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In the first phase, PPAR γ flfl; Villin Cre- (VC-) and PPAR γ flfl; Villin Cre+ (VC+) mice in a mixed FVB/C57BL/6 background were challenged with 2.5% dextran sodium sulfate (DSS) in drinking water for 0, 2, or 7 days.
SR/CR mice in the BALB/c background were challenged with J774 lymphoma (MHC haplotype H2d) or MethA sarcoma (H2d) cells.
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In the second phase, we generated VC- and VC+ mice in a C57BL/6 background that were challenged with 2.5% DSS.
5-LO deficient (5-LO−/−) mice and background wild type mice were challenged with APAP (0.3 6 g/kg) or saline.
In order to establish a two-hit model of MHV-68 infection on the background of fibrosis, mice were challenged with an oropharyngeal instillation of bleomycin (25 IU/mouse) on day 0, followed by an intranasal infection with MHV-68 (1×10 PFU) on day 14.
SR/CR mice in the C57BL/6 congenic background (generations n8 or later) were challenged with EL-4 lymphoma (H2b), LL/2 lung carcinoma (H2b), B16 melanoma (H2b) or S180 sarcoma (H2q).
After these tumours were rejected by alloantigen (H-2k/C3H background -specific effector cells, the mice were challenged with the pre-background -specific deffectorrom the original E mu/ret TGM (ret0-2).
When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of Prf-/-, Cybb-/-, or Nos2-/ did not completely abolish the SR/CR cancer resistant phenotype.
Single-housed TG and WT C57BL/6N mice were challenged with unrelated group-housed mice of C57BL/6N background.
This is true when we test tumorigenesis when mice were challenged with melanoma cells in either the mixed and or the C57/BL6 background.
That background was challenging in a home without parents.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com