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Mouse crypts develop postnatally and are the architectural unit of the stem cell niche, yet the pathways that drive their formation are not known.
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Xenografted organoids formed crypt structures distinctively different from surrounding mouse crypts, reflecting their human origin.
These mice spontaneously develop aberrant crypt foci and have increased susceptibility to dextran sulfate sodium-induced colitis [37].
Predictions of this theory were tested using mouse crypt regeneration and mouse skin as biological models.
Furthermore, 19% of all heterozygous and 37% of all homozygous gpA33ΔN-Bcat mice spontaneously developed aberrant crypt foci and adenomatous polyps, at frequencies and latencies akin to those observed in sporadic colon cancer in humans.
Indeed, double GPX1/2 knockout mice develop spontaneous colitis, which is characterized by infiltration of neutrophils and formation of crypt abscesses, (Esworthy et al., 2001; 2003,), consistent with the pathological features of S. Typhimurium-induced enteritis.
Supplementary Figure 6 Pik3cdE1020K/+ mice develop IgM autoantibodies.
Conditional inactivation of HNF4α gene in the colon in mice resulted in a failure to develop crypts, and a series of intestinal expressed genes were affected by the lack of HNF4α expression [ 27].
On the face of it, the mouse developed normally.
All but one unimmunized mouse developed tumours.
Cyclophilin C-associated protein (CyCAP -/- miCyCAP -/-aneously developed colonic micespontaneouslyia early in life comparedeveloped-type micolonic (p < 0.0001, T-test) and crypts of colonic mucosalof thyperplasia/- micearlyw hinher proliferation rate (p = 0.039, Mann-Whitney Test) and larger number of compared1-positove cells (p < 0.0001, Mann-Whitney Test).
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