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An example of distributional bias of genes induced under a particular condition is Vibrio cholerae which, when grown in an in vivo mouse intestinal model, shows a greater number of induced genes on the smaller of two replicons compared to growth on rich laboratory medium in vitro [61].
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For assessing the capability of various Vibrio species to elaborate an enterotoxin, rabbit and mouse intestinal models were used (33 ).
Intriguingly, β‐catenin itself activates transcription of TERT in cooperation with KLF4 in both a mouse intestinal tumor model and human cancer cell lines.
Two recent papers showing that B lymphocyte-induced maturation protein 1 (Blimp1) regulates postnatal epithelial stem cell reprogramming during mouse intestinal maturation support the model that adult intestinal stem cells are developed during postembryonic development in mammals, in a TH-dependent process similar to intestinal remodeling during amphibian metamorphosis.
This is in accordance with recent observations that F1C fimbriae contributed to E. coli persistence in an infant mouse intestinal colonisation and biofilm formation model [ 35].
Notch inhibition in normal colon epithelium induces premature differentiation of proliferating cells and treatment of APCmin mice, a mouse model of intestinal adenomas, with the potent γ-secretase inhibitor (GSI) dibenzazepine (DBZ) reduces adenomas [ 5].
In mouse models, intestinal fibrosis has been induced by either a single dose of radiation to the colorectum with set or varying lengths of tissue exposed or by worm parasite-induced or intra- rectal administration of trinitrobenzene sulfonic acid [ 79].
Other NSAIDs, e.g. celecoxib, can paradoxically enhance tumor progression in APCMin/+ mice, which model intestinal tumorigenesis [9].
Among others, extraction of up- or down-regulated genes specifically in K19-Wnt1/C2mE K19-Wnt1/C2mEmE respectively inferred that K19-Wnt1/C2mE mice world provide best-fit mouse model for intestinal-type gastric tumors.
A previous study compared two mouse models of intestinal tumorigenesis, ApcR850X (Min) and Apc1322T 1322Tthe the latter a model of human codon 1309 changes.
Mouse models of intestinal inflammation have also pinpointed a key role for Treg cells in intestinal homeostasis, as illustrated in a model of T cell driven colitis induced by the transfer of naive CD4+ T cells into RAG−/− mice [ 12- 14].
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