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- Axelsson, L., et al.
(författare)
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Deriving the angular variation of p(parallel to)-distributions for halo neutrons with robust statistics
- 2001
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Ingår i: Nuclear Physics A. - 0375-9474. ; 679:3-4, s. 215-230
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Tidskriftsartikel (refereegranskat)abstract
- The longitudinal neutron momentum distribution from core breakup of Li-11 and Be-11 have been measured at 29.9 MeV/u and 38.5 MeV/u, respectively. Separate measurements on Li-9 and Be-10 allowed extraction of the halo neutron distribution. The shapes of the distributions are analyzed using robust and descriptive statistics, For both isotopes the shape is changing with angle. (C) 2001 Elsevier Science B.V. All rights reserved.
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- Hugot, J-P, et al.
(författare)
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Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease
- 2001
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 411:6837, s. 599-603
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Tidskriftsartikel (refereegranskat)abstract
- Crohn's disease and ulcerative colitis, the two main types of chronic inflammatory bowel disease, are multifactorial conditions of unknown aetiology. A susceptibility locus for Crohn's disease has been mapped to chromosome 16. Here we have used a positional-cloning strategy, based on linkage analysis followed by linkage disequilibrium mapping, to identify three independent associations for Crohn's disease: a frameshift variant and two missense variants of NOD2, encoding a member of the Apaf-1/Ced-4 superfamily of apoptosis regulators that is expressed in monocytes. These NOD2 variants alter the structure of either the leucine-rich repeat domain of the protein or the adjacent region. NOD2 activates nuclear factor NF-?B, this activating function is regulated by the carboxy-terminal leucine-rich repeat domain, which has an inhibitory role and also acts as an intracellular receptor for components of microbial pathogens. These observations suggest that the NOD2 gene product confers susceptibility to Crohn's disease by altering the recognition of these components and/or by over-activating NF-?B in monocytes, thus documenting a molecular model for the pathogenic mechanism of Crohn's disease that can now be further investigated.
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