Sentence examples for mice develop intestinal from inspiring English sources
Apc heterozygous mice develop intestinal tumours on the loss of the remaining copy of Apc.
29 IL-10 is an anti-inflammatory cytokine and IL10−/− mice develop intestinal inflammation.
IL-10 knockout mice develop intestinal inflammation spontaneously, while intrarectal administration of dextran sodium sulfate (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS) in wild type mice reliably induces ulcerative colitis.
(12) The expression of Wnt target genes is significantly increased in Runx3 −/− mouse intestinal mucosa without any alteration of the expression levels of TCF4 and β-catenin, and Runx3 + /− mice develop intestinal tumors.
We correlate this clinical observation with in vivo data showing that MCD-fed mice develop intestinal permeability changes after an initial phase of liver injury and TNF α induction.
Given the relative longevity of Apc fl/+ mice and the fact that Ink4a −/− mice exhibit spontaneous tumourigenesis from 200 days of age, we approached this question by intercrossing the Ink4a −/− mice to the Apc Min/+ model of tumourigenesis where mice develop intestinal adenomas by 100 days.
The Pten-deficient male mice developed intestinal cancers (7 of 20, 35%) arising from the colorectum (n = 6) and small intestine (n = 1), whereas no female mice developed this type of cancer.
Although N1/2 cDKO mice developed intestinal hyperplasia and BCACs, we did not observe progression to adenocarcinoma in the genetic background analyzed (mixed C57B/L6-Ola129).
The Cdx2+/− mouse develops intestinal polyps with gastric differentiation and total loss of Cdx2 expression in the absence of structural loss of the second allele, suggesting a regulatory defect.
Analysis of Nod2-deficient mice confirmed decreased secretion of alpha defensins 1-6 by Paneth cells and demonstrated inability of such mice to develop intestinal inflammation, which results in their susceptibility to bacterial infection by oral administration [ 55].
To confirm our findings in zebrafish using an established mammalian model of polyposis, we examined GSK-3 and mTORC1 activity in Apc min mice, which develop intestinal adenomas through loss of heterozygosity (LOH) for Apc.
