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Tissue-based models are correlated with in vivo models for intestinal permeability studies.
In addition, necroptosis, a relatively novel programmed necrosis-like pathway associated with TNF receptor activation, seems to be also present in the pathogenesis of Crohn's disease and in specific animal models for intestinal inflammation.
Also, administration of a DNA demethylating agent, such as 5-aza-2′-deoxycytidine, suppressed tumorigenesis in animal models for intestinal tumors [ 147], prostate cancer [ 148, 149], and breast cancer [ 150].
If the mucus coating the epithelium is more abundant in guinea pigs, this is relevant in relation to the widespread use of guinea pigs as models for intestinal Listeria infections [ 26, 27], since the integrity and thickness of the intestinal mucus layer is known to affect the susceptibility to intestinal infection [ 28- 30].
Interestingly, MBD2 antisense targeting in cultured cells showed that MBD2-depleted, lung, or colorectal cancer cell lines fail to develop tumors once injected into nude mice (Campbell et al. 2004); moreover, mouse models for intestinal tumorigenesis show a reduced tumorigenesis rate in the absence of MBD2 (Sansom et al. 2003).
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Furthermore, a support vector machine-based prediction model for intestinal bowel syndrome (IBS) was built by applying MetaDP to microbial 16S sequencing data from 108 children.
Finally, we discuss organoid cultures as a tool for studying intrinsic properties of the epithelium, as a model for intestinal disease, and as a possible source for stem cell transplantations.
In order to study neutrophil-mediated formation of carcinogenic N-nitroso compounds as a mechanism of inflammation-related colon carcinogenesis, we designed an in vitro model for intestinal inflammation, consisting of a coincubation system with human colon cells (Caco-2 cells) and activated human neutrophils (PMN), as important immunoreactive cells.
To distinguish between these possibilities, we analyzed the effects of ghrelin administration on intestinal tumor formation in ApcMin/+ mice, a genetic susceptibility model for intestinal tumors.
Also, gut-specific deletion of c-Jun decreased tumour multiplicity and increased life span in the Apc Min mouse model for intestinal cancer.
We therefore crossed op/ op mice with ApcΔ 716 mice, a model for intestinal polyposis caused by Wnt activation (Oshima et al, 1995).
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