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Control mouse colon sections (Fig. 3, 0 day) showed the intact epithelium, well defined crypt length, and no edema neutrophil infiltration in mucosa and submucosa, and no ulcers or erosions.
In situ hybridisation analysis for CXCL1 found the cellular sources for this chemokine in mouse colon sections from PHIL-DSS and WT-DSS mice to be very similar.
The number of goblet cells in the upper 100 µm of the crypt were counted in IL-10−/− and WT mouse colon sections.
Fixed mouse colon sections (6 μm) were deparafinized and rehydrated in PBS; endogenous peroxidases were neutralized with 1% hydrogen peroxide and blocked with avidin/biotin (Vector Laboratories, Burlingame, CA).
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In order to assess apoptosis, immunostaining of active caspase-3 was performed on mouse small intestine and colon sections.
Frozen sections of mouse colon (10 μm) were processed for immunohistochemistry as previously described [ 25].
Sections of mouse colon were incubated with an RNA probe recognizing both Saa1 and -2 to determine whether SAA is expressed in mouse intestinal epithelium.
At the end of the experiment, sections of mouse colon were obtained, cut open longitudinally, washed in PBS containing penicillin and streptomycin and weighed.
Positive control sections included mouse colon previously treated by N-ethyl N-nitrosourea (ENU; 250 mg kg−1), which induces MT-immunopositive crypts (Cook et al, 2000).
We also investigated the spatial relationship between transduction sites and the location of tissue-associated microbeads in colon sections from mice, which received AAV2-microbead conjugates with and without the co-attachment of Con A (Fig. 5).
(B) Colon sections obtained from mice were analyzed for their outward appearance.
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