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The overall poor survival of Fyn −/− ; Yes −/ − mice prevented us from assessing the contribution of those kinases in our intestinal tumourigenesis models.
The limited life span of Aptx−/− SOD1 G93A mice prevented us from assessing other hallmarks of premature ageing such as kyphosis and grey hair.
The presence of multiple tumour nodules in the lungs of the mice prevented us from assessing FDG uptake within individual lesions.
DOI: http://dx.doi.org/10.7554/eLife.02270.006 Although we found that Pak2 is required for pre-TCR β selection and positive selection in Pak2 F/F ;Lck-Cre mice, defects that occurred in DN and DP stages in these mice prevented us from studying the impact of Pak2 on a later developmental stage, namely, the SP stage.
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Unfortunately, no motor impairment was measured in untreated Surf1 −/− mice, which prevented us from further investigating the clinical features of this model under AICAR treatment.
The inability of the clonotypic antibody to recognize all CII-specific T cells in the Vβ12-tg mouse, however, prevented us from addressing the role of T cells in the later phases of arthritis development, by means of T-cell depletion studies.
The multiple co-morbidities of the Tgfbr2fspKO mice [3], [5], [6], [33] prevented us from generating chimeric mice using these as the host to track BMDC recruitment to the prostate.
Because the perinatal lethality of DT+dox mice with strong phenotypes prevented us from analysing DT +dox ; p53−/− mice for the possible development of frank tumours and further expansion of stem cell pools, we first tested for the role of p53 on GLI1-induced NS self-renewal.
Furthermore, due to the small size of the mouse heart, technical limitations prevented us from recording endocardial data.
It would be ideal to use a singe animal model but the inherent limitations for the chinchilla nasal colonization model and mouse ear infection model have prevented us from conducting these screens in the same animal model.
Intriguingly, using antibody to neutralize IFN-γ in the mice prevented the above CTL-mediated tumour cell dormancy, suggesting that tumour-specific CTLs might release IFN-γ to induce unkilled TRCs into dormancy.
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