J. Macry

TL;DR: It is suggested that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-kB in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn’s disease that can now be further investigated.

TL;DR: The mutational analyses of CARD15 in 453 patients with CD, including 166 sporadic and 287 familial cases, 159 patients with ulcerative colitis (UC), and 103 healthy control subjects provide tools for a DNA-based test of susceptibility and for genetic counseling in inflammatory bowel disease.

TL;DR: The results suggest that CARD4 does not play a major role in genetic susceptibility to IBD, and patients carrying sequence variations in their CARD4 gene had a similar phenotype to those with a normal sequence.

TL;DR: The observed excess of affected sibling clusters indicates that birth order influences the disease status and provides evidence that familial CD is a relevant tool for further studies of environmental factors and gene-environment interaction.

TL;DR: The results show that BBH and mucosa morphology of the ileum in the rat can be modified by the molecular form of the nitrogen source and that the nutritional status interferes with this adaptation, which could have implications for the therapy of small bowel disease.