composition of enteric nerve fibres and cell bodies using whole mount

In vivo inhibition of RIPK2 kinase alleviates inflammatory disease.

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The RIPK2 kinase transduces signaling downstream of the intracellular peptidoglycan sensors NOD1 and NOD2 to promote a productive inflammatory response. However, excessive NOD2 signaling has been associated with numerous diseases, including inflammatory bowel disease (IBD), sarcoidosis and

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